TrueHealth

Natural Eradication of Cardiovascular Disease

2009-11-07T08:51:00.000-08:00

Natural Eradication of Cardiovascular Disease

Every second man and woman in the industrialized world dies from the consequences of atherosclerotic deposits in the coronary arteries (leading to heart attack) or in the arteries supplying blood to the brain (leading to stroke). The epidemic spread of these cardiovascular diseases is largely due to the fact that, until now, the true nature of atherosclerosis and coronary heart disease has been insufficiently understood.

Conventional medicine is largely confined to treating the symptoms of this disease. Calcium antagonists, beta-blockers, nitrates and other drugs are prescribed to alleviate angina pain. Surgical procedures (angioplasty and bypass surgery) are applied to improve blood flow mechanically. Rarely does conventional medicine target the underlying problem: the instability of the vascular wall, which triggers the development of atherosclerotic deposits.

Cellular Medicine provides a breakthrough in our understanding of the underlying causes of these conditions and leads to the effective prevention and treatment of coronary heart disease. The primary cause of coronary heart disease and other forms of atherosclerotic disease is a chronic deficiency of vitamins and other essential nutrients in millions of vascular wall cells. This leads to the instability of the vascular walls, lesions and cracks, atherosclerotic deposits and, eventually, heart attacks or strokes. Since the primary cause of cardiovascular disease is a deficiency of essential nutrients in the vascular wall, the daily optimum intake of these essential nutrients is the primary measure to prevent atherosclerosis and help repair artery wall damage.

Scientific research and clinical studies have already documented the particular value of vitamin C, vitamin E, beta-carotene, lysine, proline and other ingredients in Dr. Rath’s Cellular Health recommendations for preventing cardiovascular disease and improving the health of patients with existing cardiovascular disease.

Vitamins and Other Nutrients Can Halt and Reverse Coronary Heart Disease

Millions of people die every year from heart attacks because no effective treatment to halt or reverse coronary heart disease has been available. Therefore, we decided to test the efficacy of Dr. Rath’s Cellular Health recommendations for the number one health problem of our time: coronary atherosclerosis, the cause of heart attacks. If these Cellular Health recommendations were able to stop further progression of coronary atherosclerosis, the fight against heart attacks could be won and the goal of eradicating heart disease would become a reality.

To measure the success of this program, we did not primarily look at risk factors circulating in the bloodstream. We focused directly on the key problem, the atherosclerotic deposits inside the walls of the coronary arteries. A fascinating new diagnostic technique had just become available that allowed us to measure the size of the coronary deposits non-invasively: Ultrafast Computed Tomography (Ultrafast CT).

Ultrafast CT measures the area and density of calcium deposits without the use of needles or radioactive dye. The computer automatically calculates their size by determining the Coronary Artery Scan (CAS) score. The higher the CAS score, the more calcium has accumulated, which indicates more advanced coronary heart disease.

Compared to angiography and treadmill tests, Ultrafast CT is the most precise diagnostic technique available today to detect coronary heart disease already in its early stages. This diagnostic test allows the detection of deposits in the coronary arteries long before a patient notices angina pectoris or other symptoms. Moreover, since it directly measures the deposits in the artery walls, Ultrafast CT is a much better indicator of a person’s cardiovascular risk than measurements of cholesterol or other risk factors in the bloodstream.

Before following Dr. Rath’s Cellular Health recommendations, the patient had developed atherosclerotic deposits in the walls of his left coronary artery (white circled area in the left picture). The scans below are magnifications of the heart scan taken with Ultrafast CT.

We studied 55 patients with various degrees of coronary heart disease. Changes in the size of the coronary artery calcifications in each patient were measured over an average period of one year without vitamin supplementation, followed by one year with Dr. Rath’s Cellular Health recommendations. In this way, the heart scans of the same person could be compared before and after the vitamin program. This study design had the advantage of patients serving as their own controls.

The results of this study were published in the Journal of Applied Nutrition. The full text of this landmark study is documented at the end of this book. The most important findings can be summarized as follows: This study measured, for the first time, how aggressive coronary heart disease progresses until eventually a heart attack occurs. Without the use of Cellular Health recommendations, the coronary calcifications increased at an exponential rate (very fast) with an average growth of 44% every year. Thus, without vitamin protection, coronary deposits increased approximately half their size every year.

When patients followed the Cellular Health recommendations, this trend was reversed and the average growth rate of coronary calcifications actually slowed down. Most significantly, in patients with early stages of the disease, this essential nutrient program stopped further progression of coronary heart disease within one year. This study also gives us valuable information about the time it takes for the Cellular Health recommendations to show a repair effect on the artery wall.

While for the first six months the deposits in these patients continued to grow, albeit at a decreased pace, the growth essentially stopped during the second six months with the vitamin program. Of course, any therapy that stops coronary heart disease in its early stages prevents heart attacks later on.

It is not surprising that there is a delay of several months until the healing effect of these Cellular Health recommendations on the artery wall becomes noticeable. Atherosclerotic deposits develop over many years or decades, and it takes several months to control this aggressive disease and start the healing process. More advanced stages of coronary heart disease may take still longer before the vascular healing process is measurable. To determine this, we are continuing our study.

Can already existing coronary deposits be reversed in a natural way? The answer is yes. In individual patients, we documented the natural reversal and complete disappearance of early coronary artery deposits approximately within one year. The ongoing study will tell us how long the natural reversal takes in patients with advanced coronary artery disease.

The complete natural disappearance of atherosclerotic deposits with Dr. Rath’s Cellular Health recommendations confirms that this vitamin program contains the essential ingredients needed to start the natural healing process of the artery wall.

In patients with early coronary heart disease, this healing of the artery wall can lead to the complete, natural disapearance of atherosclerotic deposits.

In patients with advanced coronary artery disease, these Cellular Health recommendations can stabilize the artery walls, halt the further growth of coronary deposits, reverse them, at least in part, and contribute to the prevention of heart attacks.

Scientific Publications on Nutrients and Cardiovascular Disease
Learn more about Cellular Health
Abstract from Dr Rath Health Foundation

Coronary Heart Disease Is an Early Form of Scurvy

2009-09-13T10:00:00.000-07:00

Dr. Rath’s Scientific Discovery in Heart Disease

Dr. Rath’s research reveals that coronary heart disease occurs exactly for the same reason that clinical (early) scurvy does – a deficiency of vitamin C in the cells composing the artery wall. Humans, unlike animals, develop heart disease because their bodies cannot produce vitamin C. The average diet provides enough vitamin C to prevent scurvy, but not enough to guarantee stable artery walls. As a consequence of vitamin C deficiency, millions of tiny cracks and lesions develop in the artery walls. Subsequently, cholesterol, lipoproteins and other blood risk factors enter the damaged artery walls to repair these lesions.

In the case of chronic vitamin deficiency, this repair process becomes continuous. Over the course of many years, atherosclerotic deposits develop. Deposits in the arteries of the heart eventually lead to heart attack; deposits in the arteries of the brain lead to stroke.

Dr. Rath identified and our research has proven that atherosclerosis is nature’s plaster cast for weak and cracked arterial walls that are chronically deficient in vitamin C and other essential nutrients. One of these nutrients is the amino acid lysine. Lysine is called an essential amino acid because, similar to vitamin C, it cannot be produced in the human body. Lysine, together with another amino acid, proline, is the main component of collagen. These two amino acids comprise about 25% of all amino acids in the collagen molecule. A deficiency of lysine and proline can also trigger blood vessel wall weakness and instability.

Research and clinical studies conducted by Dr. Rath confirm that the most important function of vitamin C in preventing heart attacks and strokes is its ability to increase the production of collagen, elastin, and other reinforcement molecules in the body. This groundbreaking discovery in heart disease should be taught in every medical textbook and school and explains why other cardiovascular conditions, including heart failure, irregular heartbeat, high blood pressure and circulatory problems in diabetes, occur in the case of long-term vitamin deficiencies.

http://www.drrathresearch.org/sci_discoveries/heart_disease.html

The Cholesterol Myths

2009-09-13T09:21:00.000-07:00

UFFE RAVNSKOV
author of The Cholesterol Myths

UFFE RAVNSKOV is radical. He is so radical that, on a television show in Finland, his critics set his book on fire!

His website (or a website about him) says: If you think this is written by another internet crackpot, take a look at Dr Ravnskov's credentials and the reviews of his book.

The book in question is titled The Cholesterol Myths. Its main argument is that cholesterol is not harmful to health but, in fact, healthy. Its author is certainy no internet crackpot. His credentials are, indeed, impressive.
Uffe Ravnskov graduated with a medical degree in 1961 and, in 1973, obtained a PhD in Chemistry. Between 1975 and 1979, he was Assistant Professor at the Department of Nephrology, University Hospital, in Lund, Sweden. Ravnskov went into private practice in 1980 and, in 2000, retired to become a full-time independent researcher.

More significantly, Uffe Ravnskov has published over 80 scientific papers and letters in peer-reviewed journals criticizing what is commonly called the Lipid Hypothesis of heart disease – the belief that dietary saturated fats and cholesterol clog arteries and cause atherosclerosis and heart disease.
Uffe Ravnskov began studying cholesterol in 1989, the year Sweden launched an anti-cholesterol campaign.

“Very soon I realised that the scientific evidence behind the campaign was non-existing,” he writes.

Among the many research findings published in scientific journals, Uffe Ravnskov discovered that:

lowering cholesterol did not result in lower death rates from heart disease, but in HIGHER death rates from all causes.

drug trials with an allegedly positive outcome was cited almost only by the trial directors, although the numbers of trials with an allegedly positive and a negative outcome were identical.

the successful dissemination of the diet-heart idea is due to authors systematically ignoring or misquoting discordant studies.
Uffe Ravnskov also discovered that LDL, commonly called “bad cholesterol”, actually protects against infections. This led him to put forward the hypothesis that high cholesterol, rather than promoting atherosclerosis, in fact may protect against it.

Uffe Ravnskov first summarised his research findings in a book, first published in Sweden in 1991, whose title translates to The Cholesterol Myths.

In 1992, the book was published in Finland. That was when his critics burned the book during a television show about it.

In 2000, an updated and expanded English edition of The Cholesterol Myths was published in the United States.

In 2002, a German edition of The Cholesterol Myths was published.

In his book, Uffe Ravnskov critically analyzes and demolishes the nine main myths of the Lipid Hypothesis:

High-fat foods cause heart disease
High cholesterol causes heart disease
High fat foods raise blood cholesterol
Cholesterol blocks arteries
Animal studies prove the diet-heart idea that diet affects heart disease
Lowering your cholesterol will lengthen your life
Polyunsaturated oils are good for you
The cholesterol campaign (to have people reduce their cholesterol levels) is based on good science
All scientists support the diet-heart idea.
All the above statements, Uffe Ravnskov maintains, are NOT TRUE. And he backs his assertions with solid scientific research.

Ancel Keys' Seven Countries Study

Uffe Ravnskov starts off with a critical analysis of the original 1950s research that gave rise to the idea that saturated fats and cholesterol cause heart disease – Dr Ancel Keys Six Countries Study, which later became the more famous Seven Countries Study published in 1980.

The Seven Countries Study – which gathered data on heart disease of some 13,000 men in Greece, Italy, Croatia, Serbia, Japan, Finland and the Netherlands over several decades – is widely considered to be one of the greatest epidemological studies ever undertaken.

Ancel Keys' Seven Countries Study showed that countries with the highest animal fat intake have the highest rates of heart disease. And this is frequently cited as “proof” that saturated fats and cholesterol cause heart disease.

Uffe Ravnskov informs us, however, that Ancel Keys had deliberately hand-picked the countries he included in his studies. In other words, Ancel Keys chose to study only those countries that supported his hypothesis.

Yet there are many other countries where high consumption of animal fat DID NOT cause heart disease. But, Ufee Ravnskov points out, Ancel Keys ignored those countries.

Dangers of statins and other cholesterol lowering drugs

Uffe Ravnskov is also highly critical of statins, the cholesterol-loweing drugs that are widely hailed as miracle “wonder drugs”.

He presents scientific evidence that show:

drug trials involving statins produced only neglible reductions in the rates of heart disease
lowering cholesterol did not reduce the death rate from heart disease but INCREASED the overall death rate from all causes
whatever positive benefits associated with the use of statins are due to factors other than cholesterol-lowering.
statins are probable carcinogens and women on statins have reported higher rates of breast cancer.
Uffe Ravnskov warns that exposure to carcinogens may result in cancer only after 20 or more years. And since there has not been controlled studies on statins over such long periods, we do not know whether the use of statins will lead to increased rates of cancer in the coming decades.

"“Millions of people are being treated with medications the ultimate effects of which are not yet known.”
– Uffe Ravnskov

Of course, it is not just Uffe Ravnskov saying all this and more. What he tells us about saturated fats and high cholesterol foods comes mainly from studying the reports of other scientists. He further tells us that…

The reason why laymen, doctors and most scientists have been misled is because opposing and disagreeing results are systematically ignored or misquoted in the scientific press.

Cholesterol sceptics

Myth Number 9 in Uffe Ravnskov's book is that “All scientists support the diet-heart idea.”
This certainly is not true and Uffe Ravnskov has gathered a large – and growing – group of doctors, scientists, academics and science writers in The International Network of Cholesterol Skeptics (THINCS).

Members of the group may disagree about what causes heart disease. But they share one thing in common.

The website of THINCS state:
"For decades, enormous human and financial resources have been wasted on the cholesterol campaign, more promising research areas have been neglected, producers and manufacturers of animal food all over the world have suffered economically, and millions of healthy people have been frightened and badgered into eating a tedious and flavorless diet or into taking potentially dangerous drugs for the rest of their lives.
As the scientific evidence in support of the cholesterol campaign is non-existent, we consider it important to stop it as soon as possible."

http://www.stop-trans-fat.com/uffe-ravnskov.html

Saturated Fat - The misunderstood nutrient

2009-09-12T11:22:00.000-07:00

by by Vreni Gurd | Fri, 04/06/2007 - 11:15pm

We are told that saturated fat and trans fat are terrible for us. The distinction must be made. Saturated fats are healthy, trans fats are not.
Saturated fats have been vilified as being the cause of heart disease, some cancers, and the obesity epidemic. Although heart disease and cancer were rare before 1920, the incidences of these diseases have increased dramatically since then. By as early as 1950, heart disease was the leading killer of Americans. However, contrary to what one would expect if the saturated fat/heart disease hypothesis were true, the consumption of animal fat between 1910 and 1970 DECREASED by 21% and the consumption of butter DECREASED from eighteen pounds per person per year to only four, according to the research of Sally Fallon and Mary Enig. Furthermore, over that same time span the consumption of refined vegetable oils much of it consumed as partially hydrogenated or trans fat, INCREASED by 400%, and the consumption of sugar and processed foods INCREASED by 60%. Current Canadian 2006 data (thank you Chris Williams!) suggest that those trends are continuing, with a continued decrease in the consumption of high saturated- fat foods like full-fat milks, eggs and red meat between 1970 and 2006. Since 1981, butter consumption (a saturated fat) has decreased by a third, while the consumption of salad oil (refined and therefore rancid polyunsaturated vegetable oils) has more than tripled. Shortening consumption (a trans fat) has remained relatively constant. So considering the continued decline in saturated fat consumption, blaming heart disease on saturated fat makes no sense (see this study published in the Lancet). To fully understand how it is possible that we find ourselves in this position where we are being told to eat refined polyunsaturated vegetable oils which are disease-causing and avoid saturated fats which are health promoting, read The Oiling of America by Mary Enig, PhD, fats and oils researcher, and Sally Fallon. The insight into the politics of food is scary.

All fats and oils are made up of a mixture of saturated, mono and polyunsaturated fatty acids. Calling animal fats "saturated fats" is very misleading, as many animal fats are actually more than 50% unsaturated, and chicken fat is actually 70% unsaturated. If a fat were completely saturated it would be very solid with the consistency of hard wax. For example, beef fat or tallow is made up of about 50% saturated fatty acids (25% palmitic acid, 22% stearic acid and others), 40% monounsaturated fatty acids (oleic acid, the main fatty acid in olive oil), and the balance polyunsaturated fatty acids (linoleic and linolenic, the ratio depending on the diet of the cattle).

Saturated fatty acids are critical to maintaining the structure and rigidity of our cells by making cell membranes out of phospholipids and cholesterol, and they act as enzyme and hormone regulators thereby playing an integral role in cell messaging. When the body is fooled and incorporates trans fats into the cell membrane instead of saturated fats, cell messaging no longer works, which is one of the reasons trans fats are so dangerous.

Saturated fats are necessary for calcium to be incorporated into our bones, so no-fat or skim milk won't work as a calcium source, unless you eat some saturated fat in your meal. Saturated fats are needed to boost immune function, and to build a healthy nervous system and digestive tract. Saturated fats are the base material out of which the body makes cholesterol, which is the precursor to such critical hormones as vitamin D, cortisol, testosterone, estrogen and progesterone, as well as bile acids which are necessary for the digestion of fats. Fats also are needed as carriers for the fat soluble vitamins (the antioxidant vitamins), like vitamin A, E, D, K, and a low fat diet can lead to deficiencies in these nutrients. Saturated fats are also needed to be able to utilize omega 3 fatty acids easily. Breast milk is high in saturated fat for a reason - it is vital for the healthy development of the baby! Does it make sense that saturated fats which are vital for a baby are suddenly poison for an adult?

Fat is also needed to feel satisfied after a meal. Mary Enig says in her book Know Your Fats: The Complete Primer For Understanding the Nutrition of Fats, Oils, and Cholesterol that "as a result of the presence of fat in the small intestine, special hormones are produced that prevent hunger contractions. ... Too much fat in the diet and the loss of weight is thwarted; too little and the hunger pangs play havoc with good intentions and usually lead to overeating carbohydrates."

Saturated fatty acids can be broken down into three groups - short chain, medium chain and long chain. The short and medium chain saturated fatty acids don't turn into body fat unless consumed in very large quantities, but rather are utilized immediately by the body for energy. Therefore fats that contain more short to medium chain fatty acids have less calories than the same amount of longer chain fatty acids. According to Mary Enig, in her book Know Your Fats: the Complete Primer for Understanding the Nutrition of Fats, Oils and Cholesterol, a pound of coconut oil has 100 kilocalories less than a pound of soybean oil. And yes, butter has less calories than margarine, although not much less.

If you are eating high quality fats, such as pasture fed, non-medicated, organic eggs, dairy, poultry, and meat, you are doing your body good. If you are eating conventionally raised poultry and meat, it is a good idea to cut off the fat, as the medications, hormones and pesticides consumed by the animal will be concentrated in the fat, which will in turn be concentrated in your fat. Cook only with pasture-fed organic butter, ghee, tallow or chicken fat, or organic coconut oil, or unrefined or cold pressed extra virgin olive oil (low to medium temperatures only), as these fats are stable and won't oxidize and go rancid when heated. To find out what ratio of fat, protein and carbohydrates are appropriate for you according to your own personal biochemistry, get yourself metabolically typed at Healthexcel, and receive a food list of appropriate foods for you. Some people require more quality fats to be healthy than others.

High Cholesterol does NOT cause heart disease

2009-09-12T09:42:00.000-07:00

by Vreni Gurd | Fri, 04/13/2007 - 11:48pm

The lipid hypothesis needs to be re-evaluated - it has very serious flaws.
First of all, it is important to understand that that "risk factor" does not mean the same thing as "cause". A risk factor is a characteristic that is associated with a diagnosis. For example, for women, being tall is associated with breast cancer. Does that mean that being tall causes breast cancer? Of course not.

It is also important to understand cholesterol is an essential component of our cell membranes, it acts as an anti-oxidant, it is a precursor for the synthesis of vitamin D as well as bile for digesting fats, and is the only source out of which our steroid hormones, such as cortisol, as well as estrogen, progesterone and testosterone which are key to reproduction, can be made. Therefore it is safe to say that without cholesterol we would not survive. Cholesterol is also the precursor to calcitrol, the steroid hormone that regulates calcium levels in our bodies by helping us absorb calcium from our food, thus playing a key role in the mineralization of our bones and teeth. Cholesterol is also manufactured in the glial cells of the brain to aid with synapses.

Cholesterol is used by our bodies to repair lesions in the arteries. Dr. Mary Enig, fat researcher, suggests that blaming cholesterol for heart disease is something like blaming firefighters for starting fires. Is it really a good idea to reduce our arteries' firefighters? The key to stopping heart disease is to stop the lesions (fires) in the arteries from occurring in the first place, by minimizing glycation by eating less sugar and high fructose corn syrup, and minimizing free radical damage by not consuming refined and therefore rancid vegetable oils AND by reducing systemic stress.

Our bodies consider cholesterol to be so essential to our survival, that every cell in our body can manufacture it as needed. If we eat little or no cholesterol, our bodies manufacture more, and if we eat a lot, our bodies don't manufacture as much. This way our cholesterol levels maintain homeostasis irrespective of our diet, and this is the reason it is so difficult to reduce or raise cholesterol levels much with diet alone.

Dr. Uffe Ravnskov, MD, PhD, who wrote the book The Cholesterol Myths, goes through study after study destroying the idea that high cholesterol levels are the cause of heart disease. In the Framingham heart study done near Boston that spanned 30 years , the researchers concluded that high cholesterol was a risk factor for heart disease, but when one really dissects the data, one must question how they came to that conclusion. For example, when the participants of the study are plotted on a graph it clearly shows that those with cholesterol levels between 182 and 222 did not survive as long as those with higher cholesterol levels of between 222 and 261. The study shows that about half the people with heart disease had low cholesterol, and half the people without heart disease had high cholesterol.

Most studies have found that for women, high cholesterol is not a risk factor for heart disease at all - in fact, the death rate for women is five times higher in those with very low cholesterol. In a Canadian study that followed 5000 healthy middle-aged men for 12 years, they found that high cholesterol was not associated with heart disease at all. And in another study done at the University Hospital in Toronto that looked at cholesterol levels in 120 men that previously had heart attacks, they found that just as many men that had second heart attacks had low cholesterol levels as those that had high. The Maoris of New Zealand die of heart attacks frequently, irrespective of their cholesterol levels. In Russia, it is low cholesterol levels that are associated with increased heart disease. The Japanese are often cited as an example of a population that eat very little cholesterol and have a very low risk of heart disease. But the Japanese that moved to the US and continued to eat the traditional Japanese diet had heart disease twice as often as those that maintained the Japanese traditions but ate the fatty American diet. This suggests that it is something else, like stress perhaps, that is causing the heart disease.

Dr. Malcolm Kendrick noticed that in the MONICA study that has been going on for about 40 years, there is no association between high cholesterol levels and heart disease. See the graph for yourself at the bottom of the article. (Dr. Kendrick wrote another interesting piece about the "disappointing results" of low fat diets in the Women's Health Initiatives heart intervention study, and the lack of association between death rates from CVD and saturated fat consumption based on the MONICA study).

These are but a small sample of the studies that contradict the idea that cholesterol is the villain in heart disease. So why has this idea held on so long? Perhaps pharmaceutical companies and the processed-food industry have a lot to gain by keeping this belief alive. Statin drugs (Lipitor, Mevacor, Zocor etc.) are mega money makers, and they definitely do lower cholesterol, but if high cholesterol does not cause heart disease, why are they necessary?

Furthermore, statin drugs may not lower overall mortality rates, as lower cholesterol levels seem to be associated with higher rates of cancer. Statin drugs work by blocking the synthesis of mevalonate, which is a vital step in the body's
synthesis of cholesterol. By blocking this step, every following step is also blocked, and this is a problem, because the synthesis of Coenzyme Q10 (ubiquinone) and squalene, both precursors to cholesterol, is also blocked. Coenzyme Q10 is very important for heart function, it acts as an antioxidant in conjunction with Vitamin E, and it is important in energy metabolism in the mitochondria of muscles, which is why muscle pain is a common side effect of statin drugs. Coenzyme Q10 is important for healthy brain function as well, and when Coenzyme Q10 levels are low, through statin use or otherwise, memory is affected. Squalene is also an antioxidant and is a potent cancer fighter. If you are on statin drugs, supplementing with Coenzyme Q10 and squalene may be very helpful.

I realize that suggesting that cholesterol levels are not associated with heart disease goes against current dogma. I am not making this suggestion in order to create controversy. After looking at the evidence, I am convinced that we are going down the wrong path. I am not alone in thinking this way - there are more and more scientists and physicians that believe that cholesterol and saturated fat stand wrongly accused. For me, the epidemiological evidence is most convincing. If we ate saturated fat and cholesterol in the form of animal fats, eggs, and full-fat dairy liberally for millennia and were heart-disease free up until the early 1900s, and just as we reduced our consumption of these foods and replaced them with sugar, vegetable oils and processed food, heart disease rates began to climb - to me it seems rather obvious that we are putting the blame on the wrong thing. Feel free not to believe this idea, but please don't simply dismiss it out of hand, either. If you have high cholesterol and you are taking, or thinking about taking cholesterol-lowering drugs, please read The Cholesterol Myths: Exposing the Fallacy that Saturated Fat and Cholesterol Cause Heart Disease so that you can make an informed decision regarding this important issue. Two other very well researched books worth reading, written by scientists but geared to the lay person are Nutrition and Physical Degeneration, by Dr. Weston A. Price, on primitive cultures, their health and their eating habits versus more modern cultures, their health and their eating habits (probably the most important book on nutrition ever written), and Mary Enig's book on lipid chemistry, Know Your Fats: The Complete Primer For Understanding the Nutrition of Fats, Oils and Cholesterol. These books are each very different from the other, but they will open your eyes to the other side of the argument, and only then will you be able to come to an informed conclusion on this issue.

Vitamin E Deficiency

2009-05-24T06:55:00.001-07:00

The Untold Epidemic Vitamin E Deficiency by Ladd McNamara, M.D.

It is clear that there is an epidemic vitamin D deficiency (see posting about vitamin D below). Few people are aware that there is also a serious epidemic deficiency of vitamin E. An editorial that accompanied the largest study on vitamin E in medical history (Am J Clin Nutr 2006 Nov;84(5):1200-7) stated 93% of American men and 96% of American women do not obtain the [pathetically low] recommended dietary allowance of 15 IU of vitamin E per day. It is clear that we should be taking at least 30 to 50 times that level (400 to 1000 IU/day) to reduce the risk of chronic diseases. Taking this much vitamin E in the correct form and balance with other vitamins, is both safe and effective; more than the pharmaceutical companies would have you believe. However, it is in the economic interest of pharmaceutical companies to dissuade the public from taking supplements so that they can be on medications which often do little to nothing to reverse disease. Other health practitioners make their living by “educating” others that they can get everything they need from their food alone. The medical research indicates otherwise. The amount of vitamin E, as well as other important vitamins, required to reduce the risk of chronic diseases can only be obtained through supplementation.

Tragically many doctors and the lay person have the misconception that vitamins, such as vitamin E supplementation may be harmful. There seems to be continued misinformation put out in news media and health magazines, regarding the “dangers” of supplementation. Either they are not aware of the medical research, or they are purposefully misleading the public for their own gain. This non-stop attempt to persuade people not to supplement, but to get all their antioxidants from their food alone is at minimum unethical, at worst dangerous. Vitamin E seems to be in these detractors line of fire more than any other nutrient, probably because it is the most common supplement used today. With the thousands of medical studies showing the benefits of supplemental vitamin E, how is it that there is still controversy and confusion? The doses of vitamin E that research has shown to be of benefit can ONLY be obtained through proper supplementation.

Almost weekly a new study about the benefits of vitamin E is published. Almost all show health benefits or potential health benefits. Because vitamin E is one of the most popular supplements, it is only when a medical study or report showing a possible negative effect it is reported by the media, either to make headlines, and/or to scare people away from taking this incredible vitamin. The negative findings regarding vitamin E of a few medical reports have either shown to be excessively biased, restricting other important vitamins that work synergistically with vitamin E, poorly designed, or bearing no cause and effect of vitamin E to a detrimental health impact. The studies of vitamin E that have shown a true potential negative impact are few, but of more importance it has given us clarity regarding the synergistic impact of various vitamins as well as the importance of the formulation of vitamin E.

Vitamins must work together for optimal benefit:

Studies published many years ago showed that for vitamin E to continue to function as an antioxidant within the body, adequate levels of vitamin C must be present to regenerate (donate more electrons) to vitamin E so that it can continue to prevent oxidation of lipids. Any study about vitamin E that restricts the participants from also taking vitamin C is setting up the study to show nothing more than how vitamin E is quickly “used up,” and not regenerated to continuously provide an antioxidant benefit. It tells us nothing about the real benefits that can be obtained from proper supplementation.

The correct formulation of vitamin E is critical:

Vitamin E is a family of nutrients; alpha, delta, and gamma-tocopherols and tocotrienols. There is a difference between the synthetic (petroleum-derived) vitamin E, dl apha-tocopherol , and the natural (food-based ) vitamin E, d alpha-tocopherol. Gamma-tocopherol is a critical form of vitamin E needed to reduce the oxidation of lipids (cholesterol) in conjunction with alpha-tocopherol. (J Am Copll Cardiol. 1999 Oct:34(4):1208-15, Pro Natl Acad Sci USA, 1993 Mar 1:90(5):1771-5) In addition, studies have shown that people who supplement solely with vitamin E in the alpha-tocopherol form are at risk to lower the blood levels of a critical form of vitamin E, gamma-tocopherol. (J Nutr. 2003 Oct:133(10):3137-40; J Nutr.1985 Jun:115(6):807-13 ) The average American’s blood-stream is five times more rich in alpha-tocopherol than gamma-tocopherol, and that difference jumps 20-fold among people who take vitamin E as alpha-tocopherol without gamma tocopherol.

In 2007, a negative study about vitamin E (that lingers as the “justification” for the case against vitamin E) highlights the way the public can be mislead to make some poor decisions about supplementation. (JAMA Feb 27, 2007). This was a flawed study with flawed data that concluded that vitamins A and E “significantly increased the risk of mortality.” This meta-analysis (report) did very little to help us understand the benefits of vitamin E, but showed us just how data, and the public’s opinion, can be manipulated. The authors of this meta-analysis (which is not a study per se, but a review of previous published studies) considered 815 prior studies regarding antioxidants, but included the results of only 68 of these studies for analysis. Some of the studies excluded from their report showed significant benefits and reduction of mortality from taking supplements. Selection bias was glaringly evident. The authors essentially “cherry-picked” the studies they wanted, and ignored others, so that they could come to their desired conclusion: vitamin E can kill you!

The authors were unable to establish any cause and effect between supplementation with vitamin E and an increased risk of death, making this a poorly designed study. The elderly people who died could have just as easily died from accidents, medications, surgery, etc. …who knows? One noted researcher described this report a kin to “doing a cholesterol-lowering study without ever measuring cholesterol levels.” Furthermore, the average duration of the reviewed studies was 2.7 years, so the ridiculous conclusion that the authors wanted the public to believe was that vitamin E could kill you (somehow) in less than 3 years!

The others ignored many studies showing significant benefits derived from supplemental vitamin E. One such study that was ignored by these researchers was the November 10, 2006 study published in the American Journal of Clinical Nutrition which is the largest study on vitamin E in medical history measuring alpha-tocopherol in male smokers. (Am J Clin Nutr 2006 Nov;84(5):1200-7) This study followed 29,000 patients for over 19 years, and included over 13,000 deaths, …making possible a significant and fair analysis of vitamin E and the risk of death.

This study showed a significant reduction in overall mortality in those patients with the highest blood levels of alpha-tocopherol. Specifically, over a 19-year period men with the highest blood levels of alpha-tocopherol showed the following reduction in causes of death:
Prostate Cancer 32% Reduction of Death
Ischemic Stroke 37% Reduction of Death
Hemorrhagic Stroke 35% Reduction of Death
Lung Cancer 21% Reduction of Death
Respiratory Illness 42% Reduction of Death
The authors of this significant and powerful study stated: “As a primary fat-soluble antioxidant that protects lipids from peroxidation, alpha-tocopherol is able to scavenge mutagenic free radicals and inhibit the oxidation of LDL-cholesterol, and the abilities have important implications for the prevention of carcinogenesis and atherosclerosis ….alpha-tocopherol also has several important functions that are independent of its antioxidant activity, including modulation of gene expression, enhancements of immune responses , an suppression of tumor angiogenesis.”
The researchers further elaborated that although the patients who enjoyed the greatest health benefits had higher blood levels of alpha-tocopherol, these same subjects also had the highest levels of gamma-tocopherol, meaning that these people were taking the natural formulation of vitamin E, not dl-alpha-tocopherol without gamma-tocopherol and the tocotrienols. This study, and other significant studies are ignored by the media, and obviously by doctors who are continually visited and educated by pharmaceutical companies.

Certainly, there are tens of thousands of studies reporting the benefits of various nutritional supplements. They are both safe and effective. If doctors and the public were simply made aware of the poorly designed analyses that denigrate vitamin E supplementation, and the significant studies about the benefits of taking vitamin E, in the form of alpha-tocopherol and gamma-tocopherol (along with delta-tocopherol and the mixed tocotrienols) along with vitamin C and vitamin K, which replenishes the antioxidant abilities of vitamin E, then I believe that not only would people need less medication and reduce the economic crisis in the health care industry, but more importantly people could enjoy the true health and happiness that can be obtained by eating right, exercise, and proper supplementation with a full spectrum of quality vitamins and minerals.

Vitamin E, in the natural form (as described above), appears to be safe up to at least 2000 IU per day. I personally take 800 IU per day of the full spectrum of vitamin E. When I was in medical practice, I recommended at least that much (if not up to 1200 IU of vitamin E) to patients with diabetes. The natural form of vitamin E, along with co-enzyme Q10, the red grape extract (grape seed extract and resveratrol) and a full spectrum of other antioxidants (quercetin, alpha lipoic acid, turmeric extract, olive extract, green tea extract, etc.), vitamins (B, C, D, and K), and minerals in the chelated form, all contribute to safely and significantly reduce the risk of heart disease, stroke, cancer, Alzheimer’s disease, lung diseases, and almost every other chronic degenerative disease, as well as slow the aging process, all without the side-effects of drugs.

Posted by Ladd McNamara at 12:10 PM

Cataracts: Reduced Risk with Vitamin E, Lutein, Zeaxanthin and Grape Seed Extract

2009-05-24T06:46:00.000-07:00

In recent study published in the Archives of Ophthalmology (Arch. Ophthalmol. 2008;126:102-9) gathered from the Women's Health Study, vitamin E and the carotenoid lutein were both found to be associated with a reduced risk of cataracts.

The Women's Health Study (WHS) was a randomized, placebo-controlled trial involving nearly 40,000 women health professionals aged 45 years and older at inception of the study in 1993.

In this recent study gathered from the WHS, the researchers assessed the antioxidant intake (from food and supplements) of 35,551 women and followed them for an average of ten years. They divided the women's intake into 5 groups, ...groups with the lowest intake, to the next highest intake, to the next highest intake, etc. When women with the highest intake of lutein/zeaxanthin (mean intake of 6.7 mg/day) were compared to the group with the lowest intake (mean of 1.2 mg/day) they found an 18% decrease in the risk of cataracts.

Similarly, when women in the highest intake group of vitamin E (mean 262 mg/day, or 390 IU/day; 1 mg alpha-tocopherol = 1.49 IU) were compared to women in the lowest intake group of vitamin E (mean 4.4 mg/day, or 6.5 IU/day), there found a 14% decrease in cataracts.

This study adds to existing observational studies that xanthophyll carotenoids lutein (and its stereo-isomer, zeaxanthin) may delay cataract formation. (BTW, in animal studies, grape seed extract has been found to reduce the formation of cataracts as well.) Lutein and zeaxanthin concentrate in the tissues of the eye, ...including the lens and retina.

Personally, I take a broad spectrum multi-antioxidant and minerals in chelated form, fish oil, grape seed extract, and additional lutein/zeaxanthin and bilberry extract supplement (for a total lutein intake of 13 mg per day, ...well above the mean intake of the top fifth group of this study). In addition, I take an additional vitamin E supplement, that has the full family of vitamin E (d-alpha tocopherol, d-gamma tocopherol, delta tocopherol, and the tocotrienols), for a combined total of 600 IU/day.

For optimal eye health of the lens and retina (macular degeneration is the number one cause of blindness after the age of 40), as well as maintaining health in a time of increasing risk of chronic degenerative disease, I recommend an optimal intake of various antioxidants, vitamins, minerals, and essential fatty acids.

Posted by Ladd McNamara at 9:05 AM

Rebuttal to the Recent FLAWED Report that Antioxidants Shorten Lifespan

2009-05-24T06:42:00.000-07:00

Here we go again. It was predicted and expected ....more "bad news" for those taking supplements in the form of a recent "study" indicating that vitamins (antioxidants) may decrease your lifespan. ....Well, not so fast! I have included an article from Life Extension Foundation (see below) addressing the flawed analysis of this study ...and more importantly the lack of "cause and effect" between antioxidants and premature death. (What is so absurd about all this is that the opposite truly exists, ... that is, an association between antioxidants and the reduced risk of premature death.) Before I get to that, I have my own editorial.

Believe it or not, there is a war of information regarding the supplement industry and the pharmaceutical industry. This was not the first, and it will not be the last that some "study" comes out telling us that we, who take supplements, are going to die, or in this case not live as long due to taking antioxidant supplements. Our alternative is not to take any supplements, and therefore become eligible to take prescription drugs (which course, have side effects, incluing death ....over 100,000 people die each year in the U.S. alone DIRECTLY FROM TAKING PRESCRIPTION MEDICATIONS ....and this is under the supervision and management of doctors and nurses).

This is NOT the case for nutritional supplements. People are not dying of premature deaths from their nutritional supplements, ...but, somehow we accept that drugs are more "acceptable" than supplements in maintaining health. It makes no sense at all. It is true, that the formulation and amounts of vitamins, minerals, and antioxidants matter .... not in their risk of death, but in regard to the true benefits they can provide. For example, there is a BIG difference between taking 60 to 120 mg of vitamin C in the ascorbic acid form, and 1300 mg per day of vitamin C in the vitamin C ascorbate form. With the first, one will do little more than prevent scurvy, whereas with the later, one may prevent the onset of chronic degenerative disease and possibly extend one's longevity.

There is a difference between taking 15 to 30 IU/day of vitamin E in the dl-alpha tocopherol form, vs. 400 to 800 IU/day of vitamin E in the mixed tocopherol (d-alpha tocopherol, gamma tocopherol, delta tocopherol) and tocotrienol formulation. The first will ....well, I'm not sure what 15 to 30 IU of vitamin E does, but I do know what the studies on using the natural mixed tocopherol form of vitamin E indicates ....less risk of many types of cancer, decreased risk of heart disease, AND decreased mortality.

In regard to extending one's lifespan, the single BEST way to increase longevity is NOT TO DIE!

I have studied the medical literature, and one of the biggest frustrations regarding studies on supplements (vitamins, minerals, and antioxidants) is that they were never meant to be taken in isolation. Supplements are meant to be taken in the proper ratios, amounts, and balance. Formulations make a difference; and most of these "reports" (meta-analyses) are comparing apples and oranges.

The authors of this latest round of anti-supplement propaganda (like prior anti-supplement reports) cherry picked their studies, leaving out some powerful studies showing a decrease in heart disease, cancer, and death from any cause. Again, if we are to live longer we must not die of a chronic degenerative disease. The studies exist, but they weren't included because it did not support the aim of this meta-analysis.

My hope is that people will not be so swayed by the sensationalism of a poorly designed and selectively biased report, or meta-analysis (summary of selected studies) that in the end will NOT hold up to true medical research scrutiny. Sometimes I believe that these researchers know that their report will not hold up to scrutiny, but in the war of information it ultimately does not matter. The damage will be done because the media has already announced the "bad news," creating doubt in the minds of the less informed, ...including the minds of many doctors who do not take the time to look at the solid studies on the benefits of supplements, but rather listen (and believe) all the information doled out to them by the pharmaceutical reps who visit their office on a daily basis.

Please refer to the following article for an accurate rebuttal (the first of others to follow):

http://www.lef.org/featured-articles/Rebuttal-to-Allegation-That-Certain-Vitamins-May-Shorten-Lifespan.htm?source=eNewsLetter2008Wk16-2&key=Article+Exclusive

Big Pharma: Statin Drugs vs. Antioxidants

2009-05-24T06:35:00.000-07:00

I was concerned several years ago as the American Heart Association, backed by the pharmaceutical companies, continued to make and revise recommendations regarding how low doctors should reduce their patients' LDL cholesterol levels. At first LDL cholesterol levels were "normal" if they were 130 or below, then the standard was 100 or below, and finally, 70 or below became what we now consider medically "acceptable." With each recommendation the number of people who instantly had the made-up disease of "high cholesterol" increased, and more and more patients were prescribed statin drugs to lower their LDL cholesterol levels. Statin drugs are the top-selling drugs in the world, bringing in more money for Big Pharma than any other class of drugs. It was this con of convincing the public that high cholesterol was the cause of atherosclerosis, heart disease, and stroke that caused me to write the first edition of my book, The Cholesterol Conspiracy, in 2004. It has since been updated (2006) and is in its Second Edition; however, after the latest news from the American Heart Association conference in New Orleans on Nov. 8th, 2008 it appears that I will need to update my book again.

My contention has always been that it is NOT high cholesterol that is the main cause of plaque formation, heart disease, and stroke, but rather it is the OXIDATION of LDL cholesterol and the INFLAMMATION of the arterial lining (called the endothelium) that is the culprit to the number one cause of death for both men and women. As I discuss in my book, more than half of people who die of heart disease have NORMAL LDL cholesterol levels, ...thus it is NOT high cholesterol that is killing them, but the CONDITION of the LDL cholesterol and the inflammation of the endothelium that leads to the deadly disease. Likewise, there are cases of people with high cholesterol levels who show no signs of arterial plaque due to their high intake of vitamins, minerals, antioxidants, and the essential fatty acids that reduce the oxidation to LDL cholesterol and inflammation to the endothelium. What's more, antioxidants reduce endothelial inflammation an LDL oxidation better than any drug, ...and without the side effects.

The recent study reported at the American Heart Association in New Orleans, known as JUPITER, proved my case: if you reduce oxidation and inflammation you can reduce the risk of death from heart disease and stroke! However, unlike the JUPITER study, which proposed the way to do it is with statin drugs, I believe the best course to reduce LDL oxidation and arterial inflammation is with nutritional supplements.

If you were to believe the JUPITER study and what is being suggested by the doctors who spoke at the American Heart Association conference on Nov. 8, 2008 in New Orleans you would have to believe that "EVERYONE," young and old, sick and healthy, those with high cholesterol and those with normal cholesterol levels ALL should be on the "life-saving, miracle drugs of this or any other generation" …the statin drugs!

The JUPITER (Justification for the Use of Statins in Primary Prevention) Study, funded by AstraZeneca, makers of Crestor, was unveiled to the delight and awe of doctors and pharmaceutical companies. The study showed that 20 mg of Crestor cut in half one’s risk of heart attacks and stroke, whether they had high cholesterol or not! In other words, healthy people without elevated cholesterol levels ... could now be "saved" by the statin drugs, and like the IRS, the pharmaceutical companies are "here to help."

Doctors and pharmaceutical representatives got on the stage to proclaim that because statin drugs have been shown (in this study of just under two years) to reduce the risk of heart attack and stroke in HEALTHY people (those without signs or symptoms of heart disease and normal cholesterol levels) that governments around the world should push the campaign to put every single person on statin drugs.

As has been proposed earlier (documented in my book), they again proposed at this conference that we "drip statin drugs into our water supply" as the best way to get everyone on these "all-important" drugs. They want to take the decision out of our control and force these drugs, which ...oh, by the way, have dangerous, even deadly side effects, upon us ....and of course, run up a huge national medical cost.

Statin drugs are already the number one-selling drug in the world with over $18 billion dollars in sales, and now due to this study, they will likely double in sales. USA Today calculated that the ever-increasing prescribing of statin drugs which this study will generate would add $10 billion a year to the U.S. national debt. (http://www.usatoday.com/news/health/200 )

BUT, what are the facts of this study; what about the risks of such widespread use of statin drugs, particularly in healthy people? …and, more importantly, what about alternatives to statins? Interestingly enough, one of the authors of this study also appeared as an author on another study released the same week of the announcement of this study, showing that vitamin E and vitamin C did NOTHING to reduce the risk of heart disease; ....in fact vitamin E, they reported, might increase the risk for hemorrhagic stroke. So, in a one-two punch knock out …. Big Pharma apparently established that statin drugs are the ONLY salvation for the number one cause of death.

Now, not only are antioxidants NOT the answer, according to Big Pharma, they are the problem. It must be that we, as human beings, are born deficient of statin drugs, ….some kind of an "inborn error of metabolism," and that it is not nutrients that we lack today, but drugs! Apparently Big Pharma is not satisfied with treating the sick, they want to provide “therapy” to the healthy, by actively putting more drugs into our drinking water …as if there are not enough drugs swirling around in the water supply already.

Again, I would like to point out that this JUPITER study proves my point made in my book, The Cholesterol Conspiracy , ....that heart disease (atherosclerosis) is not caused by high cholesterol, but rather oxidation of LDL cholesterol and inflammation of the arterial lining. In my book, I make a case (backed up by medical research) that oxidized LDL cholesterol and homocysteine-induced nicking and inflammation of the arteries leads to arterial plaque and inflammation.
C reactive protein (CRP) is an indirect measure of arterial inflammation (or any inflammation). The more oxidation and inflammation of the arteries, NO MATTER WHAT THE LDL CHOLESTEROL LEVEL (normal or not), the more plaque will build within the arterial lining (known as the endothelium). By reducing oxidation and inflammation (which can be measured directly with lipid peroxides, or indirectly with CRP levels) there is less damage to the LDL cholesterol and the endothelium, and less plaque will form. Less plaque means less heart disease and death.

Vitamins, minerals, antioxidants, and omega-3 essential fatty acids have all been shown to decrease CRP, homocysteine, and lipid peroxides levels, and in some cases restore endothelial function ….without any toxic side-effects (unlike statin drugs).

Although I discuss CRP in The Cholesterol Conspiracy, as a review, CRP is a protein produced by the liver in response to inflammation. Any condition that leads to inflammation will cause the production and release of CRP. Smoking, genetics, stress, arthritis, diabetes, obesity, rheumatoid arthritis, dementia, high blood pressure colorectal cancer, the aging process, and damaged and an inflamed arterial endothelium will all cause an elevation of C reactive protein. It is an indirect, non-specific measurement of inflammation and oxidation. Statin drugs have been shown to exert an anti-inflammatory effect, and it is the modest anti-oxidant, anti-inflammatory effect that is responsible for a reduction in oxidized LDL cholesterol and arterial inflammation. Less oxidized LDL cholesterol and less arterial inflammation, the less plaque that will build up within the arterial endothelium.

However, natural antioxidants, vitamin C, turmeric extract, essential fatty acids (fish oil) do more to reduce oxidized LDL cholesterol and arterial inflammation and lower CRP than cholesterol-lowering statin drugs, AND without the dangerous side-effects of statins (liver, nerve, muscle, and heart damage, ….let alone death). The B complex vitamins and betaine (tri-methly-glycine) lower homocysteine levels, which means less “scratching up” of the endothelium, i.e., less arterial inflammation, and lower CRP levels.

The JUPITER study showed how important it is to lower inflammation of the arteries in order to reduce the risk of heart disease and stroke, ….as measured by CRP levels, and that people are susceptible to heart attack and stroke even with normal LDL cholesterol levels because oxidation and inflammation. So, let’s look at the facts and my concerns of the JUPITER Study:

Facts of the JUPITER STUDY:

1. Nearly 18,000 men and women with low LDL cholesterol levels (median 108 mg/dL), and C reactive protein levels (CRP) greater than 2.0 mg/L were placed on 20 mg of Crestor or a placebo, and followed for just under 2 years.

2. The group on 20 mg of Crestor decreased their cholesterol levels EVEN FURTHER (to as low as 53 mg/dL), reduced their triglyceride levels, and cut their risk of nonfatal heart attacks by 55%, a 48% reduction in nonfatal strokes, and a 47% reduction in hard cardiac “events” (a composite of nonfatal and fatal heart attack and stroke).

Concerns about the JUPITER STUDY:

1. What are the long-term effects of lowering one’s LDL cholesterol to such low levels? There is already concern about depression, violent behavior, suicide, etc. from lowering one’s LDL cholesterol below 70 (see my book, The Cholesterol Conspiracy). However, what other problems may arise from such low LDL cholesterol, given that the body REQUIRES LDL cholesterol to function properly? Having high LDL cholesterol levels in and of itself is not a problem, it is the oxidation of LDL cholesterol and triglycerides (lipid peroxides) and the inflammation of the endothelium (from homocysteine) that leads to plaque formation.

2. With the study only being 2 years long, AstraZeneca virtually eliminated discovering the long-term effects of such low LDL cholesterol levels AND the long-term effects of statin drugs in this population. However, we do know the long-term of statin drugs, and they are not pretty, ….dangerous and severe side-effects; occasional deadly.

3. Was the study designed to yield the desired results and minimize negative outcomes that would have been revealed had it gone on longer?

4. There was a higher incidence in insulin resistence and type 2 diabetes among those who took Crestor than in the control group. And, this was all happened within 2 years. As mentioned, what other complications would we have seen had the study gone longer than 2 years, ...especially since now all people, even those with normal cholesterol levels, are "supposed" to be on statin drugs for the REST OF THEIR LIVES? It would be good to know what people can expect.4. According to Stanford University cardiologist Dr. Mark Hlatky, about 120 people would have to take Crestor for two years in order to prevent a single heart attack, stroke or death; and how many people would then suffer moderate to severe side-effects over the long-term? Again, as people would be encouraged to be on these drugs for the rest of their lives!

5. Crestor gave clear benefit in the study, but with so few heart attacks and deaths occurred among these low-risk people that treating EVERYONE in the U.S. alone with statin drugs would cost up to $10 billion a year.

6. Big Pharma presents statin drugs as the only choice to reduce CRP levels, when this is not the case.

What We Can Learn From This Study:

1. It is important to lower C Reactive Protein levels as a means to lower inflammation, which in turn reduces the risk of heart disease and stroke.

2. This study confirms that it is NOT the lowering of LDL cholesterol that is key to reducing the risk of heart attack and stroke, but the reducing of inflammation, as is evident by the lowering of C reactive protein (CRP). Therefore, what about all the studies that show alternative means (vitamins, minerals, antioxidants, and essential fatty acids) for lowering CRP, inflammation, and lipid peroxidation without any adverse effects?

What Can You Do?

1. Know, and lower your high-sensitivy CRP levels (as mentioned in my book): a. CRP less than 1.0 mg/L = Low Risk for CardioVascular Disease (CVD) b. CRP of 1.0 – 2.9 mg/L = Moderate Risk for CVD c. CRP greater than 3.0 = High Risk for CVD 2. Know, and lower your Homocysteine levels: a. Homocysteine less than 6.5 = Low Risk for CVD b. Homocysteine 6.6 to 8.0 = Low-Moderate Risk for CVD c. Homocyseine 8.1 to 10.4 = Moderate-High Risk for CVD d. Homocysteine greater than 10.4 = High Risk for CVD 3. Know, and lower your Lipid Peroxides a. This test is not commonly performed by most labs, but can be obtained. b. Keep Lipid Peroxidation low (according to print out on lab results)

How You Can Lower CRP, Homocysteine, and Lipid Peroxidation to Reduce Heart Attack & Stroke:

1. Statin Drugs: expensive; dangerous and sometimes deadly side-effects. a. See list of side-effects in The Cholesterol Conspiracy.
OR, .... even BETTER:
2. Lifestyle Changes: inexpensive, non-dangerous, …and it promotes health! a. Maintain a Healthy Weight b. Maintain a Low-Glycemic Diet (plenty of vegetables) c. Exercise d. Don’t Smoke e. Reduce Stress f. Adequate Sleep g. Drink Plenty of Pure Water h. Maintain Gum Health (brush, floss, and use Co-Q10) i. Use Full-Range Vitamins, Minerals, Antioxidants, and Omega-3 Essential Fatty Acids: (a few examples of many vitamins and antioxidants are shown below, though I personally recommend a full-range of vitamins, minerals, antioxidants, and essential fatty acids):

Vitamin C 2000 mg/day (vitamin C alone reduces CRP similar to statins)

B Complex Vitamins

Fish Oil (4000 mg per day)

Vitamin D (1000 to 5000 IU/day)

Turmeric Extract (400 to 800 mg/day)

Olive Extract (75 to 200 mg/day)

Grape Seed Extract and Resveratrol (200 to 400 mg/day)

Co-Enzyme Q10 (200 to 400 mg/day)

Betaine (TMG) (1800 to 3000 mg/day)

Magnesium (400 mg/day)

To see references (please see http://www.laddmcnamara.com/)
Posted by Ladd McNamara at 7:51 AM

Soy vs. Whey Protein: Which is Better?

2009-05-24T06:24:00.000-07:00

Although I get asked, “Which is better, soy or whey protein?” …my question back is, “Better for what?” Each one is an excellent sources of protein, and each one has its own benefits. I suggest to use at least both sources of protein in order to obtain the benefits each provide. We need to consume protein in order to make and replace protein; and athletes and body-builders are very familiar with whey protein as an excellent source of “bio-available” protein.

Protein is essential for producing antibodies, hormones, new muscle tissue, and the oxygen-carrying protein in blood, hemoglobin. All protein lost or destroyed within the body must be replaced by bio-available protein in order for new tissue to be constructed.

Our bodies are able to manufacture many of the amino acids that are used to produce protein; however, there are nine “essential” amino acids that we cannot manufacture, but must obtain from the protein in our food. Not all protein sources provide these essential amino acids. For example, whey is an excellent source of glutathione and the branched chain essential amino acids L-leucine, L-valine and L-isoleucine.

The protein in most beans and vegetables may contain all the essential amino acids, but they are not naturally concentrated in foods, and thus vegans often do not readily obtain adequate amounts of protein, particularly the branch-chained amino acids. However, this can be compensated for by consuming concentrated protein sources, such as found within quality meal-replacement drinks.

Almost daily, I drink one or two nutritious meal-replacement drinks. These drinks not only contain a blend of both soy and whey proteins, they also contain protein from two additional sources, that of rice and pea. By obtaining a blend of proteins from these four sources one is obtaining all the essential amino acids and the benefits that each provide.

Soybeans contain high amounts of protein. Soy protein and soy isoflavones have been found to help reduce the symptoms of menopause, help reduce the risk of osteoporosis, and to help prevent a number of hormone-related diseases, such as endometrial cancer, breast cancer, and prostate cancer. (Neither soy nor soy isoflavones increase the risk of breast cancer; in fact quite the opposite, they help maintain breast health.)

In addition, soy has been observed to help maintain heart health. Even the Food and Drug Administration (FDA) has stated 25 grams of soy protein per day can reduce the chances of developing heart disease.

Soy protein has also been shown to help the thyroid, which can help with obtaining a leaner body. In the case of a soy allergy, the opposite would be true …reduced metabolism and weight gain.

If you are not allergic to soy, there are very few side effects to including soy in your diet. The most common side-effect of soy is the production of intestinal gas. Flatulence is a common side-effect of all beans (including soy), due to the bowel bacteria’s fermenting effect on the indigestible sugars contained within beans. Humans do not have the enzyme alpha-galactosidase necessary to break down the sugars that the bowel bacteria feast upon and produce gas.

Beano, purchased over-the-counter, contains alpha galactosidase, and regular use may be able to reduce gas production by breaking down the oligosaccharides (bean sugars) before the bacteria in the large bowel has a chance to ferment the sugar.

For those who are allergic to soy, gas would not be the only problem present, but significant diarrhea and abdominal bloating, hives, skin rash, and worst case, breathing problems. Soy isoflavones are not the same as pure soy protein; and even if one is allergic to soy it wound not mean they were allergic to soy isoflavones, as soy protein (the allergen of the allergy) is not found in soy isoflavones.

Whey protein is used by athletes and body builders because of the higher level of essential amino acids, particularly the branched chain amino acids that are metabolized in the muscle not the liver. Protein is critical in repairing not only muscle, but many other body tissues. Whey is helpful for weight loss and building muscle in those who work out, but will do little to help build muscle in those with sedentary lifestyles.

Whey protein affects the digestive tract in much the same way as yogurt. Therefore, it is considered to be a natural remedy for many intestinal issues. In fact, it is often used in Sweden to help prevent bowel problems, gas, and constipation. However, since whey is obtained from a dairy source (it is the liquid by-product of curdled milk … the solid becomes cheese, and the liquid protein part is dried as a source for whey). Therefore, those who are lactose intolerant should avoid whey protein, and steer towards soy protein only, as gas, constipation, and bloating can be significant. Over-the-counter Lactaid is available to help provide the enzyme necessary to break down dairy-derived lactose sugar found in whey products.

Since both soy and whey protein may lead to constipation, it is important to find a meal-replacement drink that provides adequate fiber to overcome this side-effect.

Whey protein makes a good alternative to those who are allergic to soy, and vice-versa, but the blend of soy and whey will render the user with the benefits of each, particularly if blended with adequate fiber, as mentioned. While companies selling protein supplements tout the benefits of whatever they’re selling as “the best,” whether it is soy, whey, or a combination of rice and pea protein, which together the last two alone hit numbers between 85 to 90% bioavailable protein, it is good to know that at least one company was wise enough to combine all four protein sources in their meal-replacement drinks, along with fiber, low-glycemic sugar, and vitamins and minerals. The balance is its greatest strength as a perfect meal replacement.
A summary of the benefits of Soy and Whey Proteins, and that you can have BOTH:

Soy Protein

Soy protein has been found to be higher in non-essential amino
The consumption of 25-50 grams of soy protein daily may enhance production of thyroid stimulation hormones that regulate the metabolic rate, thereby making it easier for us to lose both body weight and fat and create a leaner body
Soy is good for athletes: in a study from Romania endurance athletes experienced lean body mass, increased strength, and decrease fatigue while training. (Revue Roumaine de Physiologie 29, 3-4:63-70, 1992)
It contains more protein by weight than beef, fish or chicken, and contains less fat (especially saturated fat than meat).
The FDA has approved the following statement: ”Diets low in saturated fat and cholesterol that include 25 grams of soy protein a day may reduce the risk of heart disease.”
Other studies show that soy protein isolate has the ability to effectively lower LDL cholesterol and triglyceride levels in the blood
Soy may improve kidney functioning
Whey Protein

Whey protein assists in losing excess weight and maintaining optimal weight
Whey protein, combined with resistance training, even those who have immunosuppressive disorders (AIDS) can increase body cell mass, muscle mass and muscle strength, according to a study in AIDS (15, 18:2431-40, 2001).
Whey protein is superior to other proteins when it comes to anabolic response. It has consistently been shown to stimulate the anabolic hormones after a workout. In other words, whey protein improves athletic performance
Whey mixes well and is low in fat and lactose, and has a superior amino acid profile
Whey protein lacks no essential amino acids. It needs no fortification or additive to make it complete. It is complete in its natural form
Whey enhances the immune system because it raises glutathione levels. Glutathione is a powerful antioxidant that helps our immune cells stay charged to help ward off cancer, bacterial infection and viruses. In other words, it helps improve the immune system.
Whey is also very high in glutamine and the branch chain amino acids L-leucine, L-valine and L-isoleucine, important aminos for repairing muscle
Whey acts as a natural antibacterial or anti-viral
Whey reduces the symptoms of Chronic Fatigue Syndrome
Whey reduces liver damage
Whey improves blood pressure
Whey improves the function of the digestive system
Whey reduces gastric mucosal injury seen in ulcerative colitis
Posted by Ladd McNamara at 8:04 AM:

Calcium and vitamin D enhance heart health benefits of weight loss

2009-05-24T04:17:00.000-07:00

Weight loss and reduced waist circumference are related to an improvement in heart health and factors related to metabolic syndrome. According to a new study, supplementing with calcium and vitamin D during weight loss enhances heart health benefits in women with typically low calcium intake.

Recent research has shown that overweight individuals with low calcium and dairy consumption are at increased risk of developing metabolic syndrome. The findings suggest that adequate calcium intake could create a healthier metabolic profile similar to a balanced diet and regular exercise. In a new study, researchers investigated this issue by testing cardiovascular benefits of long-term calcium supplementation in women with usual low calcium intake. Healthy, overweight or obese women with a daily calcium intake of less than 800 mg/day were randomly assigned to 1 of 2 groups: the group consuming 2 tablets/day of a calcium + vitamin D supplement (600 mg elemental calcium and 200 IU vitamin D/tablet) or the group consuming placebo. Both groups completed a 15-week reduced calorie weight-loss program. Significant decreases in LDL cholesterol levels, as well as the ratios of Total to LDL and LDL to HDL were seen the calcium +D group. These changes were independent of the changes due to fat loss and reduced waist circumference. A tendency for more beneficial changes in HDL cholesterol, triglycerides, and total cholesterol was also observed in the calcium +D group.This was the first study to show that consumption of calcium +D during weight- loss enhances the beneficial effect of body weight loss on cardiovascular risk factors in overweight women with typically low calcium intake.

Source: Supplementation with calcium + vitamin D enhances the beneficial effect of weight loss on plasma lipid and lipoprotein concentrations, Geneviève C Major, Francine Alarie, Jean Doré, Sakouna Phouttama and Angelo Tremblay, American Journal of Clinical Nutrition, Vol. 85, No. 1, 54-59, January 2007

Supplemental vitamin D and calcium reduces risk of diabetes

2009-05-24T04:14:00.000-07:00

The incidence of type-2 diabetes is lower among women who get adequate calcium and supplement with vitamin D. Researchers used data from the Nurses Health Study, which includes over 83,000 women, to study the relationship of calcium and vitamin D intake to type-2 diabetes.

After 20 years of follow-up, it was concluded that a combined daily intake of over 1,200 mg of calcium and more than 800 IU of vitamin D was associated with a 33 percent lower risk of type-2 diabetes. Interestingly, dietary vitamin D intake did not appear to provide any statistically significant benefit. But the women who supplemented with at least 400 IU of vitamin D had a 13% lower risk of diabetes when compared to those who took less than 100 IU per day. Both dietary and supplemental calcium resulted in decreased risk of type-2 diabetes, and those with overall intakes above 1,200 mg had a 21% lower risk than those who got less than 600 mg per day. Elevated intakes of calcium and vitamin D, especially from supplements, are significantly associated with lower incidence of type-2 diabetes.

Source: Vitamin D and Calcium Intake in Relation to Type 2 Diabetes in Women, Anastassios G. Pittas et al, Diabetes Care 29:650-656, 2006

My recommendation: Active Calcium

Vitamin D and calcium supplementation reduces cancer risk

2009-05-24T04:13:00.000-07:00

A four year clinical was done that involved nearly 1200 women. This is the kind of study physicians love and always talk about when it comes to pharmaceutical trials. However, very few of them realize that there are these kinds of studies regarding the health benefits of taking supplements. Subjects were assigned to take 1400 mg of calcium alone, or 1400 mg of calcium plus 1100 IU of vitamin D, or a placebo. After only 4 years, the risk of developing any type of cancer was 60% lower in the vitamin D group. If you excluded the cancers diagnosed in the first year because these cancers were most likely already present before the study, there was a 77% reduction in all types of cancer in the vitamin D group.

The researchers pointed out that vitamin D has an effect on at least 200 human genes and is critical in the normal functioning of our immune system and cell division. When there is less than an optimal level of vitamin D, the regulatory process involving cell proliferation and differentiation becomes defective. This can lead to abnormal cell division and thus cancer growth. However, if individuals simply supplement their diet with 1100 IU of vitamin D, they can significantly decrease their risk of all cancers.

Source: Dr. Strand Health Nuggets (newsletter@Bionutrition.org)

Vitamin D prevents and improves several diseases

2009-05-24T04:12:00.001-07:00

Vitamin D has been shown to suppress inflammation in diseases like rheumatoid arthritis, congestive heart failure, and even stroke. Clinical studies have also shown that there is a decrease in the risk of both type 1 and 2 diabetes in individuals who supplement with vitamin D. There are far fewer falls in those elderly patients who supplement with vitamin D at this optimal level. Another important aspect is the fact that vitamin D is required for proper immune function. It is also known that those individuals who live in higher latitudes contract multiple sclerosis at far higher rates than those who obtain more sunshine throughout the year. Studies with supplementing even 400 IU of vitamin D have shown significant reduction in the risk of developing multiple sclerosis. The question is now arising that we need to actually be providing our bodies with much more vitamin D than we previously thought.

Source: Dr. Strand Health Nuggets (newsletter@Bionutrition.org)

Inflammation and Vitamin D

2009-05-24T04:10:00.000-07:00

Oxidative stress and inflammation is an underlying factor in the development of numerous age-related diseases. In clinical trials, vitamin D has been shown to suppress what is referred to as pro-inflammatory cytokines. This offers additional protection against conditions ranging from rheumatoid arthritis, prediabetes, heart failure, stroke, and heart disease.
It has become evident that those individuals who live in higher altitudes contract multiple sclerosis at much higher rates than those living where they get sunshine throughout the year. Scientists have identified specific vitamin D receptors in the white matter of the brain. The reduction in inflammation, which is the result of adequate vitamin D, may play a role in protecting you against developing multiple sclerosis.

Source: Dr. Strand Health Nuggets (newsletter@Bionutrition.org)

Low Vitamin D levels increase cardiovascular risk

2009-05-24T04:07:00.000-07:00

A report in the Archives of Internal Medicine (June 11,2007) added more evidence in the link of low vitamin D levels and heart disease. These researchers measured the 25-Hydroxy Vitamin D levels in over 15,000 women. Those women who had the lowest levels of vitamin D had significantly higher prevalence of hypertension, diabetes, and elevated triglyceride levels (the other fat in the blood other than cholesterol). These are all risk factors for heart disease and strokes.
These researchers again pointed out the fact that low vitamin D levels carry a significant risk factor to our health. They concluded that current intake of vitamin D is far to low for optimal health. This is why I recommend that my patients should get their vitamin D levels checked and act accordingly. First, to bring their vitamin D levels back up to the recommended level (at least greater than 50 ng/ml) and second, to maintain these levels by taking at least 1,000 to 1,200 IU of vitamin D in supplementation.

Source: Dr. Strand Health Nuggets (newsletter@Bionutrition.org)

Carotenoids decrease risk of macular degeneration

2009-05-24T04:05:00.000-07:00

One of the most concerning age-related disease is referred to as age-related macular degeneration. It is the leading cause of blindness in the elderly. This leads to the degeneration of an area in our eye called the macula, which is responsible for our central vision. When they look at someone, they are not able to see their face, but are able to see the area around their face.

Researchers have identified that the cause of this disease is oxidative stress. Several studies have been done that show that supplementation with a host of antioxidants including two carotenoids called lutein and zeaxanthin significantly decreases your risk of developing age-related macular degeneration.

Source: Neelam K, Hogg Re, et al. Carotenoids and co-antioxidants in age-related maculopathy. Ophthalmic Epidemiology. 2008 Nov-Dec;15(6):389-401.

Source: Dr. Strand Health Nuggets (newsletter@Bionutrition.org)

Lycopene and other antioxidants decrease risk of heart disease

2009-05-24T04:03:00.000-07:00

As you have been learning, oxidized LDL cholesterol and not native LDL is our enemy because it causes such inflammation of our arteries. Fat soluble vitamins are important because they can actually incorporate themselves into the LDL particle. They have been shown to have the ability to then make this LDL cholesterol less likely to be oxidized by excessive free radicals.

Lycopene and other fat soluble vitamins have been shown to protect our LDL cholesterol from becoming oxidized in epidemiological studies and human trials. Therefore, these studies show a decreased risk of developing cardiovascular disease.

Source: Riccioni G, Mancini B, et al. Protective effect of lycopene in cardiovascular disease. Eur Rev Med pharmacol Sci. 2008 May-June;12(3):183-90.

Vitamin B6 may sharply reduce the incidence of colon cancer

2009-05-24T04:00:00.000-07:00

A large Scottish study has shown that increased intake of dietary and supplemental vitamin B6 is associated with a significant decrease in colon cancers. The investigators found that the higher the level of vitamin B6 intake the lower the risk of colon cancer. Subjects with the highest level of vitamin B6 were about 20% less likely to develop colon cancer than those individuals who had the lowest levels of vitamin B6.

Source: Dietary vitamin B6 intake and the risk of colorectal cancer, Theodoratou E, et al, Cancer Epidemiol Biomarkers Prev, 2008 Jan; 17(1):171-82

Source: Dr. Strand Health Nuggets (newsletter@Bionutrition.org)

High Vitamin C level helps to prevent stroke

2009-05-24T03:40:00.000-07:00

Investigators noted that high vitamin C levels may reflect healthy lifestyles and possible supplementation. They followed 20,649 men for nearly 10 years. People with the highest levels of vitamin C had a 42% lower risk of stroke when compared to those with the lowest levels of vitamin C. All other factors were accounted for in this study.

This is just another study that shows that the higher your level of antioxidants and in this case vitamin C, the lower your risk of having a cardiovascular even like a stroke. Eating a healthy diet that contains 6 to 8 servings of fruits and vegetables along with supplementation is certainly a good idea.

Source: Myint PK, Luben RN, et al. Plasma vitamin C concentrations predict risk of incidence of stroke over 10 years. Am J Clin Nutr. 2008 Jan;87(1):64-9

Vitamin D protects against stroke

2009-05-22T19:32:00.000-07:00

Stroke is the fourth leading cause of death (140,000 per year in the US) in the US and Canada. Adverse drug reactions are the third leading cause of death (180,000 deaths per year in the US) in the US and Canada. Everyone is very concerned about having a stroke because of the major disability it can cause.
A study published in September 2008, revealed that for every small decrease in blood levels of vitamin D there was a startling 86% increase in fatal strokes. The researchers concluded that low levels of 25 hydorxyvitamin D levels are independently predictive of fatal strokes and they suggest that vitamin D supplementation is a promising approach in the prevention of strokes.

Source: Dr. Strand Health Nuggets (newsletter@Bionutrition.org)

Sunlight exposure along with low antioxidant levels increases the risk of macular degeneration

2009-05-22T19:31:00.001-07:00

A recent study suggests that protecting the eyes from sunlight exposure (using hats or protective sunglasses) and consuming high levels of dietary antioxidants may significantly reduce the risk of developing age-related macular degeneration. The researchers looked at lifetime sunlight exposure and measured blood antioxidant levels of vitamin C, vitamin E, zeaxanthin, and zinc. They evaluated 4,400 older people and found that individuals with the lowest antioxidant levels and greatest sunlight exposure significantly increased the risk of macular degeneration.

Source: Dr. Strand Health Nuggets (newsletter@Bionutrition.org)

Low antioxidant levels associated with hardening of the arteries

2009-05-22T19:24:00.000-07:00

A study looked at 220 men and women without a history of hardening of the arteries. Vitamin A, vitamin E, and Lycopene were decreased by over 50% in the participants who were found out to have hardening of the arteries (atherosclerosis) when compared to those who did not have any hardening of the arteries. The researchers concluded that regular intake of foods rich in antioxidant vitamins (nutritional supplementation) may slow the progression of hardening of the arteries and its consequences (heart attack or stroke).

Source: Plasma antioxidants and asymptomatic carotid atherosclerotic disease.http://content.karger.com/ProdukteDB/produkte.asp?Aktion=ShowFulltext&ArtikelNr=164691&Ausgabe=240434&ProduktNr=223977 Riccioni G et al. Ann Nutr Metab, 2008;53 (2):86-90

Source: Dr. Strand Health Nuggets (newsletter@Bionutrition.org)

Running for health

2009-04-28T23:41:00.000-07:00

Running for health

FOR those of you who already belong to the club where you leap out of bed before dawn for a trot round the park with an ensuing healthy, rosy glow that gets friends and colleagues asking what your secret is, thumbs up to you.

It isn’t easy to drag one’s self from a warm bed at the crack of dawn to fit in a morning run, but here are some good reasons to give it a try.

Let’s take a look at the physical and health benefits of running first.

There is no doubt running has a load of great physical benefits. According to local sports physician and marathon runner Dr William Chan, running is one of the most effective ways to lose weight and tone up.

Runners get a great cardiovascular workout which is fantastic for the heart and lungs, allowing a person to burn an average of 70 to 80 calories for each kilometre run. Of course the number of calories burnt depends on your weight, fitness level and running pace.

Local sports physician and marathon runner Dr William Chan: ‘Running helps lower blood pressure by maintaining the elasticity of the arteries.’
Running also helps reduce body fat, thus allowing for an increase in lean muscle. Compared to other popular activities, such as biking and walking, running burns far more calories.

Dr Chan explains that whilst the average human being burns about 2,000 to 2,500 calories a day by simply existing, running 5km a day can burn an additional 350 to 400 calories, making weight loss a natural result.

Regular runners also claim that the activity suppresses appetite so you would feel less inclined to eat after a good exercise. But it is also a fact that whilst beginners lose weight quickly at first, the body soon gets used to the workouts and the weight stabilises after an initial period.

Losing weight is just one of the obvious health benefits. Unseen health benefits prove to be a form of motivation as well.

“Running helps lower blood pressure by maintaining the elasticity of the arteries. Whilst running, the arteries expand and contract more than usual, which keeps them elastic and the blood pressure low,” says Dr Chan.

It is a fact that many serious runners have unusually low blood pressure. Running also helps maximise the lungs’ potential, as it keeps them strong and powerful. While deep breaths force the lungs to use more tissue, the 50% of normally unused lung potential is utilised.

Running also serves to strengthen the heart and helps prevent heart attacks. The large muscle exercise it provides helps keep the cardio system efficient and strong. In fact, the heart of an inactive person beats 36,000 more times each day than that of a runner, as running keeps the arteries open and the blood flowing smoothly.

Running makes you healthy, but can it also make you happy?

According to Avanti Kumar, author of the recently published The Science of Happiness, it can!

“In these times of increasing turmoil, it’s crucial to make moments for both internal and external aerobics. The opportunity to do good things on both an inner and outer level needs to be grasped. While you run, your big dreams will come back to you.

“Try to use your run as a session to meditate and you will find that while running, plans will form, even while the blood races around your body. When you’ve finished your run, put these plans into action,” says Kumar.

The effect of happiness that running has on your body comes from endorphins, which are powerful hormone-like substances produced in the brain that function as the body’s own natural painkillers. During exercise, there is a release of endorphins in the body that are capable of producing feelings of euphoria and a general state of well-being. The feelings produced can be so powerful that they can actually mask pain.

Proving the point, Newton Yap from Runners Malaysia says: “Running is intoxicating in a good way unlike alcohol or cigarette addiction. When the endorphins course through my veins, I get ‘high’ but without the hangover. Running calms and cleanses what even the best drug or sedative and soaps cannot get at – the mind, heart and soul. Satisfaction guaranteed almost every time I do it.

“Running keeps me sane in this insane world. Running makes me want to be a better person. Running is living.”

This article was contributed by Standard Chartered KL Marathon 2009. This article was published in The Star online on 29th Apr 2009

Boosting bone density

2009-04-28T23:29:00.000-07:00

Boosting bone density

By DR MILTON LUM

Taking vitamins, minerals and hormonal therapy are some of the ways to prevent brittle bones.

THE treatment goal in the management of osteoporosis is to increase bone density. The medicines available include vitamins, minerals, calcitriol, hormone therapy (HT), selective oestrogen receptor modulators (SERMS), bisphosphonates and recombinant parathyroid hormone.

A high calcium intake plays a crucial role as an adjunct to the other treatment options. Calcium intake has a synergistic bone protective effect along with hormone therapay in post-menopausal women, allowing a doubling or even tripling of the effect of the therapy.

Supplements

Hormones by themselves do not provide substances to form bone – they need to come from the diet. As such, the first step is to ensure that an adequate amount of calcium and vitamin is consumed daily.

Most people, particularly women, should get sufficient vitamins and minerals in their diet. A recent study found that 49% of post-menopausal Malaysian women have vitamin D levels below the normal range, despite the fact the sun is shining throughout the year. This, together with lower rates of calcium absorption and increased bone loss in post-menopausal women, contribute to the development of osteoporosis.

The daily requirement of vitamin D is 400 IU. If one is never in the sun, 800 IU of vitamin D is recommended. This has been shown to reduce fracture in the elderly who are vitamin D deficient. If calcium cannot be obtained from the diet, a calcium supplement may be required to attain the recommended daily requirement of 1,000 to 1,500mg of elemental calcium.

The risk of urinary tract stones is not increased if the calcium consumed does not exceed 1,500mg per day. It is advisable to drink plenty of water. Calcium should not be taken with fibre or iron supplements.

Calcitriol is a synthetic form of vitamin D used to treat osteoporosis. It is one of the most important active metabolites of vitamin D, which is needed for calcium absorption. Calcitriol increases intestinal calcium absorption, regulates bone mineralisation and the production of bone proteins. It prevents bone loss and increases bone mass thereby reducing fractures.

Alfacalcidol is converted in the liver to a metabolite of vitamin D3. It has a rapid onset of action and is safe and effective. It increases bone mineral density, improves biochemical markers and is effective in preventing osteoporotic fractures in the spine and those with mild to moderate osteoporosis.

Hormones

The oestrogen levels in a post-menopausal woman are about 10% that in the reproductive age group and progesterone is almost absent. Post-menopausal oestrogen is produced by the adrenal glands and fat.

Hormone therapy usually involves treatment with either oestrogen alone or in combination with progestogen to help compensate for the decrease in natural hormones. Its use only doubles the oestrogen level of a post-menopausal woman. Hence, even with hormone therapy, the oestrogen and progesterone levels of a post-menopausal woman do not reach the natural levels of a pre-menopausal woman.

The medicines used in hormone therapy are similar in certain aspects yet different in others, with different modes of action, side effects and adverse events. Hormone therapy is the only effective method for the management of menopausal symptoms..

The long-term use of hormone therapy, like all other medicines, has risks as well as benefits. It is beneficial in the prevention and treatment of osteoporosis but it is not the first line medicine as alternatives are available.

When hormone therapy is used for the treatment of menopausal symptoms, it will also decrease bone loss and prevent osteoporosis. Hence, during its intake, the alternatives need not be taken. Hormone therapy is also recommended in women who have premature menopause, that is, menopause below 40 years.

Hormone therapy is an effective method to prevent post-menopausal osteoporosis. It increases bone density at the spine, hip and peripheral sites, and reduces the risk of fractures. The beneficial effects of hormone therapy have been consistently reported in many studies. The potential risks must be weighed against the benefits.

As breast tissue is sensitive to hormones, there has been concern about breast cancer risk among hormone therapy users. Short-term use of less than five years does not appear to increase the risk of breast cancer.

There is some evidence that long-term hormone therapy use may be associated with a small increase in the incidence of breast cancer (with best evidence for combination of oestrogen and progestogen).

The Collaborative Group on Hormonal Factors in Breast Cancer, in an analysis of over 90% of breast cancer studies worldwide, estimate that there are 45 cases of breast cancer in 1,000 women at aged 50 in non-hormone therapy users.

It is estimated five years of hormone therapy use will result in two extra cases per 1,000 users; after 10 years of use, six extra cases per 1,000 users; and after 15 years of use, 12 extra cases per 1,000 users. The extra risk of developing breast cancer on hormone therapy does not persist beyond about five years after stopping its use.

There is good evidence that hormone therapy increases the risk of blood clots (venous thromboembolism) from one in 10,000 people a year to three. Most people who get a blood clot make a complete recovery with treatment. There is fair evidence that hormone therapy use is associated with a small increase in stroke incidence due mainly to an increase in thromboembolic stroke.

Unopposed oestrogen increases the development of endometrial hyperplasia and the risk of endometrial cancer. The addition of progestogen reduces the risk of endometrial cancer.

Oestrogen-only products are prescribed for women who have had a hysterectomy. All other women on hormone therapy will be prescribed an oestrogen-progestogen combination.

Prior to the commencement of hormone therapy, one needs to be assessed by the doctor particularly for conditions which would make hormone therapy unsuitable: current pregnancy, hormone dependent cancers, endometrium, venous thromboembolic disease, pulmonary embolism, severe liver disease, undiagnosed breast lump and uninvestigated abnormal vaginal bleeding.

Oestrogen is usually taken in hormone therapy unless there are contraindications. Various types of progestogens are added for endometrial protection in women with an intact uterus.

Tibolone is a synthetic steroid with mixed oestrogenic, progestogenic and androgenic actions. It is a prescribed for postmenopausal women and has to be taken continuously. It is used to treat vasomotor, psychological and libido problems, and also possesses bone protection.

Hormone therapy should be used under medical supervision. Long term use, such as more than five years, require close monitoring and a regular evaluation (at least annually).

· Dr Milton Lum is a member of the board of Medical Defence Malaysia. This article is not intended to replace, dictate or define evaluation by a qualified doctor. The views expressed do not represent that of any organisation the writer is associated with.

· This article was published in the Star online 29 Apr 2009

Passive Smoking Almost Doubles Risk Of Degenerative Eye Disease

2008-01-07T20:27:00.001-08:00

ScienceDaily (Jan. 3, 2006) — Passive smoking almost doubles the risk of the progressively degenerative eye disease, age related macular degeneration, shows research in the British Journal of Ophthalmology.

The macula lies at the centre of retina at the back of the eye. It's crucial for fine central vision, which is essential for tasks, such as reading and driving.
The risk of macular degeneration increases once someone is over the age of 60. It is a leading cause of partial sightedness and blindness in many European countries and the USA.
The researchers base their findings on 435 people with end stage macular degeneration and 280 partners who lived with them.
They found that the more a person smoked, the greater were their chances of developing age related macular degeneration, and the results showed that it was the amount smoked rather than whether someone had ever smoked that was critical.
Regularly smoking a pack or more a day for 40 years almost tripled the risk of age related macular degeneration compared with those who did not smoke, the research showed.
Smoking increased the risk of both types of macular degeneration (geographic atrophy and choroidal neovascularisation).
Giving up for 20 years or more cut the risk to levels comparable with those for non-smokers, the research found
The risks were also increased for partners who were non-smokers, and had lived with a smoker for five years or more. Their risk nearly doubled.
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Citation: Smoking and age related macular degeneration: the number of pack years of cigarette smoking is a major determinant of risk for both geographic atrophy and choroidal neovascularisation Br J Ophthalmol 2006; 90: 73-80
Adapted from materials provided by BMJ Specialty Journals.
BMJ Specialty Journals (2006, January 3). Passive Smoking Almost Doubles Risk Of Degenerative Eye Disease. ScienceDaily. Retrieved January 8, 2008, from http://www.sciencedaily.com /releases/2006/01/060102123337.htm

Smoking Doubles Risk Of Degenerative Eye Condition

2008-01-07T20:24:00.000-08:00

ScienceDaily (Apr. 15, 2005) — Smoking doubles the risk of the progressive and irreversible eye condition, macular degeneration, and may account for almost 30,000 cases in the UK, suggests research in the British Journal of Ophthalmology.

The risk of macular degeneration increases with age and is the most common cause of blindness in the UK, affecting around 200,000 elderly people.

The findings are based on a representative sample of over 4,000 people, aged 75 and older, from 49 general practices across Britain.

The participants all underwent a series of detailed eye tests and were asked about their smoking habits, and if they had given up, how long ago. After taking into account other risk factors, such as alcohol consumption and cardiovascular disease, the results showed that current smokers were twice as likely to be visually impaired as non-smokers.

Those who had kicked the habit more than 20 years previously were not at risk.

Based on the numbers of people in the UK who are blind or who are partially sighted as a result of macular degeneration, the authors calculated that smoking was likely to have caused up to 30,000 cases.

"An increased risk of [age related macular degeneration], which is the most commonly occurring cause of blindness in the United Kingdom, is yet another reason for people to stop smoking and governments to develop public health campaigns against this hazard," conclude the authors.

Adapted from materials provided by British Medical Journal.

High Insulin Levels Increase Inflammatory Markers And Beta-amyloids, May Contribute To Alzheimer's

2008-01-07T20:20:00.001-08:00

ScienceDaily (Aug. 12, 2005) — CHICAGO -- Moderately elevated levels of insulin increase the levels of inflammatory markers and beta-amyloid in plasma and in cerebrospinal fluid, and these markers may contribute to Alzheimer's disease, according to a new study posted online today from Archives of Neurology, one of the JAMA/Archives journals. The study will be published in the October print edition of the journal.

According to background information in the article, "conditions of insulin resistance and hyperinsulinemia are associated with elevated levels of inflammatory markers and increase the risk for Alzheimer disease (AD). Inflammation has been proposed as a key pathogenic factor for AD."

Mark A. Fishel, M.D., from the University of Washington, Seattle, and colleagues, raised blood insulin levels (while maintaining normal blood sugar levels) in 16 healthy older adults ranging in age from 55 to 81 years, and then measured the changes in levels of inflammatory markers, modulators, and beta-amyloid (a protein associated with AD) in plasma and cerebrospinal fluid.

"Moderate peripheral hyperinsulinemia (increased levels of insulin) provoked striking increases in CNS (central nervous system) inflammatory markers," the authors report. "Our findings suggest that insulin-resistant conditions such as diabetes mellitus and hypertension may increase the risk for AD, in part through insulin-induced inflammation."

"Although this model has obvious relevance for diabetes mellitus, hyperinsulinemia and insulin resistance are widespread conditions that affect many nondiabetic adults with obesity, impaired glucose tolerance, cardiovascular disease, and hypertension. Our results provide a cautionary note for the current epidemic of such conditions, which, in the context of an aging population, may provoke a dramatic increase in the prevalence of AD. More encouragingly, greater understanding of insulin's role in AD pathogenesis may lead to novel and more effective strategies for treating, delaying, or even preventing this challenging disease," the authors conclude.

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(Arch Neurol. 2005; 62: 1-6. Available pre-embargo for the media at www.jamamedia.org) Editor's Note: This work was supported by the Department of Veterans Affairs, Washington, D.C., by grants from the National Institute on Aging, Bethesda, Md., and by the Alvord Endowment, University of Washington, Seattle.

Adapted from materials provided by JAMA and Archives Journals.

Cytokine Resistance Contributes To Pathology Of Type 2 Diabetes

2008-01-07T20:04:00.001-08:00

ScienceDaily (Jun. 15, 2007) — In a study appearing this month in the Journal of Immunology, researchers at the University of Illinois describe how an impaired anti-inflammatory response plays a role in the pathology of type 2 diabetes.

Type 2 diabetes is classified as a metabolic disorder, but a growing number of researchers are beginning to think of it also as a disease of the innate immune system. Inflammation, a key component of the early immune response, is chronically elevated in people with type 2 diabetes. While the pro-inflammatory pathways of type 2 diabetes have received much attention, the anti-inflammatory side of the equation is less well known.

The new study focused on a number of cytokines, protein signals that bind to specific receptors on cells and set off a cascade of biochemical reactions within the cell. Interleukins, interferons, tumor necrosis factors and some growth factors are among the cytokines that direct many aspects of the immune response. Cytokines are secreted by many types of cells, including the immune cells known as macrophages.

In earlier studies, the researchers had shown that macrophages in diabetic and obese (diabese) mice secrete more pro-inflammatory and less anti-inflammatory cytokines than those of nondiabese mice. The team, led by pathology professor and department head Gregory Freund, also had demonstrated that human monocytes cultured under type 2 diabetic conditions had impaired interleukin-4 signaling. Interleukin 4 (IL-4) is an important player in the immune response in that it steers macrophages toward the production of other anti-inflammatory cytokines. It also inhibits secretion of the pro-inflammatory cytokines.

When IL-4 binds to its receptor on a target cell, it sets off one of two cascades of intracellular events.

The first of these signal transduction pathways, the Jak-STAT pathway, is well studied and well understood. The second, called the insulin receptor substrate 2 / phosphatidylinositol-3 kinase (IRS-2/PI3K) pathway, was more of a mystery, and of greater interest to Freund and his colleagues.

What drew them to this pathway was its potential role in the anti-inflammatory response, and its similarity to the cascade initiated when cells respond to insulin.

“One of the actions of diabetes is to create intracellular insulin resistance,” Freund said. “Some of the cytokines that work on cells share the same pathways as the insulin receptor.” Since diabetes causes insulin resistance, Freund said, “shouldn’t there be a resistance to cytokines, too? And that is what we found.”

The research team showed, for the first time, that the IRS-2 signaling arm of the interleukin-4 pathway directed the up-regulation of a key anti-inflammatory molecule in primary macrophages, and that this pathway was disrupted in type 2 diabetic conditions. They also showed that the loss of IL-4 function in diabese mice caused chronic over-expression of an important suppressor of cytokine signaling (SOCS) protein. This SOCS-3 protein aborts the cascade of events that normally leads to insulin uptake and/or cytokine signaling in a balanced inflammatory response.

This study supports earlier findings that inflammation is a key part of the pathology of diabetes, Freund said. Pro-inflammatory cytokines are elevated in type 2 diabetes, but the anti-inflammatory mechanisms are also impaired, leading to a multitude of major and minor health issues in the diabese.

“They get a cold. They get injured. Something happens. And it’s worse in those people with obesity or diabetes and lasts longer than it does in others,” Freund said. “Why? The imbalance may be the elevation in pro-inflammation. But it probably also includes a loss of anti-inflammatory function.”

This research was supported by grants from the National Institutes of Health, American Heart Association, and the U. of I. Agricultural Experiment Station.

Adapted from materials provided by University of Illinois at Urbana-Champaign.

Pro-inflammatory Enzyme Linked To Diabetes; Immune System's Macrophages May Be Key To Treatment

2008-01-07T19:59:00.001-08:00

ScienceDaily (Feb. 3, 2005) — An enzyme that initiates inflammation has been directly linked to insulin resistance and resulting type II diabetes by researchers at the UCSD School of Medicine. In addition, the team suggests that inhibition of the enzyme in the immune system’s macrophages may be a new diabetes therapy.

Published in the February 2005 issue of the journal Nature Medicine, the study describes research in mice that identifies enzyme IkB kinase ß (Ikk-ß) as a central coordinator of inflammatory responses in the liver and macrophages, the immune system cells which attack infections.

Both control mice and mice with Ikk-ß deleted in specific types of cells were fed a high-fat diet that normally causes metabolic syndrome and type II diabetes. While the control mice developed the diabetes and insulin-resistant symptoms, mice in which the Ikk-ß was deleted from microphages retained their healthy insulin levels.

“The potential for a new diabetes treatment is great,” said one of the study’s senior authors, Jerrold Olefsky, M.D., chief of UCSD’s Division of Endocrinology and Metabolism in the Department of Medicine, and associate dean for scientific affairs for the School of Medicine. “An inhibitor of Ikk-ß could be used, or an inhibitor of any other molecule in the inflammation pathway.”

Affecting 18.2 million Americans, diabetes is a disease in which the body does not produce or properly use insulin, a hormone necessary to convert sugar, starches and other food into energy needed for daily life. Previous studies in the past few years have implicated inflammation as playing a role in diabetes, but just how this occurred was unknown.

The researchers generated mice without Ikk-ß in liver cells that play a direct role in insulin-regulated glucose metabolism, and in systemic myeloid cells, pivotal players in inflammatory responses as they produce macrophages.

In response to challenges with a high-fat diet, mice with Ikk-ß deficient myeloid cells retained insulin sensitivity in all target tissues. Because the myeloid cells (and their macrophages) are systemic – able to travel throughout the body – they were identified by the researchers as the best target for diabetes treatments.

The mice lacking Ikk-ß only in the liver retained their insulin sensitivity in the liver but became insulin resistant in fat and muscle. Other tissue, such as muscle, was not tested in this study, because a previous study has shown that deletion of Ikk-ß in muscle has no effect on obesity-induced insulin resistance and type II diabetes, although muscle is a major insulin-responsive tissue.

In addition to Olefsky, a senior author of the paper was Michael Karin, Ph.D., UCSD professor of pharmacology, an American Cancer Society Research Professor, and the scientist who first discovered IKK and its subunits. The paper was a collaborative effort between the diabetes lab of Olefsky and Karin’s molecular signaling lab in the department of pharmacology.

Additional authors included first author Melek C. Arkan, UCSD Department of Pharmacology; and Andrea L. Hevener, UCSD Division of Endocrinology and Metabolism, Department of Medicine; Florian R. Freten, Shin Maeda, Zhi-Wei Li, UCSD Division of Endocrinology and Metabolism, Department of Medicine; Jeffrey M. Long, Ph.D., and Anthony Wynshaw-Boris, M.D., Ph.D., UCSD Departments of Pediatrics and Medicine; and Giuseppe Poli, S. Luigi Hospital, University of Turin, Italy. The study was funded by the National Institutes of Health.

Adapted from materials provided by University Of California - San Diego.

Type 2 Diabetes: Inflammation, Not Obesity, Cause Of Insulin Resistance

2008-01-07T18:11:00.000-08:00

ScienceDaily (Nov. 7, 2007) — Researchers at the University of California, San Diego (UCSD) School of Medicine have discovered that inflammation provoked by immune cells called macrophages leads to insulin resistance and Type 2 diabetes. Their discovery may pave the way to novel drug development to fight the epidemic of Type 2 diabetes associated with obesity, the most prevalent metabolic disease worldwide.

In recent years, it has been theorized that chronic, low-grade tissue inflammation related to obesity contributes to insulin resistance, the major cause of Type 2 diabetes. In research done in mouse models, the UCSD scientists proved that, by disabling the macrophage inflammatory pathway, insulin resistance and the resultant Type 2 diabetes can be prevented.

The findings of the research team, led by principle investigators Michael Karin, Ph.D., Professor of Pharmacology in UCSD's Laboratory of Gene Regulation and Signal Transduction, and Jerrold Olefsky, Distinguished Professor of Medicine and Associate Dean for Scientific Affairs, will be published as the feature article of the November 7 issue of Cell Metabolism.

"Our research shows that insulin resistance can be disassociated from the increase in body fat associated with obesity," said Olefsky.

Macrophages, found in white blood cells in the bone marrow, are key players in the immune response. When these immune cells get into tissues, such as adipose (fat) or liver tissue, they release cytokines, which are chemical messenger molecules used by immune and nerve cells to communicate. These cytokines cause the neighboring liver, muscle or fat cells to become insulin resistant, which in turn can lead to Type 2 diabetes.

The UCSD research team showed that the macrophage is the cause of this cascade of events by knocking out a key component of the inflammatory pathway in the macrophage, JNK1, in a mouse model. This was done through a procedure called adoptive bone marrow transfer, which resulted in the knockout of JNK1 in cells derived from the bone marrow, including macrophages.

With this procedure, bone marrow was transplanted from a global JNK1 knockout mouse (lacking JNK1 in all cell types) into a normal mouse that had been irradiated to kill off its endogenous bone marrow. This resulted in a chimeric mouse in which all tissues were normal except the bone marrow, which is where macrophages originate. As a control, the scientists used normal, wild-type mice as well as mice lacking JNK1 in all cell types. These control mice were also subjected to irradiation and bone marrow transfer.

The mice were all fed a high-fat diet. In regular, wild-type mice, this diet would normally result in obesity, leading to inflammation, insulin resistance and mild Type 2 diabetes. The chimeric mice, lacking JNK1 in bone marrow-derived cells, did become obese; however, they showed a striking absence of insulin resistance -- a pre-condition that can lead to development of Type 2 diabetes.

"If we can block or disarm this macrophage inflammatory pathway in humans, we could interrupt the cascade that leads to insulin resistance and diabetes," said Olefsky. "A small molecule compound to block JNK1 could prove a potent insulin-sensitizing, anti-diabetic agent."

The research also proved that obesity without inflammation does not result in insulin resistance. Olefsky explained that when an animal or a human being becomes obese, they develop steatosis, or increased fat in the liver. The steatosis leads to liver inflammation and hepatic insulin resistance.

The chimeric mice did develop fatty livers, but not inflammation. "Their livers remained normal in terms of insulin sensitivity," said Olefsky, adding that this shows that insulin resistance can also be disassociated from fatty liver.

"We aren't suggesting that obesity is healthy, but indications are promising that, by blocking the macrophage pathway, scientists may find a way to prevent the Type 2 diabetes now linked to obesity and fatty livers," Olefsky said.

Co-first authors of the paper are Giovanni Solinas, UCSD Department of Pharmacology and Cristian Vilcu, UCSD Division of Endocrinology and Metabolism.

Additional contributors include Jun-Li Luo, Willscott Naugler and Sergei Grivennikov, UCSD Department of Pharmacology; Jaap G. Neels, and Gautam K. Bandyopadhyay, UCSD Division of Endocrinology and Metabolism; Anthony Wynshaw-Boris, UCSD Departments of Pediatrics and Medicine; and Miriam Scadeng, UCSD Department of Radiology.

This research was supported by National Institutes of Health grants ES004151, ES006376, DK033651 and DK074868. Additional funding was provided by a fellowship from the Swiss National Science Foundation, a University of California Discovery Grant and Mentor-Based Postdoctoral Fellowships from the American Diabetes Association.

Adapted from materials provided by University of California - San Diego.

University of California - San Diego (2007, November 7). Type 2 Diabetes: Inflammation, Not Obesity, Cause Of Insulin Resistance. ScienceDaily. Retrieved January 8, 2008, from http://www.sciencedaily.com /releases/2007/11/071106133106.htm

Diabetes, Depression Together Increase Risk For Heart Patients

2008-01-07T18:06:00.000-08:00

ScienceDaily (Mar. 11, 2007) — Having both depression and type 2 diabetes increases the risk of death for heart patients. Each factor had been known to increase the risk of heart disease deaths by itself, but together they're even more deadly.

In an analysis of more than 900 patients with established coronary artery disease, Duke University Medical Center psychologists found that those with both type 2 diabetes and symptoms of depression were more likely to die than heart patients without those conditions.

The study showed that among type 2 diabetes patients, having high depression scores increased the risk of dying by 20 to 30 percent compared to patients with similar depression scores but no type 2 diabetes.

"We found a trend showing that the probability of death increases as the level of depression increases in diabetic patients with coronary artery disease," said Duke researcher Anastasia Georgiades, Ph.D. "Our data appear to show an important interaction between type 2 diabetes and depression, meaning that physicians should closely monitor their heart patients who have both of these disorders."

"There is some sort of synergistic effect between type 2 diabetes and depression that we don't fully understand," Georgiades said. "In our analysis, we controlled for factors that could influence mortality, such as heart disease severity and age. For whatever reasons, these patients were still at higher risk of dying, and future research will aim to investigate the mechanisms for this association."

The research was supported by the National Heart, Lung, Blood Institute.

The researchers followed 933 heart patients for more than four years and correlated the 135 deaths that occurred during that period with the presence of type 2 diabetes and depression alone and together.

Georgiades said there are some possible explanations for the link between depression and diabetes.

"Patients with type 2 diabetes typically have an extensive self-care regimen involving special diet, medications, exercise and numerous appointments with their doctor," she said. "It may be that such patients who are depressed might not be as motivated to carry out all these activities, thereby putting them at higher risk."

Depression has also been linked to other cardiovascular risk factors such as insulin resistance, hypertension, obesity, increased cigarette smoking, alcohol abuse and physical inactivity.

Adapted from materials provided by Duke University Medical Center.

New Study Confirms Diabetics Face Significantly Higher Risks Of Colorectal Cancer

2008-01-07T18:03:00.000-08:00

ScienceDaily (Nov. 1, 2005) — A new study confirms that patients with diabetes are significantly more likely to have colon cancer than individuals without diabetes. Researchers at the Medical University of South Carolina reported results from a large cross-sectional analysis assessing the risk of colon cancer among patients with diabetes at the 70th Annual Scientific Meeting of the American College of Gastroenterology.

Researchers analyzed data from a comprehensive nationally representative sample of patients using the 1997-2003 National Health Interview Survey. Of the 226,953 patients in the study, 5.9 percent had a history of diabetes. Researchers controlled for age, race, gender, obesity, alcohol use, tobacco use, and physical activity. Adjusting for potentially confounding factors, researchers found that people with diabetes were 1.4 times more likely to have colon cancer as individuals without diabetes.

"This work is important because it suggests that people with diabetes may be at higher risk of colon cancer. Until we know for sure, diabetics should pay particular attention to their doctor's recommendations for colorectal screening," said Donald Garrow, M.D. one of the investigators.

Adapted from materials provided by American College of Gastroenterology.

Scientists Discover Connection Between Obesity And Diabetes

2008-01-07T17:56:00.001-08:00

ScienceDaily (Dec. 15, 2003) — DENVER (December 11, 2003) -- Scientists with the Eleanor Roosevelt Institute at the University of Denver have made a revolutionary discovery that for the first time establishes a biochemical connection between obesity and Type 2 Diabetes. This study was published in this month's Journal of Endocrinology.

Type 2 Diabetes occurs when the body either doesn't make enough insulin or becomes resistant to insulin, preventing it from storing sugar thus increasing the body's sugar levels to beyond what is normal and healthy. In the United States, it is estimated that approximately 16 million people suffer from this disease.

In this landmark study, tests in mice found that diabetes in obese mice requires a hormone known as MSH, which is made by the POMC gene that is found in both mice and humans. The study found that obese mice without the MSH hormone were obese but did not develop diabetes. Administration of the MSH hormone to these mice increased resistance to insulin and directly affected blood sugar levels. Therefore, MSH may be a factor in the development of Type 2 Diabetes.

"Our findings show that obese people with high levels of the hormone MSH may be more likely to be diabetic than obese people with low levels of the MSH hormone," explained the study's lead author Miles B. Brennan, Ph.D., and ERI scientist. "While we knew that there was a connection between obesity and diabetes, this is the first time that the link between the hormone MSH and blood sugar levels has been established."

According to Brennan, this study will possibly lead to more preventive treatments for diabetes. Preventive treatments, such as testing the MSH hormone levels in obese individuals and then administering a medication if the levels are too high, are currently being studied.

###

Denver's Eleanor Roosevelt Institute was founded in 1961 as a private, independent research center. ERI merged with the University of Denver in 2003. The Institute is staffed by leading scientists from around the world who study Down syndrome, Lou Gehrig's disease, cancer, obesity, Type 2 Diabetes and other diseases and conditions. It is the mission of the Institute's scientists to seek an in-depth understanding of the process of life and through this understanding work towards unlocking the mysteries of human health and disease.

Adapted from materials provided by Eleanor Roosevelt Institute.

2008-01-06T22:15:00.000-08:00

Vitamins: tested and rated

Reporter: Helen Wellings
Broadcast Date: August 07, 2007

From A to zinc, a staggering 70 per cent of Australians buy nutritional supplements, spending on average $200 per year: a total of $2.3 billion.

But it is hard to know which to choose, from a mind-blowing 30,000 different types on the market. An extraordinary scientific analysis by a team of Canadian and US biochemists may come to the rescue.

They have thoroughly examined more than 100 leading multivitamins available in Australia and New Zealand, evaluating and comparing their formulations by separating and measuring each ingredient: vitamins, minerals antioxidants and other components.

Dr Lesley Braun, Pharmacist and Naturopath from the National Herbalists Association of Australia and Dr Marc Cohen, Professor of Complementary Medicine at RMIT are the authors of Herbs and Natural Supplements.

We showed them the latest comparison of multivitamin products which scores brand by brand.

"What you've got is seven experts from the US that have put together what I would call a wish list, a list of ingredients they believe would be the ultimate to have in a multivitamin," Dr Braun said.

Professor Cohen added: "It was done on a range of issues, which include how absorbable the vitamins were, the range of vitamins and minerals that were in the tablet and whether they were in the appropriate amounts and in the appropriate form" says Professor Marc Cohen.

Dr Braun explained the research further.

"Their aim is to try to find a product on the market that is as close as possible to their wish list of the most comprehensive, of the highest doses, for them what they would consider the best," Dr Braun said.

"It is very important when you look at a vitamin supplement that not only have you got the key ingredients, but you've got them in the right combinations."

They say the absolutely perfect multivitamin tablet would be a huge "poly-pill", the size of a walnut, but Professor Cohen says we should be aiming for the following.

"The full range of vitamins e.g. A, the full range of vitamin Bs - and B should be done in a complex, not just 1 or 2 of the vitamins - certainly vitamin C and a range of minerals," Prof Cohen said.

"There is also an argument to say you should not put everything in the one pill because things absorb differently, e.g. the fat soluble vitamins."

Now the results

First, the final top 5 scorers. Remember they're rated against an ideal multi-vitamin pill.

Best: USANA Health Sciences Essentials scores a very high 74 per cent, followed by Solgar Omnium at 56.5 per cent.

Thorn Research Al's Formula scored 47 percent, Clinicians Vitamin and Mineral Boost 45 per cent, and NFS Nutraceuticals Ultimate Sports Multi 44.5 per cent.

But you won't find them at the supermarket nor pharmacies: they're available online, some through naturopaths and herbalists.

What is it that gave these brands such top ratings?

"They do contain a lot of the B group vitamins, the antioxidants that are traditional vitamins, so bioflavonoids. And they contain a few other little bits and pieces as well in high doses, such as the minerals with magnesium and calcium," Dr Braun said.

"A lot of the key ingredients are in very high doses. So when you match it up to the wish list that the US experts put together, it looks very good."

Most of the multivitamins tested scored lower than 20 per cent. Again though, all were rated against the ideal.

About one-third only managed single figure scores. Bottom of the list, unbelievably, some of our top supermarket and pharmacy brands: Myadec and Nature's Own Multivitamins and Minerals both with just 2.4 per cent,

Herron Clinical Nutrition All-in-One Multi-Vitamin and Mineral scored 2 per cent, Guardian Multi Vitamins and Minerals Hi Potency also 2 per cent, and last was Advocare Macro-Mineral Complex at just 1 per cent.

But at a fraction of the price of the top scorers, our expert nutritionists say you do get what you pay for.

"They tend to have fewer number of ingredients compared to the ones that rated very highly," Dr Braun said.

"Also the strength of the ingredients tended to be lower.

"So I see them as just a very basic stopgap for someone whose diet really needs some work, whereas as they go higher in the list, they become more sophisticated and have better combinations."

Professor Cohen said: "I think the ones in the supermarkets and pharmacies are competing on price. You could have the vitamin on the label and only a very tiny amount. It won't actually do anything for you, but it is still on the label and consumers don't really know how much is the correct amount."

So are the right vitamins worth the money?

"Go with the ones that are comprehensive in good doses, the ones on the list," Dr Braun said. "Ideally though, go to a health professional, get your diet looked at, start working on the diet and get the right supplement for you."

"There is strong evidence now that everyone over the age of 55 should be taking a multivitamin every day to prevent long-term diseases," Prof Cohen said.

"I'd extend that to say everyone should be taking a multivitamin because the risks are very low and the benefits are potentially very high."

So what does an expert take daily? Here's a tip: don't waste your money taking multivitamins with a cup of tea.

"The best way to take them is in the morning with breakfast, big glass of water," Prof Braun said. "Tea not so good because it binds some of the iron and you won't get the absorption, cancels out the iron."

Dr Lesley Braun takes:

"Dona Glucosamine" by Your Health.
"CoQ10", Co-enzyme Q10 by BioCeuticals for healthy cardio-vascular function and good for people taking statins for lowering cholesterol. Lesley also takes them for migraine.
"Multi-biocomplex" with selenium, a multivitamin by Nutrimedicine.
A bowl of blueberries which are neuro regenerative - to combat the loss of brain-cells due to ageing. If she can't buy fresh in season, she buys frozen blueberries.

National Herbalists Association of Australia.
Website: www.nhaa.org.au

Dr Lesley Braun and Professor Marc Cohen wrote "Herbs and Natural Supplements: An Evidence Based Guide. Published by Elsevier, November 2004. ISBN 0729536823. Contains 567 pages. Price $A40.

TEST RESULTS
The scores and brand analysis of multi-vitamins, as mentioned in our story, are in Comparative Guide to Nutritional Supplements. A Compendium of over 100 Products available in Australia and New Zealand, written by Lyle MacWilliam BSc, MSc, FP. (Northern Dimensions Publishing, Vernon, British Columbia, Canada. Revised 1st Edition).

But it is not in bookshops in Australia. Go to www.uniprotools.com.au. You can order the book from that site by selecting Lyle MacWilliam's name on the left-hand side of the page. Price is $40 including postage and handling.

Nutritional Supplements sorted by score
USANA Health Sciences Essentials 73.7
Solgar Omnium 56.5
Thorne Research Al's Formula 46.9
Clinicians Vitamin and Mineral Boost 45.1
NFS Nutraceuticals Ultimate Sports Multi 44.5
Thorne Research Basic Nutrients V 44.4
Thorne Research Basic Nutrients III 38.7
Solgar VM-2000 37.9
Pharmanex Lifepak 28.1
Amway NutriWay Double X 27.3
GNC LiveWell Women's Ultra Mega 26.1
Pharmanex Lifepak Women 25.6
BioCeuticals Multi Essentials 25.3
Pharmalliance OxiChel 24.8
Neways Orachel 24.1
Solgar Formula VM-75 23.1
Radiance Multi-Power 22.6
Nutra Life Active Men's Multi 22.3
GNC LiveWell Mega Men 21.2
Pharmanex Lifepak Prime 21.0
Nature's Sunshine Supplemental Vitamins & Minerals 20.6
Thompson's Multifort 17.5
Nature's Way Mega Multi 17.1
Thompson's Immunofort 16.9
Nutra Life Active Women's Multi Plus 16.4
Eagle Tresos B PluSe 16.4
Nature's Way Women's Energy Mega Multivitamin 16.4
Pharm-a-Care Women's Mega Strength Multi-Vitamins 16.4
Bioglan Women's Complete Multi Compex 16.4
Pretorius Women's Live Better Multi Vitamin & Mineral 16.3
Kordel's Men's Multi (without Iron) 15.4
Nutrition Care Formula SF88 15.1
Blackmores Women's Vitality Multi 14.1
Metagenics Multigenics 14.1
Red Seal Women's Multi 14
Nature's Own Daily Multi Peak Performance 14
Mannatech GlycoLEAN Catalyst 13.9
Natural Nutrition Mega Potency Women's Multi Vitamin with Selenium 13.7
Nature's Sunshine Mega-Chel 13.5
Metagenics Multigenics Phyto Plus 13.5
Blackmores Women's Multi & Evening Primrose Oil 13.4
Natural Nutrition Mega Potency Fifty Plus Multi Vitamins 13.4
Blackmores Sustained Release Women's Multi Vitamins & Minerals 13.3
Natural Nutrition Mega Potency Men's Multi Vitamin with Selenium 13.3
Red Seal Men's Multi 13.3
Pharm-a-Care Men's Mega Strength Multi-Vitamin 11.7
Bioglan Men's Complete Multi Complex 11.6
Nature's Way Men's Energy Mega Multi-Vitamin Iron-Free 11.6
Blackmores Sustained Release Multi Vitamins and Minerals 11.5
Swisse Women's Ultivite Formula 1 11.5
Pluravit Time-Release Multi 11.5
Thompson's Men's Multi with Antioxidants 11.3
Herbs of Gold Executive Multi Vitamin & Mineral 11.1
Golden Glow Senior's One-A-Day Multi 11.1
Swisse Women's Ultivite No Iron or Iodine 10.9
Swisse Men's Ultivite Formula 1 10.8
Blackmores Sustained Release Multi Vitamins & Minerals + Selenium 10.7
Melaleuca Vitality for Women 10.6
Reliv Now 10.4
Nature's Own Multivitamin Plus Omega 3 Fish Oil 9.1
Avon VitAdvance Women's Complete II 9.1
Good Health Men's Multi-Plus 9.1
Pharma Foods Pharma Day with Selenium 8.7
Herbalife Formula 3 8.7
Kordel's Women's Multi Plus EPO 8.6
Cenovis Mega Multi 8.4
Thompson's Femmefort 8.3
Microgenics Mega Multivitamin 8
Melaleuca Vitality for Men 7.5
Reliv Classic 7.5
Nutrition Care Formula 33SE 7.4
Microgenics Women's Pro Active Multi Vitamin 6.8
Golden Glow Super One-A-Day 6.7
Herron Clinical Nutrition Men's Multi-Vitamin & Minerals 6.2
Blackmores Men's Performance Multi 6.2
Good Health Women's Multi-Plus 6
Vitaplex Professional One a Day Multivitamin 5
New Vision Essential Vitamins 4.7
Centrum Select 50+ 4.3
Amway NutriWay Daily 4.2
Microgenics Men's Essential Multivitamin 4.1
Myadec Gold A-Z Guard 4
Red Seal Total Multi with Minerals 3.9
Centrum Complete from A to Zinc 3.9
Cenovis 50+ Multi 3.8
Guardian Women's Multi Vitamins & Minerals 3.6
Herron Clinical Nutrition One-a-Day Women's Multi-Vitamins & Minerals 3.6
Cenovis Multivitamin and Minerals 3.4
Amcal One-A-Day 3.3
Berocca Performance 3.2
Healtheries Women's Multi (AU) 3.2
Cenovis Women's Multi 3.1
Nature's Own Daily Multi Essentials 3.1
Pluravit Women 3.1
Golden Glow Women's One-a-Day Multi 3.1
Blackmores Multi + Gingko for 55+ 3
Pluravit 50 Plus 3
Healtheries Women's Multi (NZ) 2.7
Hivita LiquiVita 2.6
Red Seal One-a-Day Multi & Minerals 2.6
Amcal Multivitamin & Mineral Effervescent 2.6
Golden Glow Men's One-a-Day Multi 2.5
Bioglan Daily Plus Max 2.5
Cenovis Men's Multi 2.5
Myadec Multivitamins and Minerals 2.4
Nature's Own Multivitamin & Mineral 2.4
Herron Clinical Nutrition All-in-One Multi-Vitamin & Mineral 2.1
Guardian Multi Vitamins & Minerals Hi Potency 2.1
Advocare Macro-Mineral Complex 1.1

Source: Comparative Guide to Nutritional Supplements by Lyle MacWilliam, BSc, MSc, FP (Northern Dimensions Publishing, ISBN 0-9732538-3-5

Diet and Inflammation

2008-01-06T02:11:00.000-08:00

In addition to toxic cytokines, there are other inflammatory pathways that can be mediated via diet modification. A common problem involves overproduction of pro - inflammatory hormone-like "messengers" (such as prostaglandin E2) and underproduction of anti-inflammatory "messengers" (such as prostaglandin E1 and E3).

The good news is that omega-3 fatty acids found in fish oil help to suppress the formation of undesirable prostaglandin E2 and promote synthesis of beneficial prostaglandin E3 (Kelley et al. 1985; Watanabe et al. 2000). Gamma - linolenic acid (GLA) induces production of the anti-inflammatory prostaglandin E1 (Das et al. 1989; Fan et al. 1997). What you eat can significantly affect whether you have more of the beneficial prostaglandins (E1 and E3) as opposed to the pro-inflammatory prostaglandin E2.

Because prostaglandin E2 is a culprit in inflammation, reducing the consumption of foods that are high in omega-6 fatty acids and increasing the consumption of omega-3 rich foods, such as salmon and other fish, can be beneficial. Limiting foods that convert to arachidonic acid can help reduce inflammation. Arachidonic acid is a precursor to both prostaglandin E2 and the pro-inflammatory cytokine leukotriene B(4) (Brock et al. 1999). Another dietary factor that can lead to high levels of arachidonic acid is the overconsumption of high-glycemic index carbohydrates that cause excess production of insulin (Kreisberg et al. 1983). These quickly digestible foods include fruit juices or rice cakes. Food heavy in polyunsaturated fats or saturated fats can also increase prostaglandin E2.

Additionally, a study of elderly patients with heart disease requiring elective surgery (Tepaske et al. 2001) found that nutritional supplements containing omega-3 polyunsaturated fatty acids (as well as yeast and L-arginine) improved the outlook for high-risk patients when given a minimum of 5 days prior to surgery.

The number of inflammatory-related diseases that could be successfully treated with cytokine-lowering therapy is staggering. PTX and supplements such as fish oil, nettle leaf, DHEA, and vitamin K possess mechanisms of suppressing inflammatory cytokines. Unfortunately, there are no side-by-side comparisons to enable us to categorically state whether PTX or natural agents (such as DHA fish oil) work better.

Foods cooked at high temperatures can produce a browning effect in which glycotoxins are formed from the reaction of sugars and oxidized fats with protein. Glycotoxins may contribute to low-grade chronic inflammation. High glycemic foods may also contribute to the inflammatory process. Dietary modifications to reduce inflammation should include elimination of foods and cooking processes that contribute to a chronic state.

For those who have multiple degenerative diseases, the cytokine profile blood test and the C-reactive protein blood test are highly recommended. This may be done through your own physician or the Life Extension Foundation. If your cytokine test reveals excess levels of cytokines such as TNF-a, IL-1(b), or both, nutritional supplementation, dietary modifications, and low-cost prescription medications such as PTX are advised.

The following supplements are suggested:

The docosahexaenoic acid (DHA) fraction of fish oil may be the most effective nonprescription supplement to suppress pro-inflammatory cytokines. Gamma-linolenic acid (GLA) is a precursor of PGE1, a potent anti-inflammatory agent. A product called Super EPA/DHA provides 1400 mg of EPA and 1000 mg of DHA in 4 capsules.
DHEA is a hormone that decreases with age. DHEA has been shown to suppress IL-6, an inflammatory cytokine that often increases as people age. Typical doses of DHEA are 25-50 mg daily, although some people take 100 mg daily. Refer to the DHEA Replacement protocol for suggested blood tests to safely and optimally use DHEA.
Nettle leaf has been shown to suppress the proinflammatory cytokine TNF-a. Take 1000 mg daily.
Vitamin E and N-acetyl-cysteine (NAC) are protective antioxidants with anti-inflammatory properties. Vitamin E that contains gamma-tocopherol and tocotrienols provides the most broad-spectrum protection. Take 1 capsule daily of Gamma E Tocopherols with Sesame Lignans and Tocotrienols with Sesame Lignans. NAC is an amino acid with antiviral and liver protectant properties. One 600 mg capsule daily is recommended.
Vitamin K helps reduce levels of IL-6, a pro-inflammatory messenger. Vitamin K also helps in the treatment of osteoporosis by regulating calcium and promoting bone calcification. One 10 mg capsule daily is recommended for prevention purposes. Do not take vitamin K if you are taking Coumadin or some other type of anticoagulant medicine.
Consuming at least 1000 mg per day of carnosine and/or 300 mg of the European drug aminoguanidine can inhibit pathological glycation reactions in the body.

See Full article by Health Concerns below for more details

http://www.lef.org/protocols/prtcl-146b.shtml

Chronic Inflammation and Degenerative Diseases

2008-01-06T02:05:00.000-08:00

Chronic systemic inflammation is an underlying cause of many seemingly unrelated, age-related diseases. As humans grow older, systemic inflammation can inflict devastating degenerative effects throughout the body (Ward 1995; McCarty 1999; Brod 2000). This fact is often overlooked by the medical establishment, yet persuasive scientific evidence exists that correcting a chronic inflammatory disorder will enable many of the infirmities of aging to be prevented or reversed.

The pathological consequences of inflammation are well-documented in the medical literature (Willard et al. 1999; Hogan et al. 2001). Regrettably, the dangers of systemic inflammation continue to be ignored, even though proven ways exist to reverse this process. By following specific prevention protocols suggested by the Life Extension Foundation, the inflammatory cascade can be significantly reduced.

The Causes of Age-Related Inflammation
Aging results in an increase of inflammatory cytokines (destructive cell-signaling chemicals) that contribute to the progression of many degenerative diseases (Van der Meide et al. 1996; Licinio et al. 1999). Rheumatoid arthritis is a classic autoimmune disorder in which excess levels of cytokines such as tumor necrosis factor-alpha (TNF-a), interleukin-6 (IL-6), interleukin 1b [IL-1(b)], and/or interleukin-8 (IL-8) are known to cause or contribute to the inflammatory syndrome (Deon et al. 2001).

Chronic inflammation is also involved in diseases as diverse as atherosclerosis, cancer, heart valve dysfunction, obesity, diabetes, congestive heart failure, digestive system diseases, and Alzheimer's disease (Brouqui et al. 1994; Devaux et al. 1997; De Keyser et al. 1998). In aged people with multiple degenerative diseases, the inflammatory marker, C-reactive protein, is often sharply elevated, indicating the presence of an underlying inflammatory disorder (Invitti 2002; Lee et al. 2002; Santoro et al. 2002; Sitzer et al. 2002). When a cytokine blood profile is conducted on people in a weakened condition, an excess level of one or more of the inflammatory cytokines, e.g., TNF-a, IL-6, IL-1(b), or IL-8, is usually found (Santoro et al. 2002). (See the Suggested Reading reference list for additional citations.)

Protecting Against Inflammatory-Related Disease

The New England Journal of Medicine published several studies in the year 2000 showing that the blood indicators of inflammation are strong predictive factors for determining who will suffer a heart attack (Lindahl et al. 2000; Packard et al. 2000; Rader 2000). The January 2001 issue of Life Extension Magazine described these studies and explained how individuals could protect themselves against these inflammatory markers (such as C-reactive protein, homocysteine, and fibrinogen).

A growing consensus among scientists is that common disorders such as atherosclerosis, colon cancer, and Alzheimer's disease are all caused in part by a chronic inflammatory syndrome.

Seemingly unrelated diseases have a common link. People who have multiple degenerative disorders often exhibit excess levels of pro-inflammatory markers in their blood.

See Full article by Health Concerns below for more details

http://www.lef.org/protocols/prtcl-146.shtml

Preventing Chronic Degenerative Disease and Obesity – Get in the Anti-Inflammatory Zone Naturally

2008-01-06T01:40:00.001-08:00

A recent headline in USA Today, and an article in Men’s Health (Dec. 04), and a book by Dr. Barry Sears, The Anti-Inflammation Zone, all highlight the dangers of silent inflammation that occurs within the cells of the body.

The USA Today article by Steve Sternberg quotes studies that appeared in New England Journal of Medicine. It says: “Inflammation is as potent as bad cholesterol: Two leading research groups independently report today that lowering blood levels of a protein that promotes artery inflammation is just as important as reducing bad cholesterol for preventing heart attacks and strokes. Their conclusions reflect a major shift away from the notion that bad cholesterol, or LDL, is the primary villain in heart disease. Levels of C-reactive protein (CRP) also must be reduced to halt the disease’s progression, researchers said.”

The article in Men’s Health, Bonfires of the Arteries, sites “Inflammation is the slow burn that sparks thousands of heart attacks and strokes every year.”

“Half of all heart attacks and strokes in the United States each year occur among people with essentially normal cholesterol levels, says Paul Ridker, M.D., a professor of medicine at Havard medical school. There’s more to heart disease than just lipids. In addition to the problem of cholesterol, there’s the problem of the immune system or the inflammation response. A heart attack occurs when plaque ruptures inside your blood vessels. But that rupturing hinges not just on how much plaque you have but also on the degree of inflammation, Dr. Ridker says. Your level of CRP – measured by a simple blood test – helps detect this condition so you can predict whether you’re in danger of cardiovascular disease and stroke.”

Many people take drugs to dampen down inflammation. After numerous months of controversy, the FDA removed Bextra from the market this month amidst reports that it posed health risks to the heart and stomach, and can cause a potentially fatal skin condition. Vioxx was also taken off the market in September 2004 because of dangerous and life-threatening cardiovascular side effects. The FDA established new warning labels for anti-inflammatory drugs, both prescribed and over-the-counter and older, popular non-steroidal anti-inflammatories (NSAIDs), such as ibuprofen (Motrin, Advil) and naproxen (Aleve, Naprosyn), are also coming under increased scrutiny.
This is a big step in protecting the consumer from the dangers of these drugs, but it’s left many wondering what to do now.

Top Ten Tips to help reduce inflammation (CRP) levels in the body naturally

Take a High Quality Multi-Antioxidant - A study in the American Journal of Medicine showed that people who took a multivitamin each morning for 6 months decreased their CRP by 0.7 milligrams per liter. And a University of California at Berkeley study found that people who took 500 mg of vitamin C saw a 24 percent drop in CRP after just 2 months.
Get in Anti-Inflammatory Food Zone - people who most closely followed a Mediterranean diet – one rich in olive oil – had CRP numbers 20 percent lower than those of their less oily brethren. Here are some other specific diet tips.

Reduce your intake of high glycemic foods. White foods of all kinds (pasta, French fries, white bread, white sugar products) all produce inflammatory chemicals in the cells. Eliminating or greatly reducing these will make a difference immediately. To speed up the process and see for yourself, I recommend a digestive cleanse process.
Avoid all partially hydrogenated fat. These fats create inflammatory chemicals and also damage cell membrane function.
Hold the red meat, eggs, and night shade vegetables. Some people are intensely sensitive to the arachidonic acid in red meat and eggs. When they stop eating these foods, their joint pain goes away quickly. Others are sensitive to the nightshade vegetables, which include tomatoes, potatoes, eggplant, and zucchini. It’s easy enough to stop them for ten days to see if you notice a difference. Sometimes this is all that is necessary!
Get enough omega-3 fats in your diet. Getting enough omega-3 fats in your diet is a natural and highly effective way to help the body resist inflammation. Wild Alaskan salmon is loaded with omega-3 fats, as are omega-3 rich eggs, sardines, and flax seeds. You can also get omega-3 fats in supplement form. I recommend 1000-5000 mg per day in divided doses.
Eat colorfully! Follow a diet rich in plant foods of all types, especially the highly pigmented ones such as blueberries, raspberries, kale, collard greens, sweet potatoes, and squash. These are loaded with naturally-occurring antioxidants that decrease inflammation and thwart oxidative stress caused by free radicals. For more information about this, see the book The Color Code.

Floss - inflammation effects of periodontal disease also cause inflammation of your arteries.
Stop Smoking - Smokin takes toxic chemicals into the lungs and distributes them to every cell in the body, accelerating the aging and inflammatory process exponentially.
Get Good Fats - In a new Harvard study, people who consumed the most omega-3 fatty acids (1.6 grams per day) had 29 percent lower CRP readings than those who ate the least. Fish oil has a direct anti-inflammatory effect by either: inhibiting the formation of arachidonic acid (AA), or inhibiting the enzymes that transform AA into pro-inflammatory eicosanoids.” Dr Barry Sears tells us “On a scale of 1 to 10 for supplements, I give high-dose fish oil a 12. It’s the number-one anti-inflammatory supplement you can take – as long as you take an ultra-refined product that has had the vast majority of the inherent toxins removed… If you only take one supplement in your life, make sure it’s high-dose fish oil…
Increase Lean Muscle Mass and Reduce Body - Reducing fat helps reduce CRP.
Get Fiber - Consume your recommended 20-plus grams of fiber..
Practice the Friendship Solution - Social interaction helps reduce depression which helps to lower CRP.
Release Resentment - According to Louise Hay, author of You Can Heal Your Life and the famous little blue book Heal Your Body, arthritis is associated with feelings of criticism and resentment. A good affirmation for this is the following.

I now lovingly release all past hurts, resentments, and grievances and open myself up to love and approval on all levels.
Be Moderate - It is certainly true that some people need a bit of NSAID or COX-2 inhibitor to get through their day at least while they’re making other lifestyle changes. If this is true for you, don’t spend a moment worrying about it. This just leads to more stress chemicals. Sometimes taking a small risk for significant pain relief is worth it. Just use the least amount that does the job, make the changes you can make as lsuited, and then let it go.

As an alternative to the drugs removed from the market by the FDA, consider other joint-healthy supplements. Two of the most powerful and beneficial are glucosamine sulfate and OPCs.

Glucosamine sulfate is found naturally in high amounts in joint tissue. It stimulates the body to make cartilage, thus helping repair the joints; glucosamine also helps protect joints against destruction. When taken orally, it is absorbed selectively by joint tissues where it exerts a powerfully therapeutic effect in those with osteoarthritis. Many good studies have shown that it works better than NSAIDs and placebos at relieving the pain and inflammation of osteoarthritis in at least 50 percent of people—with only minor side effects Recommended dosage is 500 mg, three times per day.
Oligomeric Proanthocyanidins (OPCs) are a powerful group of antioxidants found in both pine bark and grape seeds. There’s good research on both grape seed extract and pine bark. Because OPCs help repair connective tissue, they are also very good for bones, hair, nails, and skin.

Inflammation = Degenerative Disease-by Bonnie C. Minsky

2008-01-06T01:21:00.001-08:00

June 2004 | Health Conscious

Inflammation has long been linked to both rheumatoid arthritis and osteoarthritis. Now, there’s emerging research that also links chronic inflammation to allergies, asthma, Alzheimer’s disease, cancer, diabetes, digestive disorders, heart disease, hormonal imbalances and osteoporosis. Andrew Weil, holistic health M.D., Nicholas Perricone, M.D., an anti-aging expert, Jeffrey Bland, Ph.D., a biochemist who popularized the concept “genetic nutritioneering,” and health writer Jack Challem, author of The Inflammation Syndrome, have spoken widely about the damage that inflammation causes.

Injured tissues become inflamed and result in redness, heat, swelling, pain and loss of function. When acute inflammation doesn’t shut down, it becomes chronic and causes damage to the injured tissues. Bland, the nutritional biochemist, says, “Inflammatory stimuli, such as bacterial infection, trauma, ischemic events, stress-related events, toxic exposures, allergens and chronic viral infections activate the inflammatory response.”

According to the health experts I mention, the biggest culprit in causing abnormal inflammation is the pathetic “standard American diet” (SAD) of heavily processed convenience and fast foods. Perricone believes that “Inflammation equals aging. Inflammation is the reason you get wrinkles; why you forget everything from where you left your car keys to your neighbor’s first name; why you can be irritable and depressed and why you lose the healthy bloom of youth.”

Inflammation is what causes arthritic pain, stiffness when using your muscles, the wheezing of asthma and the discomfort of allergies. It is even possible that the progression of atherosclerosis is directly related to chronic inflammation in up to 50 percent of cases. Excess acid production also increases the inflammatory response leading to loss of bone and joint tissues.

To reduce degenerative disease, it’s necessary to avoid pro-inflammatory foods and rely exclusively on anti-inflammatory foods:

Pro-inflammatory foods to avoid:

* red meats from corn-fed, antibiotic/hormone laden animals

* saturated fats such as lard and meat fats

* fried foods

* partially hydrogenated (trans fats) found in margarines, chips, candies, cereals and baked goods

* cooking oils that are exclusively corn, safflower, sunflower or soy based

* soft drinks (both high sugar and diet varieties)

* excess sugar (both from heavily processed sources, such as candy and from naturally occurring sources such as fruit juice)

Perricone describes sugar as one of the most serious causes of inflammation, rapid aging and weight gain. Sugary foods quickly elevate blood sugar, creating an insulin release along with free radicals that oxidize fats. When oxidized, the fats form plaque deposits in our arteries, leading to disease. Thus, a diet high in sweets, pasta, fruit juices, cereals and even rice cakes can actually lead to heart disease. Insulin release also increases stored body fat and release of pro-inflammatory chemicals causing cell damage and accelerated aging.

Anti-inflammatory foods and dietary supplements to include:

* foods high in omega-3 fatty acids, especially cold water, wild-caught fish (or fish oil supplements)

* raw nuts and seeds (especially pecans, almonds, walnuts and flaxseeds)

* homemade soups made with poultry or meat bones (boiling the bones releases glucosamine and chondroitin into the soup which, when ingested becomes bioavailable in the body. They can reduce inflammation and helps repair cartilage)

* dark green vegetables (especially kale, seaweed and greens)

* antioxidants in supplement form (especially vitamins C and E, and quercetin)

* zinc taken in supplement form which assists healing and reduces inflammation

* extra virgin organic olive oil, expeller pressed grapeseed and avocado oils

If you are already showing chronic inflammatory symptoms, I recommend that you adopt the following 10 dietary recommendations:

1) Eat lean meats and poultry that are free-range, organic and not corn-fed (i.e. grass-fed preferably).

2) Eat a wide variety of vegetables (the deeper the colors, the better).

3) Use cold-pressed, uncooked olive oil (in salad dressings) and grapeseed or avocado oil for cooking.

4) Avoid products that contain added sugars (especially white sugar and high fructose corn syrup).

5) Avoid or limit your intake of cow’s milk products.

6) Avoid or limit your intake of heavily processed grains and grains containing gluten if you suspect an intolerance to them (brown rice, wild rice and millet are gluten-free).

7) Eat organic foods whenever possible.

8) Identify and avoid foods to which you have an allergy or sensitivity.

9) Eat wild, cold water fish at least three times weekly, especially salmon.

10) Eliminate all trans fats. Avoid added saturated fats.

Andrew Weil commented at a recent conference, “The idea on the medical horizon is that chronic inflammation is a root cause of degenerative diseases.”

It is time for medical schools to improve nutrition education. If physicians are trained to use “food as medicine,” they may not need to rely upon drugs (and their distressing side-effects) to treat the inflammatory process.

Disclaimer: This column is for information only and no part of its contents should be construed as medical advice, diagnosis, recommendation or endorsement by Ms. Minsky.

Bonnie Minsky is a Licensed and Certified Nutrition Specialist, Public Health Educator and Certified menopause Educator with a private practice in Northbrook, IL. She can be reached at nutritionalconcepts.com.

Persistent Overeating By The Obese Generates Massive Free Radical Load, Initiating Artery Disease

2008-01-06T01:15:00.000-08:00

ScienceDaily (Jan. 22, 2001) — BUFFALO, N.Y. -- Endocrinologists at the University at Buffalo have pinpointed one of the mechanisms that place the obese at higher risk of atherosclerosis and subsequent heart attack.

Their study, published in the January issue of The Journal of Clinical Endocrinology and Metabolism, shows that persistent overeating in the obese exposes them to excessive oxidative damage from free radicals, the hyperactive oxygen molecules that damage arterial walls and initiate the accumulation of fatty deposits that eventually inhibit or block blood flow to the heart.

Moreover, the researchers found that severely restricting caloric intake decreased the production of free radicals by more than 50 percent, lowering the risk of developing heart disease without medication.

"Our research has shown for the first time that the obese carry a massive oxidative load," said Paresh Dandona, M.D., UB professor of medicine and primary author on the study. "This oxidative load causes the kind of changes in the blood stream that make obese people prone to heart disease.

"We've also shown for the first time that diet restriction alone can change their risk," he said. "Taking a pill is easier, but lifestyle change is just as effective and should be considered."

Dandona and colleagues at the Diabetes-Endocrinology Center of Western New York at Kaleida Health, which Dandona heads, set out to determine whether the generation of free radicals and other indices of oxidative damage decrease as a result of short-term calorie restriction and weight loss.

Their study subjects were nine obese nondiabetic men and women who were taking neither antioxidant vitamins nor medication for heart disease. Their weight ranged from 183 lbs. to 360 lbs., with a mean body mass index (BMI) -- a ratio of weight to height -- of 40.7. An individual with a BMI over 30 is considered obese.

After taking fasting blood samples, researchers placed the participants on 1,000-calorie diets, consisting of a 200-calorie commercial liquid diet drink for breakfast and lunch and a home-cooked 600-calorie dinner. They remained on the diet for four weeks, returning to the clinic weekly to be weighed and provide fasting blood samples. Participants were asked to maintain their normal level of physical activity.

At the end of four weeks, participants had lost an average of 10 pounds. Analysis of blood samples showed a marked decrease in both markers of oxidative damage and the generation of free radicals. The more than 50 percent fall in free radical concentrations was accompanied by a significant decrease in markers of oxidative damage to lipids, proteins and amino acids.

"This finding is important because it represents a dramatic reversal in the cardinal processes affecting atherogenesis without the use of any drug or antioxidant," Dandona said. "Despite the wide variation in BMI, the changes were consistent and therefore are intrinsic to the process of dietary restriction and weight loss."

All participants gained weight after the four-week intervention, and at three months post-study, the concentration of free radicals and indices of oxidative damage were higher than at its inception, the researchers found.

Additional authors on the study are Ahmad Aljada, Ph.D., UB research assistant professor of medicine; Richard Browne, Ph.D., UB research instructor in the Department of Social and Preventive Medicine; and Priya Mohanty, Husam Ghanim, Wael Hamouda, Anu Prabhala, Aqeela Afzal and Rajesh Garg, doctoral students working with Dandona.

The study was supported in part by the William G. McGowan Charitable Fund.

Adapted from materials provided by University At Buffalo.

How Eating Less Might Make You Live Longer

2008-01-06T01:09:00.001-08:00

ScienceDaily (Mar. 6, 2007) — Caloric Restriction in non-obese people translates into less oxidative damage in muscle cells, according to a new study by Anthony Civitarese, Eric Ravussin, and colleagues (Pennington Biomedical Research Center). As oxidative damage has been linked to aging, this could explain how limiting calorie intake without malnutrition extends life span.

A calorie-restricted diet provides all the nutrients necessary for a healthy life but minimizes the energy (calories) supplied in the diet. This type of diet increases the life span of mice and delays the onset of age-related chronic diseases such as cancers, heart disease, and stroke in rodents. There are also hints that people who eat a calorie-restricted diet might live longer than those who overeat. In addition, calorie-restricted diets beneficially affect several biomarkers of aging, including decreased insulin sensitivity (a precursor to diabetes). But how might caloric restriction slow aging? A major factor in the age-related decline of bodily functions is the accumulation of "oxidative damage" in the body's proteins, fats, and DNA. Oxidants--in particular, chemicals called "free radicals"--are produced when food is converted to energy by cellular structures called mitochondria. One theory for h ow caloric restriction slows aging is that it lowers free-radical production by inducing the formation of efficient mitochondria.

Civitarese and colleagues enrolled 36 healthy overweight but non-obese young people into their study. A third of them received 100% of their energy requirements in their diet; the caloric restriction (CR) group had their calorie intake reduced by 25%; and the caloric restriction plus exercise (CREX) group had their calorie intake reduced by 12.5% and their energy expenditure increased by 12.5%. The researchers found that a 25% caloric deficit for 6 months, achieved by diet alone or by diet plus exercise, decreased 24hr whole body energy expenditure (i.e. overall calories burned), which suggests improved mitochondrial function. Their analysis of genes involved in mitochondria formation indicated that CR and CREX both increased the number of mitochondria in muscle. Both interventions also reduced the amount of DNA damage--a marker of oxidative stress--in the participants' muscles.

The researchers also examined gene expression in the study participants. In yeast, worms, and flies the activation of the Sir2 gene increases life span and regulates cellular metabolism. An important question is whether caloric restriction can regulate SIRT1 (the mammalian equivalent of Sir2) in humans. Civitarese and colleagues found that indeed fewer calories can improve whole body metabolism in conjunction with an increase in SIRT1 gene expression in skeletal muscle. These results raise the possibility that SIRT1 may contribute to more efficient metabolism, less oxidative stress, and increase longevity in humans as it does in lower organism.

The results suggest that even short-term caloric restriction can produce beneficial physiological changes leading to improved health. Whether caloric restriction and the associated health benefits can be sustained over longer term remains to be established in humans.

Citation: Civitarese AE, Carling S, Heilbronn LK, Hulver MH, Ukropcova B, et al. (2007) Calorie restriction increases muscle mitochondrial biogenesis in healthy humans. PLoS Med 4(3): e76. (http://dx.doi.org/10.1371/journal.pmed.0040076)

Adapted from materials provided by Public Library of Science.

Risk Of Stroke Doubles If Diagnosed With Type 2 Diabetes

2008-01-06T01:04:00.001-08:00

ScienceDaily (Jun. 15, 2007) — Individuals diagnosed with Type 2 diabetes are at double the risk of having a stroke compared to those without diabetes, according to new research from the University of Alberta. It was found that the risk of a stroke is considered high within the first five years of treatment for Type 2 diabetes and more than doubles the rate of occurrence.

For this study, the researchers entered 12,272 subjects into a Type 2 diabetes cohort. All subjects were recently diagnosed with Type 2 diabetes and had a mean age of 64 years. After five years of monitoring, stroke incidence rates were compared between the cohort and the general population.

"What we found is that 9.1 per cent of the diabetes cohort had a stroke within the first five years of their diagnosis," Dr. Thomas Jeerakathil, an assistant professor in neurology, at the University of Alberta. "We also found that compared to persons from the general population of a similar age, the relative risk for stroke was much greater in younger persons with diabetes than for older persons.

As it has been more common to study stroke prevalence within 10 years after diagnosis, this is the first study to specifically examine stroke-related outcomes immediately after the diagnosis of and initiation of treatment for Type 2 diabetes.

Jeerakathil indicates it is possible that physicians are undertreating stroke risks because of a prevailing attitude among physicians and patients that the cardiovascular complications of diabetes occur long after diagnosis rather than in the first five years.

"We hope our findings will help to dispel the notion that the risk of stroke occurs only in the long term and will improve the motivation of both patients and health care providers to aggressively control cardiovascular risk factors soon after diagnosis." said Jeerakathil.

The research recently appeared in the American Heart Association's Stroke journal.

Adapted from materials provided by University of Alberta.

Low Glycemic Index Diet Best For Weight Loss And Cardiovascular Health

2008-01-06T00:55:00.001-08:00

ScienceDaily (Jul. 26, 2006) — The most effective diet for weight loss and cardiovascular health is a high carbohydrate plan based on low glycemic index (GI) foods, according to a study by University of Sydney researchers.

Published in the most recent issue of Archives of Internal Medicine, the world's first 12 week parallelled, randomised, controlled trial compared the relative effects on weight loss and cardiovascular risk of low GI and high-protein diets.

Undertaken by Professor Jennie Brand-Miller and Joanna McMillan-Price from the University of Sydney Human Nutrition Unit, the findings show that there is no 'one diet fits all' solution, and although both high protein and low GI diets will help you to shed fat. However, it did show that a diet containing low GI carbohydrate significantly reduces your risk of heart disease.

The trial, which was led by Joanna McMillan-Price, enrolled 129 overweight or obese young adults (aged 18-40 years) and randomly assigned them to one of four reduced calorie, reduced fat diets over a 12 week period. Two of the diets were high-carbohydrate diets and the other two high in protein - one of each had a high GI and the other had a low GI.

Between the two high-carbohydrate diets, lowering the glycemic index doubled fat loss - this effect was strongest in women. Participants on the high-protein, high GI diet was equally effective for fat loss as the high carbohydrate, low GI diet, the two had diverse effects on LDL (bad) cholesterol - the high protein, high-GI group showed increased levels of LDL or 'bad' cholesterol, while there were significant reductions in those on the high carbohydrate, low-GI diet. However those on the high-protein, low GI diet did not experience the same rise in total LDL cholesterol suggesting the importance of low GI foods alongside a high meat intake.

"Our findings suggest that dietary glycemic load, and not just overall energy intake influences weight loss and postprandial glycaemia (blood sugar levels after eating)," said Joanna McMillan-Price.

"We found that moderate reductions in glycemic load appear to increase the rate of body fat loss, particularly in women. Diets based on low-glycemic index, whole grain products, tend to be better for the heart, maximising cardiovascular risk reduction - particularly if protein intake is high," said Joanna McMillan-Price.

Adapted from materials provided by University Of Sydney.

High-glycemic Index Carbohydrates Associated With Risk For Developing Type 2 Diabetes In Women

2008-01-06T00:49:00.000-08:00

ScienceDaily (Nov. 27, 2007) — Eating foods high on the glycemic index, which measures the effect of carbohydrates on blood glucose levels, may be associated with the risk for developing type 2 diabetes in Chinese women and in African-American women, according to two new studies. However, eating more cereal fiber may be associated with a reduced risk for type 2 diabetes in African-American women.

Researchers remain uncertain regarding exactly how diet, including carbohydrate intake, affects the development of type 2 diabetes, according to background information in the articles. Studies have revealed that the body absorbs carbohydrates from different foods at different rates. This leads to varying effects on levels of blood glucose and the hormone insulin, which converts glucose into energy.

Foods high on the glycemic index, such as rice and other simple carbohydrates, cause a rapid spike and then a drop in blood glucose, whereas high-fiber foods tend to be lower on the glycemic index and have a more gradual effect. Some evidence has linked high--glycemic index foods with the risk of developing type 2 diabetes.

In one study, Supriya Krishnan, D.Sc., of Boston University School of Public Health, and colleagues examined data from 40,078 U.S. black women who filled out a food questionnaire in 1995. The glycemic index and glycemic load--a measure of the amount of carbohydrates from glucose--were calculated. Every two years through 2003, the women answered follow-up questionnaires about their weight, health and other factors.

During eight years of follow-up, 1,938 participants developed type 2 diabetes. Women who ate high--glycemic index foods or a diet with a high glycemic load had a higher risk for diabetes. However, women who ate more fiber from grains (cereal fiber) had a reduced risk; for women with a body mass index (BMI) of less than 25, women who ate about 1.5 grams of fiber per day were 59 percent less likely to develop diabetes than women who ate about 8.3 grams per day.

Because high--glycemic index foods increase blood glucose levels significantly, they increase the body's demand for insulin, the authors note. This can contribute to problems with the pancreas (which produces insulin) that may eventually lead to diabetes. In addition, high--glycemic index foods can directly decrease the body's response to insulin by increasing the production of fatty acids after meals.

"Our results indicate that black women can reduce their risk of diabetes by eating a diet that is high in cereal fiber," the authors write. "Incorporating fiber sources into the diet is relatively easy: a simple change from white bread (two slices provides 1.2 grams of fiber) to whole wheat bread (two slices provides 3.8 grams of fiber) or substituting a cup of raisin bran (5 to 8 grams of fiber) or oatmeal (4 grams of fiber) for a cup of corn chex (0.5 grams of fiber) or rice chex (0.3 grams of fiber) will move a person from a low fiber intake category to a moderate intake category, with a corresponding 10 percent reduction in risk."

In another study, Raquel Villegas, Ph.D., of Vanderbilt University Medical Center, Nashville, Tenn., and colleagues followed a group of 64,227 Chinese women for an average of five years. During in-person interviews conducted every two years between 2000 and 2004, the researchers collected data on dietary habits, physical activity and other health-related information.

During the study, 1,608 of the women developed diabetes. Women who consumed more carbohydrates overall were more likely to develop diabetes--when they were split into five groups based on carbohydrate intake, those in the group consuming the most (about 337.6 grams per day) had a 28 percent higher risk than those in the group consuming the least (about 263.5 grams per day). Women who ate diets with a higher glycemic index and who ate more staples such as bread, noodles and rice specifically also had an increased risk. Women who ate 300 grams or more of rice per day were 78 percent more likely to develop diabetes than those who ate less than 200 grams per day.

"Given that a large part of the world's population consumes rice and carbohydrates as the mainstay of their diets, these prospective data linking intake of refined carbohydrates to increased risk of type 2 diabetes mellitus may have substantial implications for public health," the authors conclude.

Journal reference: Arch Intern Med. 2007;167(21):2304-2309, 2310-2316.

Adapted from materials provided by JAMA and Archives Journals.

Exercise Pivotal In Preventing And Fighting Type II Diabetes

2008-01-06T00:44:00.001-08:00

ScienceDaily (Feb. 9, 2007) — One in three American children born in 2000 will develop type II diabetes, according to the U.S. Centers for Disease Control and Prevention (CDC). A new study at the University of Missouri-Columbia says that acute exercise - as little as 15 minutes a day - can have a profound influence on preventing and fighting the disease.

This research adds to the body of evidence that indicates exercise can fight type II diabetes, one of the most widespread self-inflicted healthcare struggles in the United States, and could save Americans millions of dollars in pills, injections and medical treatment. Acute exercise is a bout of activity in which people actively participate, as opposed to activity resulting from everyday activities.

"Many people can fight type II diabetes through diet and exercise alone," said John Thyfault, professor in the MU College of Human Environmental Sciences' Department of Nutritional Sciences. "It is important to ward off diabetes early. Exercise has proven to be effective at all levels. At any stage of type II diabetes, from an obese child to a person dependent for 20 years on insulin injections, exercise could have a dramatic effect on improving insulin sensitivity."

Type II diabetes results from a lack of insulin production and insulin resistance in skeletal muscle cells. Insulin is necessary to help drive glucose out of the blood and into the tissues of the body. As a result of insulin resistance, cells do not respond appropriately to insulin, causing more insulin to be released to have a measurable effect and ultimately causing insulin and glucose to build up dangerously in the blood.

Thyfault's study found that relatively short periods of acute muscle exercise in diabetic Zucker rats significantly increased insulin sensitivity in the previously insulin resistance skeletal muscles. Since 80 to 90 percent of all glucose goes into muscle after a meal, it is reasonable that more active muscles on a day- to-day basis will result in increased insulin sensitivity, Thyfault said.

"In relation to a person with type II diabetes, this would mean that they could lessen their dependence on insulin therapy to control their blood glucose levels or potentially control glucose levels without any drug by just increasing their daily activity levels in addition to the right diet," Thyfault said.

The study, "Contraction of insulin resistant muscle normalizes insulin action in association with increased mitochondrial activity and fatty acid catabolism," will be published in the American Journal of Physiology-Cell.

Adapted from materials provided by University of Missouri-Columbia.

Rate Of Cellular Energy Production Lower In Persons At Risk For Type 2 Diabetes

2008-01-06T00:43:00.001-08:00

ScienceDaily (Aug. 26, 2005) — New Haven, Conn.-The rate of insulin-stimulated energy production is significantly reduced in the muscles of lean, healthy young adults who have already developed insulin resistance and are at increased risk of developing diabetes later in life, according to a Yale School of Medicine study.

The new research by Gerald Shulman, M.D., professor of internal medicine, endocrinology, and senior author of the study, indicates that a decreased ability to burn sugars and fats efficiently is an early and central part of the diabetes problem. The new data also suggest that the basic defect lies within the mitochondria, which are the energy factories inside cells that produce most of the chemical power needed to sustain life.

The young adults studied by the research team are the offspring of parents who have type 2 diabetes, adding support to the idea that the risk can be inherited and that the problem begins well before diabetes symptoms become evident. The researchers observed that the mitochondria in the subjects' muscle cells responded poorly to insulin stimulation. Normal mitochondria react to insulin by boosting production of an energy-carrying molecule, ATP, by 90 percent. But the mitochondria from the insulin-resistant people they tested only boosted ATP production by five percent.

Among their findings was also evidence for a severe reduction in the amount of insulin stimulated phosphorus transport into the muscle cells of the insulin-resistant participants. This also points to a dramatic defect in insulin signaling and may explain the observed abnormalities in insulin-stimulated power production in the insulin-resistant study subjects. Phosphorus is a key element in the mithochondrion's complex energy-production process.

###

The co-authors were Kitt Petersen and Sylvie Dufour.

PLoS Medicine 2: www.plosmedicine.org (September 2005)

Adapted from materials provided by Yale University.

Lots Of Low-fat Food Is Better Than Small Portions Of High-fat Food

2008-01-06T00:38:00.000-08:00

ScienceDaily (Feb. 6, 2004) — Dutch research has shown that a diet of low-fat products is better than smaller portions of normal high-fat food for preventing diabetes in obese people. Mice put on a low-fat diet were more sensitive to insulin than mice that received the same amount of energy in the form of high-fat food.

Martin Muurling put obese mice on different diets in which the total energy intake and the final body weight were the same. He then studied the effect of these diets on insulin sensitivity.

Mice that received just low-fat products were more sensitive to insulin than mice that ate small portions of high fat food. A low-fat diet is, therefore, a more effective remedy for diabetes than eating less calories.

Muurling also discovered that in mice, the consumption of fish oil had no positive effects whatsoever on reduced insulin sensitivity. From this he concluded that a diet with fish oil cannot prevent or remedy diabetes in the case of somebody who is already less sensitive to insulin due to a high-fat diet.

Clinically obese people sometimes suffer from a certain form of diabetes, type II diabetes mellitus. This is because far more fatty acids are released from the adipose tissue during obesity. These fatty acids can reduce the functioning of the beta cells in the pancreas as well as the sensitivity of various tissues to insulin.

Fat accumulation in adipose tissue is less harmful than fat accumulation in organs such as the liver and muscles. Treatment methods that lead to a reduction of fat accumulation in the liver and muscles might also remedy type II diabetes mellitus in obese patients.

In diabetics, the regulation of the blood glucose level and the transport of glucose from the blood to tissue cells are disrupted. This is due to either an inadequate production of insulin or the insulin available not being effective enough. Obesity and type II diabetes mellitus will probably be the health problems of the 21st century, as the number of obese people has risen sharply over the last few decades.

The research was funded by the Netherlands Organisation for Scientific Research.

Adapted from materials provided by Netherlands Organization For Scientific Research.

Type 2 Diabetes

2008-01-06T00:36:00.000-08:00

Diabetes mellitus type 2 or Type 2 Diabetes (formerly called non-insulin-dependent diabetes (NIDDM), obesity-related diabetes, or adult-onset diabetes) is a metabolic disorder that is primarily characterized by insulin resistance, relative insulin deficiency and hyperglycemia. It is often managed by engaging in exercise and modifying one's diet. It is rapidly increasing in the developed world, and there is some evidence that this pattern will be followed in much of the rest of the world in coming years. The CDC has characterized the increase as an epidemic.^[1] In addition, whereas this disease used to be seen primarily in adults over age 45, in contrast to Diabetes mellitus type 1, it is now increasingly seen in children and adolescents, an increase thought to be linked to rising rates of obesity in this age group. ^[2]

Unlike Type 1 diabetes, there is little tendency toward ketoacidosis in Type 2 diabetes, though it is not unknown. One effect that can occur is nonketonic hyperglycemia which also quite dangerous, though it must be treated very differently. Complex and multifactorial metabolic changes very often lead to damage and function impairment of many organs, most importantly the cardiovascular system in both types. This leads to substantially increased morbidity and mortality in both Type 1 and Type 2 patients, but the two have quite different origins and treatments despite the similarity in complications.

Pathophysiology

Insulin resistance means that body cells do not respond appropriately when insulin is present.

Other important contributing factors:

increased hepatic glucose production (e.g., from glycogen degradation), especially at inappropriate times
decreased insulin-mediated glucose transport in (primarily) muscle and adipose tissues (receptor and post-receptor defects)
impaired beta-cell function—loss of early phase of insulin release in response to hyperglycemic stimuli
Cancer survivors who received allogenic Hematopoietic Cell Transplantation (HCT) are 3.65 times more likely to report type 2 diabetes than their siblings. Total body irradiation (TBI) is also associated with a higher risk of developing diabetes.

Type 2 may go unnoticed for years in a patient before diagnosis, since the symptoms are typically milder (no ketoacidosis) and can be sporadic. However, severe complications can result from improperly managed Type 2 diabetes, including renal failure, blindness, wounds that are slow to heal (including surgical incision), and arterial disease, including coronary artery disease. The onset of Type 2 is most common in middle age and later life, though a form of it, called MODY is being much more frequently seen in adolescents.

Diabetes mellitus type 2 is presently of unknown etiology (i.e., origin). Diabetes mellitus with a known etiology, such as secondary to other diseases, known gene defects, trauma or surgery, or the effects of drugs, is more appropriately called secondary diabetes mellitus. Examples include diabetes mellitus caused by hemochromatosis, pancreatic insufficiencies, or certain types of medications (e.g. long-term steroid use).

About 90–95% of all North American cases of diabetes are type 2^[3], and about 20% of the population over the age of 65 has diabetes mellitus type 2. The fraction of type 2 diabetics in other parts of the world varies substantially, almost certainly for environmental and lifestyle reasons, though these are not known in detail. Diabetes affects over 150 million people worldwide and this number is expected to double by 2025^[3]. There is also a strong inheritable genetic connection in type 2 diabetes: having relatives (especially first degree) with type 2 increases risks of developing type 2 diabetes very substantially. In addition there is also a mutation to the Islet Amyloid Polypeptide gene that results in an earlier onset, more severe, form of diabetes^[4],[5]. About 55 percent of type 2 are obese^[6] —chronic obesity leads to increased insulin resistance that can develop into diabetes, most likely because adipose tissue is a (recently identified) source of several chemical signals to other tissues (hormones and cytokines). Other research shows that type 2 diabetes causes obesity.^[7]

Diabetes mellitus type 2 is often associated with obesity, hypertension, elevated cholesterol (combined hyperlipidemia), and with the condition often termed Metabolic syndrome (it is also known as Syndrome X, Reavan's syndrome, or CHAOS). It is also associated with acromegaly, Cushing's syndrome and a number of other endocrinological disorders. Additional factors found to increase risk of type 2 diabetes include aging^[8], high-fat diets^[9] and a less active lifestyle^[10].

From Wikipedia, the free encyclopedia

Insufficient Sleep Raises Risk Of Diabetes, Study Suggests

2008-01-06T00:31:00.001-08:00

ScienceDaily (Dec. 2, 2007) — The most common factors believed to contribute to diabetes are a decreased amount of physical activity and access to highly palatable processed foods. However, there is growing evidence that another aspect of our modern lifestyle, short sleep duration, is also contributing toward the "diabetes epidemic", according to a new study.

The study, authored by James E. Gangwisch, PhD, of Columbia University in New York, explored the relationship between sleep duration and the diagnosis of diabetes over an eight-to-10-year follow-up period between 1982 and 1992 among 8,992 subjects who participated in the Epidemiologic Follow-Up Studies of the first National Health and Nutrition Examination Survey. The subjects' ages ranged from 32 to 86 years.

According to the results, subjects who reported sleeping five or fewer hours and subjects who reported sleeping nine or more hours were significantly more likely to have incident diabetes over the follow-up period than were subjects who reported sleeping seven hours, even after adjusting for variables such as physical activity, depression, alcohol consumption, ethnicity, education, marital status, age, obesity and history of hypertension.

The effect of short sleep duration on diabetes incidence is likely to be related in part to the influence of short sleep duration upon body weight and hypertension, said Dr. Gangwisch. Experimental studies have shown sleep deprivation to decrease glucose tolerance and compromise insulin sensitivity by increasing sympathietic nervous system activity, raising evening cortisol levels and decreasing cerebral glucose utilization. The increased burden on the pancreas from insulin resistance can, over time, compromise â-cell function and lead to type two diabetes, warned Dr. Gangwisch.

"If short sleep duration functions to increase insulin resistance and decrease glucose tolerance, then interventions that increase the amount and improve the quality of sleep could potentially serve as treatments and as primary preventative measures for diabetes," said Dr. Gangwisch.

It is unknown as to how long sleep duration contributes to diabetes, although increased time in bed to compensate for poor sleep quality is one possible explanation, noted Dr. Gangwisch.

Recent estimates show that at least 171 million people worldwide suffer from diabetes, and that, by the year 2030, this number is projected to double.

Lawrence Epstein, MD, medical director of Sleep HealthCenters, an instructor of medicine at Harvard Medical School, a past president of the American Academy of Sleep Medicine (AASM) and a member of the AASM board of directors, said that this study is one of several large studies that have shown that people who don't get enough sleep have higher rates of diabetes.

"Restricting sleep to four hours a night for only a few days causes abnormal glucose metabolism, suggesting the mechanism for increased rates of diabetes in sleep deprived individuals," said Dr. Epstein. "Additionally, sleep disorders that disrupt sleep, such as obstructive sleep apnea, also increase the likelihood of developing diabetes. Treating the sleep disorders improves glucose metabolism and diabetes control. These studies underscore the fact that sleep is integral to good health."

On average, most adults need seven to eight hours of sleep each night to feel alert and well-rested. Adolescents should sleep about nine hours a night, school-aged children between 10-11 hours a night and children in pre-school between 11-13 hours a night.

The article, "Sleep Duration as a Risk Factor for Diabetes Incidence in a Large U.S. Sample", is published in the December 1 issue of the journal Sleep.

Adapted from materials provided by American Academy of Sleep Medicine

Study Adds To Links Between Sleep Loss And Diabetes

2008-01-06T00:28:00.000-08:00

ScienceDaily (Sep. 19, 2006) — Short or poor quality sleep is associated with reduced control of blood-sugar levels in African Americans with diabetes, report researchers from the University of Chicago in the Sept. 18, 2006, issue of the Archives of Internal Medicine.

The finding suggests that one inexpensive way to improve the health of patients with type 2 diabetes might be to improve the duration and quality of their sleep.

"Sleep is modifiable," said Kristen Knutson, research associate (assistant professor) in the department of health studies at the University of Chicago and first author of the paper. "We've known for some time that skimping on sleep can impair glucose tolerance even for healthy people. Now we have evidence connecting chronic partial sleep deprivation and reduced blood-sugar control in patients with diabetes."

"Although we can't be certain whether sleep loss makes diabetes worse or the diabetes interferes with sleep, it only makes sense for everyone, but especially patients with diabetes, to give themselves the opportunity to get enough sleep," Knutson said.

The study focused on 161 African-American patients being treated at the University of Chicago Hospitals for type 2 diabetes. The researchers asked participants how much sleep they thought they needed at night and how much sleep they managed to get on weeknights and weekends. They also assessed the quality of their sleep using a standard 19-item questionnaire, the Pittsburgh Sleep Quality Index (PSQI).

To assess blood sugar control they measured glycosylated hemoglobin, a standard tool for management of patients with diabetes. Glycosylated hemoglobin, or HbA1c, reflects the average blood glucose level over the previous three months. A normal HbA1c result is between four and six percent. Higher levels represent poor glucose control. Patients with diabetes are considered to be under good control if they can keep their levels below seven percent.

The researchers found that, on average, the 161 diabetes patients got very little sleep and had poor glucose control. Mean sleep duration was six hours a night. Only six percent reported getting eight hours of sleep on weeknights and only 22 percent reported getting at least seven hours. Seventy-one percent had poor sleep quality. The median HbA1c score was 8.3 percent.

Many patients with diabetes have painful complications that can interfere with sleep. Even after the researchers excluded 39 patients who reported such pain, however, two out of three of the remaining 122 patients reported poor quality sleep. The average HbA1c among those patients was almost as high: 8.2 percent.

Insufficient or poor quality sleep was closely associated with higher HbA1c results. For patients with no complications of their diabetes, a three-hour "perceived sleep debt"--the difference between how much sleep they felt they needed and how much they think they got--was associated with a 1.1 percentage-point increase in HbA1c levels, for example from 7.5 percent up to 8.6 percent.

For patients with at least one complication of diabetes--such as nerve pain, kidney damage or coronary artery disease--decreased sleep quality appeared to be more important. An increase of five points (out of 21) on the PSQI was associated with a 1.9 percentage-point increase in HbA1c, for example from 8.7 percent up to 10.6 percent.

"The magnitude of these effects," the authors note, "is comparable to those of widely used oral antidiabetic agents."

A long series of laboratory and epidemiologic studies has suggested that cutting back on sleep has a harmful effect on glucose control, insulin secretion and metabolism in ways that might increase diabetes risk, said Eve Van Cauter, professor of medicine at the University of Chicago and senior author of the study. The current study asks the question: is glucose control in subjects who already have diabetes adversely affected by too little sleep or poor sleep?

"Our findings suggest, at least in this study population, that short or poor sleep is associated with decreased blood-sugar control in patients who already have diabetes," she said. "The growing tendency to burn the candle at both ends may be a significant contributor to the current epidemic of diabetes. One way to slow down this epidemic may be to avoid building a chronic sleep debt."

The MacArthur Foundation, the American Diabetes Association and the National Institutes of Health funded this study. Additional authors are Armand Ryden, of the University of Chicago, and Bryce Mander, now at Northwestern University.

Adapted from materials provided by University of Chicago Medical Center.

Lack Of Deep Sleep May Increase Risk Of Type 2 Diabetes

2008-01-06T00:25:00.000-08:00

ScienceDaily (Jan. 2, 2008) — Suppression of slow-wave sleep in healthy young adults significantly decreases their ability to regulate blood-sugar levels and increases the risk of type 2 diabetes, report researchers at the University of Chicago Medical Center.

Deep sleep, also called "slow-wave sleep," is thought to be the most restorative sleep stage, but its significance for physical well-being has not been demonstrated. This study found that after only three nights of selective slow-wave sleep suppression, young healthy subjects became less sensitive to insulin. Although they needed more insulin to dispose of the same amount of glucose, their insulin secretion did not increase to compensate for the reduced sensitivity, resulting in reduced tolerance to glucose and increased risk for type 2 diabetes. The decrease in insulin sensitivity was comparable to that caused by gaining 20 to 30 pounds.

Previous studies have demonstrated that reduced sleep quantity can impair glucose metabolism and appetite regulation resulting in increased risk of obesity and diabetes. This current study provides the first evidence linking poor sleep quality to increased diabetes risk.

"These findings demonstrate a clear role for slow-wave sleep in maintaining normal glucose control," said the study's lead author, Esra Tasali, MD, assistant professor of medicine at the University of Chicago Medical Center. "A profound decrease in slow-wave sleep had an immediate and significant adverse effect on insulin sensitivity and glucose tolerance."

"Since reduced amounts of deep sleep are typical of aging and of common obesity-related sleep disorders, such as obstructive sleep apnea these results suggest that strategies to improve sleep quality, as well as quantity, may help to prevent or delay the onset of type 2 diabetes in populations at risk," said Eve Van Cauter, PhD, professor of medicine at the University of Chicago and senior author of the study.

The researchers studied nine lean, healthy volunteers, five men and four women between the ages of 20 and 31. The subjects spent two consecutive nights in the sleep laboratory, where they went to bed at 11 P.M., slept undisturbed but carefully monitored, and got out of bed 8.5 hours later, at 7:30 A.M.

The same subjects were also studied for three consecutive nights during which they followed identical nighttime routines. During this session, however, when their brain waves indicated that they were drifting into slow-wave sleep they were subtly disturbed by sounds administered through speakers beside the bed.

These sounds were loud enough to disrupt deep sleep but not so loud as to cause a full awakening. This technique enabled the researchers to decrease slow-wave sleep by about 90 percent, shifting the subjects from the onset of deep sleep (stage 3 or 4) to a lighter sleep (stage 2) without altering total sleep time.

"Our system proved quite effective," Tasali said. When asked about the sounds the next morning, study subjects vaguely recalled hearing a noise "three or four times," during the night. Some recalled as many as 10 to 15. On average, however, subjects required about 250-300 interventions each night, fewer the first night but more on subsequent nights as "slow-wave pressure," the body's need for deep sleep, accumulated night after night.

"This decrease in slow-wave sleep resembles the changes in sleep patterns caused by 40 years of aging," Tasali said. Young adults spend 80 to 100 minutes per night in slow-wave sleep, while people over age 60 generally have less than 20 minutes. "In this experiment," she said, "we gave people in their 20s the sleep of those in their 60s."

At the end of each study, the researchers gave intravenous glucose (a sugar solution) to each subject, then took blood samples every few minutes to measure the levels of glucose and insulin, the hormone that controls glucose uptake.

They found that when slow-wave sleep was suppressed for only three nights, young healthy subjects became about 25 percent less sensitive to insulin. As insulin sensitivity decreased, subjects needed more insulin to dispose of the same amount of glucose. But for eight of the nine subjects, insulin secretion did not go up to compensate for reduced effects. The result was a 23 percent increase in blood-glucose levels, comparable to older adults with impaired glucose tolerance.

Those with low baseline levels of slow-wave sleep had the lowest levels after having their sleep patterns disrupted and the greatest decrease in insulin sensitivity.

The alarming rise in the prevalence of type 2 diabetes is generally attributed to the epidemic of obesity combined with the aging of the population. "Previous studies from our lab have demonstrated many connections between chronic, partial, sleep deprivation, changes in appetite, metabolic abnormalities, obesity, and diabetes risk," said Van Cauter. "These results solidify those links and add a new wrinkle, the role of poor sleep quality, which is also associated with aging."

"Chronic shallow non-REM sleep, decreased insulin sensitivity and elevated diabetes risk are typical of aging," the authors conclude. "Our findings raise the question of whether age-related changes in sleep quality contribute to the development of these metabolic alterations."

This research was reported in the "Early Edition" of the Proceedings of the National Academy of Science, available online Dec. 31, 2007.

The National Institutes of Health funded this research. Additional authors include Rachel Leproult and David Ehrmann of the University of Chicago Medical Center.

Adapted from materials provided by University of Chicago Medical Center.

Why Wounds Are Slow To Heal In Diabetics

2008-01-06T00:23:00.001-08:00

ScienceDaily (May 6, 2007) — Individuals with diabetes often experience slow or limited wound healing. Endothelial progenitor cells (EPCs), which derive from bone marrow, normally travel to sites of injury and are essential for the formation of blood vessels and wound healing.

In a study reported in the May 1st issue of the Journal of Clinical Investigation, Omaida Velazquez and colleagues from University of Pennsylvania Medical Center reveal why the numbers of these vital EPCs are decreased in the circulation and at wound sites in diabetes.

The authors examined diabetic mice and found that increased oxygen levels (hyperoxia) enhanced the mobilization of EPCs from the bone marrow to the peripheral blood circulation. The high oxygen levels increased the activation of the bone marrow enzyme eNOS, which stimulated nitric oxide production, helping to produce greater numbers of EPCs.

However, local injection of the chemokine stromal cell--derived factor 1 alpha (SDF-1alpha) was required to recruit these EPCs from the circulation to the wound site. The increased presence of EPCs at the wound site resulted in accelerated wound healing. The authors concluded that impaired eNOS activation and decreased SDF-1alpha expression in diabetes are responsible for the defect in diabetic wound healing.

In an accompanying commentary, Harold Brem and Marjana Tomic-Canic from Columbia University and Cornell University, respectively, reinforce that future therapeutics for diabetic wound healing will have to correct multiple deficiencies simultaneously. Therapeutic interventions, including correcting EPC activation via hyperbaric oxygen therapy and correcting EPC homing via administration of SDF-1alpha, may significantly accelerate diabetic wound healing by correcting the deficit in EPC number that is inherent to diabetic wounds.

Article: Diabetic impairments in NO-mediated endothelial progenitor cell mobilization and homing are reversed by hyperoxia and SDF-1alpha

Adapted from materials provided by Journal of Clinical Investigation.

2007-12-13T02:49:00.001-08:00

Journal of The American Medical Association Announces Recommendation that All Adults Should Take Vitamins

July 2002 -- In a landmark article published June 19, 2002, The Journal of The American Medical Association (JAMA) announced that all adults should take vitamin supplements to help prevent chronic diseases.

Clinical Applications

Robert H. Fletcher, MD,MSc; Kathleen M. Fairfield, MD,DrPH
JAMA. 2002;287:3127-3129.

Vitamin deficiency syndromes such as scurvy and beriberi are uncommon in Western societies. However, suboptimal intake of some vitamins, above levels causing classic vitamin deficiency, is a risk factor for chronic diseases and common in the general population, especially the elderly. Suboptimal folic acid levels, along with suboptimal levels of vitamins B6 and B12, are a risk factor for cardiovascular disease, neural tube defects, and colon and breast cancer; low levels of vitamin D contribute to osteopenia and fractures; and low levels of the antioxidant vitamins (vitamins A, E, and C) may increase risk for several chronic diseases. Most people do not consume an optimal amount of all vitamins by diet alone. Pending strong evidence of effectiveness from randomized trials, it appears prudent for all adults to take vitamin supplements. The evidence base for tailoring the contents of multivitamins to specific characteristics of patients such as age, sex, and physical activity and for testing vitamin levels to guide specific supplementation practices is limited. Physicians should make specific efforts to learn about their patients' use of vitamins to ensure that they are taking vitamins they should, such as folate supplementation for women in the childbearing years, and avoiding dangerous practices such as high doses of vitamin A during pregnancy or massive doses of fat-soluble vitamins at any age.

Author Affiliations: Department of Ambulatory Care and Prevention, Harvard Medical School/Harvard Pilgrim Health Care, and Department of Epidemiology, Harvard School of Public Health (Dr Fletcher); Division of General Medicine and Primary Care, Beth Israel Deaconess Medical Center, and Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School (Dr Fairfield), Boston, Mass.

How should adults who haven't been taking vitamins choose the right ones for them?

The Dietary Supplement Information Bureau (DSIB), a non-profit information resource created specifically to provide consumers with scientifically accurate, up-to-date information, offers some practical advice. According to Dr. Jeffrey Blumberg, a member of the DSIB Scientific Advisory Board and a nutrition scientist who is an authority on disease prevention through vitamin supplementation, here are some guidelines for choosing vitamins:

The JAMA study recommends multivitamins for all adults. Choose one that contains minerals as well as vitamins.
Read the ingredients panel carefully. Your goal is to come as close as possible to the RDA, which is the minimum daily requirement of each vitamin and mineral your body needs.
Remember to take your vitamins every day, preferably with meals. Taking them only occasionally, or seasonally, will not be as effective.
You also may need other supplements to achieve the minimum daily requirement of certain vitamins and minerals (calcium, for example) beyond the amount contained in any multivitamin. Read directions carefully.
Check the expiration date on the bottle. Reliable companies all list them.
Consider formulations made specifically for your age group and life stage. There are multivitamins designed for children, for adults, for seniors, and for pregnant women.
Select a brand name you trust. Your health care professional can provide advice on brands.

Much more detailed information can be found on The Dietary Supplement Information Bureau's Web site, which provides medically and scientifically accurate, up-to-date information to consumers and does not sell any product. The Web site can be found at: http://www.supplementinfo.org.

The Dietary Supplement Information Bureau(TM) (DSIB (TM)) is a national non-profit organization created to provide accurate information to consumers and to the professional healthcare community about vitamins, minerals, herbs and other supplements for the purpose of improving quality of life through better health.

The DSIB (TM) Scientific Advisory Board oversees the development and dissemination of all information with IMAGINutrition, Inc. (http://www.imaginutrition.com), a nutrition technology innovation and research think tank based in Laguna Niguel, CA. IMAGINutrition collaborates with academic research centers on clinical trials using dietary supplements and regularly collects, analyzes, and disseminates the latest research on dietary supplements.

For more information about the DSIB(TM) or dietary supplements, visit the DSIB(TM) Web site at http://www.supplementinfo.org.

More Support for Vitamins!

Consistent use of multivitamins and other key supplements can promote good health and help prevent disease, according to a new report released from the Council for Responsible Nutrition. The report found that ongoing use of multivitamins and other supplements (like calcium or folic acid) can have a demonstrable impact on health. Read Research Documents Benefits of Vitamins and Supplements.

Source: PR Newswire

http://jama.ama-assn.org/cgi/content/abstract/287/23/

Why you need Supplements

2007-12-13T01:09:00.001-08:00

Cancer an Overview : Risk Factors

2007-12-12T21:40:00.000-08:00

Doctors often cannot explain why one person develops cancer and another does not. But research shows that certain risk factors increase the chance that a person will develop cancer. These are the most common risk factors for cancer:

Growing older
Tobacco
Sunlight
Ionizing radiation
Certain chemicals and other substances
Some viruses and bacteria
Certain hormones
Family history of cancer
Alcohol
Poor diet, lack of physical activity, or being overweight

Many of these risk factors can be avoided. Others, such as family history, cannot be avoided. People can help protect themselves by staying away from known risk factors whenever possible.

If you think you may be at risk for cancer, you should discuss this concern with your doctor. You may want to ask about reducing your risk and about a schedule for checkups.

Over time, several factors may act together to cause normal cells to become cancerous. When thinking about your risk of getting cancer, these are some things to keep in mind:

Not everything causes cancer.
Cancer is not caused by an injury, such as a bump or bruise.
Cancer is not contagious. Although being infected with certain viruses or bacteria may increase the risk of some types of cancer, no one can "catch" cancer from another person.
Having one or more risk factors does not mean that you will get cancer. Most people who have risk factors never develop cancer.
Some people are more sensitive than others to the known risk factors.

The sections below have more detailed information about the most common risk factors for cancer. You also may want to read the NCI booklet Cancer and the Environment.

Growing Older

The most important risk factor for cancer is growing older. Most cancers occur in people over the age of 65. But people of all ages, including children, can get cancer, too.

Tobacco

Tobacco use is the most preventable cause of death. Each year, more than 180,000 Americans die from cancer that is related to tobacco use.

Using tobacco products or regularly being around tobacco smoke (environmental or secondhand smoke) increases the risk of cancer.

Smokers are more likely than nonsmokers to develop cancer of the lung, larynx (voice box), mouth, esophagus, bladder, kidney, throat, stomach, pancreas, or cervix. They also are more likely to develop acute myeloid leukemia (cancer that starts in blood cells).

People who use smokeless tobacco (snuff or chewing tobacco) are at increased risk of cancer of the mouth.

Quitting is important for anyone who uses tobacco - even people who have used it for many years. The risk of cancer for people who quit is lower than the risk for people who continue to use tobacco. (But the risk of cancer is generally lowest among those who never used tobacco.)

Also, for people who have already had cancer, quitting may reduce the chance of getting another cancer.

There are many resources to help people stop using tobacco:

· Staff at the NCI's Smoking Quitline (1-877-44U-QUIT) and at LiveHelp (click on "Need Help?" at http://www.cancer.gov) can talk with you about ways to quit smoking and about groups that help smokers who want to quit. Groups may offer counseling in person or by telephone.

· A Federal Government Web site, http://www.smokefree.gov, has an online guide to quitting smoking and a list of other resources.

· Doctors and dentists can help their patients find local programs or trained professionals who help people stop using tobacco.

· Doctors and dentists can suggest medicine or nicotine replacement therapy, such as a patch, gum, lozenge, nasal spray, or inhaler.

Sunlight

Ultraviolet (UV) radiation comes from the sun, sunlamps, and tanning booths. It causes early aging of the skin and skin damage that can lead to skin cancer.

Doctors encourage people of all ages to limit their time in the sun and to avoid other sources of UV radiation:

It is best to avoid the midday sun (from mid-morning to late afternoon) whenever possible. You also should protect yourself from UV radiation reflected by sand, water, snow, and ice. UV radiation can penetrate light clothing, windshields, and windows.
Wear long sleeves, long pants, a hat with a wide brim, and sunglasses with lenses that absorb UV.
Use sunscreen. Sunscreen may help prevent skin cancer, especially sunscreen with a sun protection factor (SPF) of at least 15. But sunscreens cannot replace avoiding the sun and wearing clothing to protect the skin.
Stay away from sunlamps and tanning booths. They are no safer than sunlight.

Protect yourself from the sun.

Ionizing Radiation

Ionizing radiation can cause cell damage that leads to cancer. This kind of radiation comes from rays that enter the Earth's atmosphere from outer space, radioactive fallout, radon gas, x-rays, and other sources.

Radioactive fallout can come from accidents at nuclear power plants or from the production, testing, or use of atomic weapons. People exposed to fallout may have an increased risk of cancer, especially leukemia and cancers of the thyroid, breast, lung, and stomach.

Radon is a radioactive gas that you cannot see, smell, or taste. It forms in soil and rocks. People who work in mines may be exposed to radon. In some parts of the country, radon is found in houses. People exposed to radon are at increased risk of lung cancer.

Medical procedures are a common source of radiation:

Doctors use radiation (low-dose x-rays) to take pictures of the inside of the body. These pictures help to diagnose broken bones and other problems.
Doctors use radiation therapy (high-dose radiation from large machines or from radioactive substances) to treat cancer.

The risk of cancer from low-dose x-rays is extremely small. The risk from radiation therapy is slightly higher. For both, the benefit nearly always outweighs the small risk.

You should talk with your doctor if you are concerned that you may be at risk for cancer due to radiation.

If you live in a part of the country that has radon, you may wish to test your home for high levels of the gas. The home radon test is easy to use and inexpensive. Most hardware stores sell the test kit.

You should talk with your doctor or dentist about the need for each x-ray. You should also ask about shields to protect parts of the body that are not in the picture.

Cancer patients may want to talk with their doctor about how radiation treatment could increase their risk of a second cancer later on.

Certain Chemicals and Other Substances

People who have certain jobs (such as painters, construction workers, and those in the chemical industry) have an increased risk of cancer. Many studies have shown that exposure to asbestos, benzene, benzidine, cadmium, nickel, or vinyl chloride in the workplace can cause cancer.

Follow instructions and safety tips to avoid or reduce contact with harmful substances both at work and at home. Although the risk is highest for workers with years of exposure, it makes sense to be careful at home when handling pesticides, used engine oil, paint, solvents, and other chemicals.

Some Viruses and Bacteria

Being infected with certain viruses or bacteria may increase the risk of developing cancer:

Human papillomaviruses (HPVs): HPV infection is the main cause of cervical cancer. It also may be a risk factor for other types of cancer.
Hepatitis B and hepatitis C viruses: Liver cancer can develop after many years of infection with hepatitis B or hepatitis C.
Human T-cell leukemia/lymphoma virus (HTLV-1): Infection with HTLV-1 increases a person's risk of lymphoma and leukemia.
Human immunodeficiency virus (HIV): HIV is the virus that causes AIDS. People who have HIV infection are at greater risk of cancer, such as lymphoma and a rare cancer called Kaposi's sarcoma.
Epstein-Barr virus (EBV): Infection with EBV has been linked to an increased risk of lymphoma.
Human herpesvirus 8 (HHV8): This virus is a risk factor for Kaposi's sarcoma.
Helicobacter pylori : This bacterium can cause stomach ulcers. It also can cause stomach cancer and lymphoma in the stomach lining.

Do not have unprotected sex or share needles. You can get an HPV infection by having sex with someone who is infected. You can get hepatitis B, hepatitis C, or HIV infection from having unprotected sex or sharing needles with someone who is infected.

You may want to consider getting the vaccine that prevents hepatitis B infection. Health care workers and others who come into contact with other people's blood should ask their doctor about this vaccine.

If you think you may be at risk for HIV or hepatitis infection, ask your doctor about being tested. These infections may not cause symptoms, but blood tests can show whether the virus is present. If so, the doctor may suggest treatment. Also, the doctor can tell you how to avoid infecting other people.

If you have stomach problems, see a doctor. Infection with H. pylori can be detected and treated.

Certain Hormones

Doctors may recommend hormones (estrogen alone or estrogen along with progestin) to help control problems (such as hot flashes, vaginal dryness, and thinning bones) that may occur during menopause. However, studies show that menopausal hormone therapy can cause serious side effects. Hormones may increase the risk of breast cancer, heart attack, stroke, or blood clots.

A woman considering menopausal hormone therapy should discuss the possible risks and benefits with her doctor.

Diethylstilbestrol (DES), a form of estrogen, was given to some pregnant women in the United States between about 1940 and 1971. Women who took DES during pregnancy may have a slightly higher risk of developing breast cancer. Their daughters have an increased risk of developing a rare type of cancer of the cervix. The possible effects on their sons are under study.

Women who believe they took DES and daughters who may have been exposed to DES before birth should talk with their doctor about having checkups.

Family History of Cancer

Most cancers develop because of changes (mutations) in genes. A normal cell may become a cancer cell after a series of gene changes occur. Tobacco use, certain viruses, or other factors in a person's lifestyle or environment can cause such changes in certain types of cells.

Some gene changes that increase the risk of cancer are passed from parent to child. These changes are present at birth in all cells of the body.

It is uncommon for cancer to run in a family. However, certain types of cancer do occur more often in some families than in the rest of the population. For example, melanoma and cancers of the breast, ovary, prostate, and colon sometimes run in families. Several cases of the same cancer type in a family may be linked to inherited gene changes, which may increase the chance of developing cancers. However, environmental factors may also be involved. Most of the time, multiple cases of cancer in a family are just a matter of chance.

If you think you may have a pattern of a certain type of cancer in your family, you may want to talk to your doctor. Your doctor may suggest ways to try to reduce your risk of cancer. Your doctor also may suggest exams that can detect cancer early.

You may want to ask your doctor about genetic testing. These tests can check for certain inherited gene changes that increase the chance of developing cancer. But inheriting a gene change does not mean that you will definitely develop cancer. It means that you have an increased chance of developing the disease.

Alcohol

Having more than two drinks each day for many years may increase the chance of developing cancers of the mouth, throat, esophagus, larynx, liver, and breast. The risk increases with the amount of alcohol that a person drinks. For most of these cancers, the risk is higher for a drinker who uses tobacco.

Doctors advise people who drink to do so in moderation. Drinking in moderation means no more than one drink per day for women and no more than two drinks per day for men.

Poor Diet, Lack of Physical Activity, or Being Overweight

People who have a poor diet, do not have enough physical activity, or are overweight may be at increased risk of several types of cancer. For example, studies suggest that people whose diet is high in fat have an increased risk of cancers of the colon, uterus, and prostate. Lack of physical activity and being overweight are risk factors for cancers of the breast, colon, esophagus, kidney, and uterus.

Choose a diet rich in fruits and vegetables.

Having a healthy diet, being physically active, and maintaining a healthy weight may help reduce cancer risk. Doctors suggest the following:

Eat well: A healthy diet includes plenty of foods that are high in fiber, vitamins, and minerals. This includes whole-grain breads and cereals and 5 to 9 servings of fruits and vegetables every day. Also, a healthy diet means limiting foods high in fat (such as butter, whole milk, fried foods, and red meat).
Be active and maintain a healthy weigh Physical activity can help control your weight and reduce body fat. Most scientists agree that it is a good idea for an adult to have moderate physical activity (such as brisk walking) for at least 30 minutes on 5 or more days each week.

Adapted from Article by US National Cancer Institute, www.cancer.gov

2007-12-12T21:35:00.001-08:00

Defining Cancer

Cancer is a term for diseases in which abnormal cells divide without control and can invade other tissues. Cancer cells can spread to other parts of the body through the blood and lymph systems.

Cancer is not just one disease but many diseases. There are more than 100 different types of cancer. The main categories of cancer include:

Carcinoma - cancer that begins in the skin or in tissues that line or cover internal organs.
Sarcoma - cancer that begins in bone, cartilage, fat, muscle, blood vessels, or other connective or supportive tissue.
Leukemia - cancer that starts in blood-forming tissue such as the bone marrow and causes large numbers of abnormal blood cells to be produced and enter the blood.
Lymphoma and myeloma - cancers that begin in the cells of the immune system.
Central nervous system cancers - cancers that begin in the tissues of the brain and spinal cord.

(For definitions of other cancer-related terms, see NCI's Dictionary of Cancer Terms.)

Origins of Cancer

All cancers begin in cells, the body's basic unit of life. To understand cancer, it's helpful to know what happens when normal cells become cancer cells.

The body is made up of many types of cells. These cells grow and divide in a controlled way to produce more cells as they are needed to keep the body healthy. When cells become old or damaged, they die and are replaced with new cells.

But sometimes this orderly process goes wrong. The genetic material (DNA) of a cell can become damaged or changed, producing mutations that affect normal cell growth and division. When this happens, cells do not die when they should and new cells form when the body does not need them. The extra cells may form a mass of tissue called a tumor.

(Image from Understanding Cancer Series: Cancer.)

Not all tumors are cancerous; tumors can be benign or malignant.

Benign tumors aren't cancerous. They can often be removed, and, in most cases, they do not come back. Cells in benign tumors do not spread to other parts of the body.
Malignant tumors are cancerous. Cells in these tumors can invade nearby tissues and spread to other parts of the body. The spread of cancer from one part of the body to another is called metastasis.

Most cancers are named for the organ or type of cell in which they begin. For example, cancer that begins in the stomach is called stomach cancer.

Some cancers do not form tumors. For example, leukemia is a cancer of the bone marrow and blood.

Cancer Statistics

A new report from the nation's leading cancer organizations shows cancer death rates decreased on average 2.1 percent per year from 2002 through 2004, nearly twice the annual decrease of 1.1 percent per year from 1993 through 2002. (Read more about the Annual Report.)

Estimated new cases and deaths from cancer in the United States in 2007:

New cases: 1,444,920 (does not include nonmelanoma skin cancers)
Deaths: 559,650

NCI's Cancer Stat Fact Sheets provide frequently requested cancer statistics for a number of cancer types.

Adapted from article by National Cancer Institute of US www.cancer.gov

2007-12-12T21:29:00.001-08:00

Effects of Grape Seed Extracts

Human case reports and results from some laboratory and animal studies appear to show that grape seed extract may help to prevent and treat heart diseases such as high blood pressure and high cholesterol. By limiting oxidation, antioxidants in grape seed extract may help prevent changes, including damage to blood vessels, that may contribute to the development of heart disease. Substances in grape seed extract may also block the effects of enzymes that process fats, including cholesterol, from the diet. Consequently, less fat may be absorbed and more may be eliminated from the body. Other research shows that grape seed extract may help to prevent or control damage to body cells that is caused by drugs, pollution, tobacco, and other toxins. While all of these studies appear promising, much more research including long-term studies in humans is needed to confirm initial findings.

Proanthocyanidins are also believed to block the deterioration of blood vessels, therefore, grape seed extract may improve conditions involving veins and arteries. It has been used to prevent, delay, and treat a condition known as chronic venous insufficiency, which occurs when valves in the veins that carry blood back to the heart are weak or damaged. The blood that collects in the veins of the legs can lead to varicose veins, spider veins, or sores on the legs. Results that are more serious may include blood clots in the legs or sores that do not heal and may become infected. This blood vessel strengthening effect of grape seed extract may also help to prevent and treat hemorrhoids.

Since proanthocyanidins in grape seed extract strengthen the walls of all blood vessels, they may also help to keep damaged, stretched, or stiff blood vessels from leaking. In one area of research, grape seed extract may be effective for slowing retinopathy, the gradual break down of the retinas in the eyes, usually due to blood vessel damage. Individuals with arteriosclerosis (a build up of fatty deposits in the arteries), diabetes, or other conditions that increase the likelihood for damage to the small blood vessels in the eyes are more likely to have serious vision problems as a result of that damage. Grape seed extract may also reduce eye stress caused by bright lights. In studies of laboratory animals, it has shown some possible effectiveness in preventing cataract formation, but further study is needed to determine whether this effect may pertain to humans.

One of the polyphenols contained in grape seed extract is called resveratrol. In laboratory and animal studies, resveratrol from grape seeds has appeared to interfere with cancer cell growth and division, as well as causing some cancer cells to disintegrate faster than they would ordinarily. In addition, it may also block enzymes that prolong the survival of several cancer cell types, including skin cancer, prostate cancer, and breast cancer. As a result, tumors may either stop growing or actually shrink because higher than usual numbers of cancer cells die. Therefore, resveratrol may have direct anticancer activity. It may also increase the effectiveness and/or lower the side effects of drugs currently used for cancer chemotherapy. One possible result is that taking resveratrol during chemotherapy may allow lower doses of cancer drugs to be effective, thereby limiting the potential for debilitating side effects. A similar effect was seen in laboratory studies of grape seed extract against HIV, the virus that causes AIDS. Although the exact ways that grape seed extract may fight HIV and other viruses are not known, it is thought that grape seed extract interferes with viral multiplication, possibly by preventing viral attachment to host cells. How high doses of resveratrol and other chemicals in grape seed extract may affect normal human cells is not yet known.

Grape seed extract may also have topical uses. In preliminary research, grape seed extract appears to be moderately effective for preventing tooth decay. It is believed to delay or stop the breakdown of sugars in the mouth and also to inhibit the growth of certain oral bacteria that may play a role in forming dental cavities. In other studies, injuries to the skin of laboratory animals may have healed better when grape seed extract was applied. Through several possible effects that include promoting the regrowth of connective tissues, grape seed extract is believed to encourage faster, stronger healing with less scarring.

Oil pressed from grape seeds is used as a dietary supplement. It contains a relatively high percentage of linoleic acid, which belongs to a group of nutrients known as essential fatty acids (EFAs). The body needs EFAs to regulate activities that include heart function, insulin utilization, and mood balance. However, the body cannot produce EFAs, so they must be obtained from foods or dietary supplements. EFAs are thought to block the production of chemicals that promote the formation of deposits in the blood vessels. Consequently, blood pressure and blood cholesterol levels may be lowered and the risk of heart disease may decrease. Additional studies are needed to confirm the effects of both linoleic acid and grape seed oil for lowering the risk of heart disease.

From article by Wikipedia

http://en.wikipedia.org/wiki/Grape_seed_extract

2007-12-12T21:06:00.001-08:00

Higher Trans Fat Levels In Blood Associated With Elevated Risk Of Heart Disease

ScienceDaily (Mar. 28, 2007) — High consumption of trans fat, found mainly in partially hydrogenated vegetable oils and widely used by the food industry, has been linked to an increased risk of coronary heart disease (CHD). New York and Philadelphia have passed measures eliminating its use in restaurants, and other cities are considering similar bans. A new study from the Harvard School of Public Health (HSPH) provides the strongest association to date between trans fat and heart disease. It found that women in the U.S. with the highest levels of trans fat in their blood had three times the risk of CHD as those with the lowest levels. The study will appear in the April 10, 2007 print issue of Circulation: Journal of the American Heart Association.

“The strength of this study is that the amount of trans fatty acid levels was measured in blood samples from the study population. Because humans cannot synthesize trans fatty acids, the amount of trans fat in red blood cells is an excellent biomarker of trans fat intake,” said senior author Frank Hu, associate professor of nutrition and epidemiology at HSPH.

Clinical trials have shown that trans fatty acids increase LDL cholesterol and lower HDL cholesterol, making them the only class of fatty acids, which includes saturated fat, to have this dual effect. HDL (high-density lipoprotein) is considered a “good” cholesterol; LDL (low-density lipoprotein) a “bad” cholesterol.

The researchers, led by Hu and lead author Qi Sun, a graduate research assistant at HSPH, set out to test the assumption that higher trans fatty acid levels in erythrocytes—red blood cells—were associated with a higher risk of heart disease among U.S. women. Blood samples collected in 1989 and 1990 from 32,826 participants in the Brigham and Women’s Hospital-based Nurses’ Health Study were examined. During six years of follow-up, 166 cases of CHD were diagnosed and matched with 327 controls for age, smoking status, fasting status and date of blood drawing.

After adjusting for age, smoking status and other dietary and lifestyle cardiovascular risk factors, the researchers found that a higher level of trans fatty acids in red blood cells was associated with an elevated risk of CHD. The risk among women in the top quartile of trans fat levels was triple that of the lowest quartile. “Positive associations have been shown in earlier studies based on dietary data provided by the participants, but the use of biomarkers of trans fatty acids is believed to be more reliable than self-reports. This is probably the reason why we see an even stronger association between blood levels of trans fat and risk of CHD in this study,” said Sun.

“These data provide further justifications for current efforts to remove trans fat from foods and restaurant meals,” said Hu. “Trans fat intake in the U.S. is still high. Reducing trans fat intake should remain an important public health priority.”

The study was supported by the National Institutes of Health.

“A Prospective Study of Trans Fatty Acids in Erythrocytes and Risk of Coronary Heart Disease,” Qi Sun, Jing Ma, Hannia Campos, Susan E. Hankinson, JoAnn E. Manson, Meir J. Stampfer, Kathryn M. Rexrode, Walter C. Willett, Frank B. Hu, Circulation, April 10, 2007.

Adapted from materials provided by Harvard School of Public Health.

2007-12-12T21:02:00.001-08:00

Trans Fat Leads To Weight Gain Even On Same Total Calories, Animal Study Shows

ScienceDaily (Jun. 19, 2006) — The "apple" body shape that increases the risk of diabetes and heart disease may be accelerated by eating trans fat such as partially hydrogenated vegetable oil, according to new animal research at Wake Forest University School of Medicine.

"Diets rich in trans fat cause a redistribution of fat tissue into the abdomen and lead to a higher body weight even when the total dietary calories are controlled," said Lawrence L. Rudel, Ph.D., professor of pathology and biochemistry and head of the Lipid Sciences Research Program.

"What it says is that trans fat is worse than anticipated," Rudel said. "I was surprised."

According to the U.S. Food and Drug Administration (FDA), consumption of saturated fat, trans fat, and dietary cholesterol raises low-density lipoprotein (LDL), or "bad" cholesterol, levels, which increases the risk of coronary artery disease.

Kylie Kavanagh, D.V.M., presented the findings today at the 66th annual Scientific Sessions of the American Diabetes Association in Washington, D.C. She said that over six years, male monkeys fed a western-style diet that contains trans fat had a 7.2 percent increase in body weight, compared to a 1.8 percent increase in monkeys that ate monounsaturated fats, such as olive oil.

All that extra weight went to the abdomen, and some other body fat was redistributed to the abdomen. Computed tomography (CT) scans showed that the monkeys on the diet containing trans fats had dramatically more abdominal fat than the monkeys on the monounsaturated fat. "We measured the volume of fat using CT," Kavanagh said. "They deposited 30 percent more fat in their abdomen."

The monkeys all were given the same amount of daily calories, with 35 percent of the calories coming from fat. The amount of calories they got should only have been enough to maintain their weight, not increase it, Rudel said. "We believed they couldn't get obese because we did not give them enough calories to get fat."

One group of monkeys got 8 percent of their calories from trans fat while the other group received those calories as monounsaturated fat. The researchers said that this amount of trans fat is comparable to people who eat a lot of fried food.

"We conclude that in equivalent diets, trans fatty acid consumption increases weight gain," said Kavanagh.

Over the entire course of the study, there was a small but significant difference in weight between the two groups. "In the world of diabetes, everybody knows that just 5 percent weight loss makes enormous difference," Kavanagh said. "This little difference was biologically quite significant."

Rudel said, "The study was specifically funded to look at the role of trans fatty acids in atherosclerosis."

He said that at the time he got a grant from the National Heart, Lung and Blood Institute, there was not much evidence in the literature and no animal models that documented the hazards of trans fats, though there are data showing it was a risk factor for atherosclerosis.

Kavanagh said the six-year length of the study was equivalent to 20 years in people.

According to the FDA, trans fat is found in vegetable shortenings, some margarines, crackers, cookies, snack foods, and other foods made with or fried in partially hydrogenated oils. Unlike other fats, the majority of trans fat is formed when food manufacturers turn liquid oils into solid fats like shortening and hard margarine by adding hydrogen.

Since Jan. 1, the FDA has required the amount of trans fat to be listed in the nutrition facts panel on all foods. But the restaurant industry is exempt.

Other researchers on the American Diabetes Society report include Janice D. Wagner, Ph.D., D.V.M., John Jeffrey Carr, M.D., Kate Jones, B.S., Janet Sawyer, M.S., and Kathryn Kelly., B.S., all from Wake Forest University School of Medicine.

Adapted from materials provided by Wake Forest University Baptist Medical Center.

2007-12-12T21:01:00.001-08:00

Trans Fatty Acids: What Are They And Why Shouldn't You Eat Them?

ScienceDaily (Sep. 24, 2003) — Just what is the skinny on those trans fatty acids that are so bad for you? Donuts, stick margarines, French fries, cookies and other tasty snacks are loaded with them. And this summer the Food and Drug Administration decreed that as of Jan. 1, 2006, manufacturers must break the trans fats category out of the total fat listing on labels.

Chemical &Engineering News, in its Sept. 22 issue, describes the chemistry of these culprits. C&EN is the newsmagazine of the American Chemical Society, the world's largest scientific society.

In issuing its order, the FDA relied mainly on an Institute of Medicine report that concluded that consuming foods containing trans fatty acids raises LDL (bad) cholesterol and the risk of coronary heart disease, according to C&EN. The IOM recommended people keep their consumption of trans fats as low as possible, and to help consumers do this the FDA issued the labeling requirement.

What are trans fatty acids?

Unsaturated fats, found in such foods as avocados and olive and corn oils are heart healthy, but in the air they can go rancid by absorbing oxygen and then decompose, C&EN explains. Manufacturers can stop this process by bubbling hydrogen (hydrogenation) through the fat at a high temperature in the presence of a catalyst like nickel and in the absence of oxygen.

The process raises a fat's melting point, turning liquid vegetable oil into products ranging from soft margarine to solid shortening, according to the newsmagazine. When the healthful unsaturated fats are partially hydrogenated, the double bonds are rearranged, converting some to the trans configuration and shifting the double bonds along the chain. Unfortunately, this newly created trans fatty acid is an artery-clogger.

Amid the criticism of cookies, chips and other products containing trans fat, a number of companies have either developed foods without partially hydrogenated oils or have pledged to explore ways of replacing the fat. PepsiCo's Frito Lay, for example, has already eliminated trans fats from some of its products.

To access the C&EN article on trans fats, go to: http://pubs.acs.org/cen/science/8138/8138sci4.html

Adapted from materials provided by American Chemical Society.

2007-12-12T20:50:00.001-08:00

Omega-3 Boosts Grey Matter, May Explain Improved Moods

ScienceDaily (Mar. 7, 2007) — Omega-3 fatty acids, found in fatty fish like salmon, are associated with increased grey matter volume in areas of the brain commonly linked to mood and behavior according to a University of Pittsburgh study.

Findings will be presented today by Sarah M. Conklin, Ph.D., postdoctoral scholar at the Cardiovascular Behavioral Medicine Program in the department of psychiatry at the University of Pittsburgh, at the American Psychosomatic Society's Annual Meeting, held in Budapest, Hungary.

Animal research has shown that raising omega-3 intake leads to structural brain changes. In a separate study presented by Dr. Conklin at the society's meeting last year, Pitt researchers reported that people who had lower blood levels of omega-3 fatty acids were more likely to have a negative outlook and be more impulsive. Conversely, those with higher blood levels of omega-3s were found to be more agreeable and less likely to report mild or moderate symptoms of depression. In the study being presented today, the researchers sought to investigate if grey matter volume was proportionally related to long-chain omega-3 intake in humans, especially in areas of the brain related to mood, helping them attempt to explain the mechanisms behind the improvement in mood often associated with long-chain omega-3 intake.

Researchers interviewed 55 healthy adult participants to determine their average intake of long-chain omega-3 fatty acids. Grey matter volume was evaluated using high-resolution structural MRI. The researchers discovered that participants who had high levels of long-chain omega-3 fatty acid intake had higher volumes of grey matter in areas of the brain associated with emotional arousal and regulation -- the bilateral anterior cingulate cortex, the right amygdala and the right hippocampus.

While this finding suggests that omega-3s may promote structural improvement in areas of the brain related to mood and emotion regulation -- the same areas where grey matter is reduced in people who have mood disorders such as major depressive disorder -- investigators note that more research is needed to determine whether fish consumption actually causes changes in the brain.

Adapted from materials provided by University of Pittsburgh Schools of the Health Sciences.

2007-12-12T20:48:00.001-08:00

Study Links Brain Fatty Acid Levels To Depression

ScienceDaily (May 25, 2005) — Bethesda, MD -- A group of researchers from Israel has discovered that rats exhibiting the signs of depression have increased levels of the omega-6 fatty acid, arachidonic acid, in their brains. The details of their findings appear in the June issue of the Journal of Lipid Research, an American Society for Biochemistry and Molecular Biology journal.

During recent years, omega-3 fatty acids have enjoyed increased popularity as numerous studies have shown that supplementing diets with fish oil (a natural source of this polyunsaturated fatty acid) does everything from reducing the risk of heart disease to preventing arthritis. There is also evidence that depression may be associated with a dietary deficiency in omega-3 fatty acids. This "phospholipid hypothesis" of depression has been supported by research showing that omega-3 fatty acid concentration in the blood of depressed patients is lower than that in control patients.

"The "phospholipid hypothesis" of depression postulates that decreased omega-3 fatty acid intake, and hence, perhaps decreased brain omega-3 fatty acid content, could be responsible for the disease," explains Dr. Pnina Green of Tel Aviv University. "In humans, because of high dietary variability and the obvious inability to examine brain tissue, the theory is backed up mainly by indirect evidence. The availability of the Flinders Sensitive Line rat, an animal model of depression, overcomes both these obstacles."

In the Journal of Lipid Research study, Dr. Green in collaboration with Dr Gal Yadid of Bar-Ilan University, Ramat Gan, used the Flinders Sensitive Line rats to investigate the link between omega-3 fatty acids and depression. They examined the brains of the depressed rats and compared them with brains from normal rats. Surprisingly, they found that the main difference between the two types of rats was in omega-6 fatty acid levels and not omega-3 fatty acid levels. Specifically, they discovered that brains from rats with depression had higher concentrations of arachidonic acid, a long-chain unsaturated metabolite of omega-6 fatty acid.

Arachidonic acid is found throughout the body and is essential for the proper functioning of almost every body organ, including the brain. It serves a wide variety of purposes, from being a purely structural element in phospholipids to being involved in signal transduction and being a substrate for a host of derivatives involved in second messenger function.

"The finding that in the depressive rats the omega-3 fatty acid levels were not decreased, but arachidonic acid was substantially increased as compared to controls is somewhat unexpected," admits Dr. Green. "But the finding lends itself nicely to the theory that increased omega-3 fatty acid intake may shift the balance between the two fatty acid families in the brain, since it has been demonstrated in animal studies that increased omega-3 fatty acid intake may result in decreased brain arachidonic acid."

Although far less attention has been paid to dietary requirements for omega-6 fatty acids, which can be found in most edible oils and meat, perhaps in the future depression may be controlled by increasing omega-3 fatty acid intake and decreasing omega-6 fatty acid intake.

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The American Society for Biochemistry and Molecular Biology (ASBMB) is a nonprofit scientific and educational organization with over 11,000 members in the United States and internationally. Most members teach and conduct research at colleges and universities. Others conduct research in various government laboratories, nonprofit research institutions, and industry.

Founded in 1906, the Society is based in Bethesda, Maryland, on the campus of the Federation of American Societies for Experimental Biology. The Society's primary purpose is to advance the sciences of biochemistry and molecular biology through its publications, the Journal of Biological Chemistry, the Journal of Lipid Research, Molecular and Cellular Proteomics, and Biochemistry and Molecular Biology Education, and the holding of scientific meetings.

Adapted from materials provided by American Society For Biochemistry And Molecular Biology.

2007-12-12T20:46:00.001-08:00

Omega-3 Fatty Acids Affect Risk Of Depression, Inflammation

ScienceDaily (Mar. 29, 2007) — A new study suggests that people whose diets contain dramatically more of one kind of polyunsaturated fatty acid than another may be at greater risk for both clinical depression and certain inflammatory diseases.

The report, published online in the journal Psychosomatic Medicine, suggests that we need to balance out our intake of omega-6 and omega-3 fatty acids. The current typical American diet contains 20 times more omega-6 than omega-3, a ratio that researchers say should be lowered to 4-to-1, or even 2-to-1.

This is the most recent in a long series of experiments Ohio State University researchers have conducted on the links between psychological stress and immunity. The addition of dietary questions to studies that have previously focused solely on emotional and biochemical markers may yield important new clues about the immune system.

"In this study, we're looking at the intersection of behavior, immune function and diet. In past experiments, we concentrated only on the first two," explained Jan Kiecolt-Glaser, professor of psychiatry and psychology at Ohio State and lead author on the paper.

"It now appears that diet is a very important variable in the equation as to how people respond to depression and stress."

The study, conducted in OSU's Institute for Behavioral Medicine Research, focused on a group of 43 middle-aged to elderly men and women, nearly half of which were the caregiver spouses of people with Alzheimer's or other dementias. By including caregivers who typically report greater stress and more depression than similar ad ults who are not caregiving, the researchers could look at how depression and diet might interact to affect inflammation.

Blood samples were drawn from each person in the study and tested for interleukin-6 (IL-6), tumor necrosis factor -alpha (TNF-alpha ) and the receptor molecule for IL-6. Participants also completed a survey questionnaire that gauged their level of depression.

The analysis showed that participants who had much more omega-6 -- compared to omega-3 -- fatty acids, and who also were reporting more symptoms of depression, had much higher levels of IL-6 and TNF-alpha, two cytokines which enhance inflammation.

"The data suggest that higher depression and a poorer diet in terms of omega-3 can work together to promote inflammation. Other researchers have shown that clinically depressed people -- those with more severe depression -- often have lower omega-3 levels in their blood, and several studies have shown that supplementing diets with omega-3 improves depression," Kiecolt-Glaser said, although the reason isn't clear.

"People who are depressed don't eat well, or it might be that there is something about depression that affects how well people process such foods."

In recent years, research has shown that an increase in omega-3 fatty acids in the diet has specific health benefits, especially in patients with depression, cardiovascular disease and inflammatory and autoimmune diseases.

Martha Belury, an associate professor of human nutrition, endocrinology, diabetes & metabolism at Ohio State and co-author of the study, said the design of the study was important.

"We looked at people who were experiencing real depression, not those whose depression arose as a part of some experiment, and we could clearly see a relationship between lower omega-3 fatty acids and certain markers of depression and inflammation."

Belury said that current recommendations allow up to two servings each week of cold-water fish -- the best source of omega-3 -- such as salmon or trout. This would not apply to pregnant women, she said, where concerns are greater about the heavy metal contamination such fish might contain. Omega-3 is also available as nutritional supplements

"This study has shown that even in people who did not take supplements, maybe just a little bit more omega-3, could help reduce their markers for both stress and depression," Belury said.

"The important message for consumers is that they don't have to take mega-doses of omega-3 to have some impact. It might not take a whole lot to have a significant clinical impact," Belury said.

The researchers are now starting a larger, more comprehensive randomized and controlled trial of omega-3 in adults between the ages of 50 and 80 in hopes of testing the questions raised in this pilot study.

Ron Glaser, professor of internal medicine, molecular virology, immunology and medical genetics; David Beversdorf, an assistant professor of neurology; Stanley Lemeshow, dean of the College of Public Health, and Kyle Porter, a statistician in the Center for Biostatistics, were also part of the project. The research was supported in part by the National Institutes of Health.

Adapted from materials provided by Ohio State University.

2007-12-12T20:38:00.001-08:00

Omega-3 Supplements Can Help With Alzheimer's Symptoms, Study Suggests

ScienceDaily (Jun. 22, 2007) — Omega-3 supplements can, in certain cases, help combat the depression and agitation symptoms associated with Alzheimer's disease, according to a clinical study conducted at the Swedish medical university Karolinska Institutet.

A number of epidemiological studies have shown that eating fatty fish provides a certain degree of protection against Alzheimer's and other dementia diseases--an effect often thought attributable to the omega-3 fatty acids it contains. Some studies also suggest that omega-3 can have a therapeutic effect on some psychiatric conditions.

Researchers at Karolinska Institutet and Uppsala University have now examined whether omega-3 supplementation has any effect on the psychiatric symptoms associated with Alzheimer's disease. Just under 200 patients with mild Alzheimer's were divided into two groups, one of which received omega-3, and one a placebo. The study lasted for one year.

There was no observable difference in therapeutic effect between the patients receiving the omega-3 and the placebo group. However, when the researchers took into account which of the patients carried the susceptibility gene APOE4 and which did not, an appreciable difference appeared. Carriers of the gene who had received active treatment responded positively to the omega-3 as regards agitation symptoms, while non-bearers of the gene showed an improvement in depressive symptoms.

The team points out that no general therapeutic recommendations can be made from the results until larger studies on individuals with more pronounced neuropsychiatric symptoms are conducted.

Reference: "Omega-3 supplementation in mild to moderate Alzheimer's disease: effects on neuropsychiatric symptoms," Yvonne Freund-Levi, Hans Basun, Tommy Cederholm, Gerd Faxén-Irving, Anita Garlind, Mikaela Grut, Inger Vedin, Jan Palmblad, Lars-Olof Wahlund and Maria Eriksdotter-Jönhagen, International Journal of Geriatric Psychiatry, doi 10.1002/gps.1857, Published online 21 June 2007

Adapted from materials provided by Karolinska Institutet.

2007-12-12T20:37:00.001-08:00

Omega-3 Fatty Acids May Slow Cognitive Decline In Some Patients With Very Mild Alzheimer's Disease

ScienceDaily (Oct. 11, 2006) — Omega-3 fatty acid supplements may slow cognitive decline in some patients with very mild Alzheimer's disease, but do not appear to affect those with more advanced cases, according to results of a clinical trial published in the October issue of Archives of Neurology, one of the JAMA/Archives journals.

Alzheimer's disease is a severely debilitating condition that affects thinking, learning and memory, beginning with declines in episodic memory (including memory about events in one's own life), according to background information in the article. Medications are available to treat the symptoms, but these drugs do not affect the underlying cause and progression of the disease. Several studies have shown that eating fish, which is high in omega-3 fatty acids, may protect against Alzheimer's disease, leading researchers to question whether supplements could have similar effects.
Yvonne Freund-Levi, M.D., Karolinska Institutet, Stockholm, Sweden, and colleagues compared the effects of supplements containing two omega-3 fatty acids with placebo in 204 patients with Alzheimer's disease, 174 of whom completed the entire study. For six months, 89 patients (51 women and 38 men) took 1.7 grams of docosahexaenoic acid (DHA) and .6 grams of eicosapentaenoic acid (EPA), while 85 patients (39 women and 46 men) took placebo. For an additional six months, both groups took the omega-3 fatty acids. Patients had physical examinations, which included blood tests and blood pressure measurement, and took cognitive tests at the beginning of the study and at the six- and 12-month marks.
After six months, there was no difference in the rate of cognitive decline between the two groups. However, among a subgroup of 32 patients with very mild cognitive impairment at the beginning of the study, those who took the fatty acids experienced less decline in six months compared with those who took placebo. Among those who took placebo during the first six months, decline decreased during the second six months, when they also began taking the omega-3 supplements. The supplements appeared safe and well-tolerated, with no change in blood pressure or blood test results other than a higher ratio of fatty acids in the blood.
"The mechanisms by which omega-3 fatty acids could interfere in Alzheimer's disease pathophysiologic features are not clear, but since anti-inflammatory effects are an important part of the profile of fish oils, they are conceivable also for Alzheimer's disease," the authors write. This could potentially explain why effects were seen only in those with very early-stage disease--recent evidence suggests that there is a critical period two or more years before patients develop dementia when levels of chemicals that signal the presence of inflammation are elevated. "It is possible that when the disease is clinically apparent, the neuropathologic involvement is too advanced to be substantially attenuated by anti-inflammatory treatment."
The authors also point out that "these findings cannot serve as a basis for general recommendations for treatment of Alzheimer's disease with dietary DHA-rich fish oil preparations. However, studies in larger cohorts with mild cognitive impairment, including those at risk for Alzheimer's disease, are needed to further explore the possibility that omega-3 fatty acids might be beneficial in halting initial progression of the disease."
Adapted from materials provided by JAMA and Archives Journals.

2007-12-12T20:34:00.001-08:00

Omega-3 Supplements Can Help With Alzheimer's Symptoms, Study Suggests

The team points out that no general therapeutic recommendations can be made from the results until larger studies on individuals with more pronounced neuropsychiatric symptoms are conducted.

Adapted from materials provided by Karolinska Institutet.

2007-12-12T20:30:00.000-08:00

Scientists Say Vitamin C May Alleviate The Body's Response To Stress

ScienceDaily (Aug. 23, 1999) — NEW ORLEANS, La., Aug. 22 -- Large doses of vitamin C can prevent illness by alleviating the body's normal response to stress, according to a scientist at the University of Alabama in Huntsville. This study was described here today at a national meeting of the American Chemical Society, the world's largest scientific society.

The study tested the effects of vitamin C on the adrenal function of laboratory animals subjected to stress, said P. Samuel Campbell, Ph.D., chairman of the university's department of biological sciences. In both animals and humans, the adrenal gland reacts to stress by releasing corticoids, such as corticosterone and cortisol. These and other hormones trigger the "fight or flight" reaction that allows us to spring into action when in danger. They also suppress the immune system, the body's first line of defense against disease.

The Alabama researchers put laboratory rats under stress by immobilizing them for one hour a day over a three-week period. To check whether vitamin C would reduce the production of stress hormones, the rats were fed 200 milligrams a day, the equivalent of several grams a day for humans. This dosage far exceeds the present recommended daily allowance (RDA) of 60 milligrams, a figure based on the amount required to prevent deficiency diseases such as scurvy. The study showed that vitamin C reduced the levels of stress hormones in the blood-and also reduced other typical indicators of physical and emotional stress, such as loss in body weight, enlargement of the adrenal glands, and reduction in the size of the thymus gland and the spleen, according to Campbell.

In addition, the vitamin C treatment elevated the levels of circulating IgG antibody, the body's principal defense against systemic infection, he said.

In the control group-rats who were not subjected to stress-vitamin C increased the production of IgG antibody to a somewhat higher level than it did in the stressed rats. This suggests that stress may create a tolerance for vitamin C. Consequently, animals-and perhaps people-who are under emotional stress may require higher doses of vitamin C to protect immune function.

Paradoxically, the vitamin C treatment may work by suppressing production and/or utilization of the vitamin C that naturally exists in the adrenal cortex of humans and animals, Campbell noted. This endogenous vitamin C appears to support the production of stress hormones, he said.

Campbell said his results help explain other evidence of the value of vitamin C in protecting immune function. For example, according to reports in the medical literature, vitamin C boosted immune function in a test group of elderly women. It also reduced the incidence of stress-related upper-respiratory infections in marathon runners.

Recommending a sharper look at the present RDA, Campbell said he believes that our prehistoric ancestors probably consumed large amounts of vitamin C in a tropical diet rich in fruits. "If so, the physiological constitution we have inherited may require doses far larger than the present RDA to keep us healthy under varying environmental conditions, including stress."

Adapted from materials provided by American Chemical Society.

2007-12-12T20:16:00.000-08:00

Study Citing Antioxidant Vitamin Risks Based On Flawed Methodology, Experts Argue

ScienceDaily (Mar. 1, 2007) — A study recently published on possible health risks of antioxidant supplements is based on flawed methodology and ignores the broad totality of evidence that comes to largely opposite conclusions, say experts from the Linus Pauling Institute at Oregon State University.

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The research, which was published in this week’s edition of the Journal of the American Medical Association, concluded that antioxidant supplements such as vitamins A and E may “significantly increase mortality,” and that there was no evidence for any positive effect of vitamin C in the reduction of mortality rates.

However, Balz Frei, professor and director of one of the world’s leading institutes that studies the possible health value of vitamins, phytochemicals and micronutrients, said that the new study’s focus on a selected group of clinical trials disregards the results of other more positive trials, as well as huge amounts of laboratory, animal, and human observational and experimental data.

“This is a flawed analysis of flawed data, and it does little to help us understand the real health effects of antioxidants, whether beneficial or otherwise,” Frei said.

“Instead of causing harm, the totality of the evidence indicates that antioxidants from foods or supplements have many health benefits, including reduced risk for cardiovascular disease, some types of cancer, eye disease and neurodegenerative disease,” he said. “In addition, they are a key to an enhanced immune system and resistance to infection.”

The “meta-analysis” published in JAMA, which is a statistical analysis of previously published data, looked at 815 antioxidant trials but included only 68 of them in its analysis, Frei said. And two of the studies excluded – which were published in the Journal of the National Cancer Institute and the prominent British medical journal Lancet – found substantial benefits and reduced mortality from intake of antioxidant supplements.

“If these two large studies had been included, none of the reported effects on increased mortality would have been significant, with the exception of the effects of beta carotene,” Frei said. “And the research showing a higher incidence of lung cancer in smokers who take supplements of beta carotene or vitamin A is old news, that’s been known for many years. Very high doses of vitamin A are known to have multiple adverse health effects.”

All the new study really demonstrates, Frei said, is a bias toward identifying studies or research that show harm caused by antioxidants, and selective removal of research that shows benefits.

The mean duration of the reviewed trials was 2.7 years, so the implied conclusion is that taking antioxidant supplements can kill people in less than three years, Frei said. It is absurd to think that vitamin supplements could have such an effect, he said, and no biological mechanism has been identified that would explain it. In addition, the causes of death were not considered or were not determined in many of the studies reviewed, and may include accidents or other causes that have nothing to do with diet or oxidative stress.

Most trials cited in the study, Frei said, tested multiple antioxidants and additional interventions in the treatment of disease, including a long list of other dietary supplements and pharmaceutical drugs. The underlying health problems or multiple types of medical, drug and surgical treatments could all interfere with or mask the effects that can be attributed directly to antioxidants, he said.

“These trials don’t tell us anything about the usefulness of antioxidants in the prevention of disease, or whether the supplements had the intended effect of lowering oxidative stress in the body,” Frei said. “It’s like doing a cholesterol-lowering trial without ever measuring serum cholesterol. How can you draw any conclusions from such a poorly-designed study?”

About the Linus Pauling Institute: The Linus Pauling Institute at OSU is a world leader in the study of micronutrients and their role in promoting optimum health or preventing and treating disease. Major areas of research include heart disease, cancer, aging and neurodegenerative disease.

Adapted from materials provided by Oregon State University.

2007-12-12T20:01:00.001-08:00

Altering Fatty Acid Levels In Diet May Reduce Prostate Cancer Growth Rate

ScienceDaily (Aug. 1, 2006) — UCLA researchers found that altering the fatty acid ratio found in the typical Western diet to include more omega-3 fatty acids and decrease the amount of omega-6 fatty acids may reduce prostate cancer tumor growth rates and PSA levels.

Published in the Aug. 1 issue of the journal Clinical Cancer Research, this initial animal-model study is one of the first to show the impact of diet on lowering an inflammatory response known to promote prostate cancer tumor progression and could lead to new treatment approaches.

The omega-6 fatty acids contained in corn, safflower oils and red meats are the predominant polyunsaturated fatty acids in the Western diet. The healthier marine omega-3 fatty acids are found in cold-water fish like salmon, tuna and sardines.

"Corn oil is the backbone of the American diet. We consume up to 20 times more omega-6 fatty acids in our diet compared to omega-3 acids," said principal investigator Dr. William Aronson, a professor in the department of urology at the David Geffen School of Medicine at UCLA and a researcher with UCLA's Jonsson Cancer Center. "This study strongly suggests that eating a healthier ratio of these two types of fatty acids may make a difference in reducing prostate cancer growth, but studies need to be conducted in humans before any clinical recommendations can be made."

Scientists used a special mouse model for hormone-sensitive prostate cancer that closely mirrors the disease in humans. Researchers fed one group of mice a diet comprised of 20 percent fat with a healthy one-to-one ratio of omega-6 to omega-3 fatty acids. A second group of mice were fed the same diet but with the fat derived from mostly omega-6 fatty acids.

The study showed that tumor cell growth rates decreased by 22 percent and PSA levels were 77 percent lower in the group receiving a healthier balance of fatty acids compared with the group that received predominantly omega-6 fatty acids.

The most likely mechanism for the tumor reductions, according to researchers, was due to an increase of the prostate tumor omega-3 fatty acids DHA and EPA and a lowering of the omega-6 acid known as arachidonic acid. These three fatty acids compete to be converted by cyclooxgenase enzymes (COX-1 and COX-2) into prostaglandins, which can become either pro-inflammatory and increase tumor growth, or anti-inflammatory and reduce growth.

Researchers found that pro-inflammatory prostaglandin (PGE-2) levels were 83 percent lower in tumors in the omega-3 group than in mice on the predominantly omega-6 fatty acid diet, demonstrating that higher levels of DHA and EPA may lead to development of more anti-inflammatory prostaglandins.

"This is one of the first studies showing changes in diet can impact the inflammatory response that may play a role in prostate cancer tumor growth," Aronson said. "We may be able to use EPA and DHA supplements while also reducing omega-6 fatty acids in the diet as a cancer prevention tool or possibly to reduce progression in men with prostate cancer."

Currently, the research team is conducting a clinical trial with men who are undergoing prostate removal due to cancer to compare the effects of a low-fat diet using omega-3 supplements and a balanced Western diet. Aronson said that positive findings from this study may lead to larger clinical trials.

In addition, Aronson said that further study might show that COX-2 inhibitors or non-steroidal anti-inflammatories (NSAIDS) combined with omega-3 supplements also may lower the inflammatory response in prostate cancer development.

The study was funded by the Department of Veterans Affairs, the National Institute of Health Grants: Specialized Programs of Research Excellence and UCLA's Jonsson Cancer Center.

Other study authors include: Naoko Kobayashi, R. James Barnard, Susanne M. Henning, David Elashoff, Srinivasa T. Reddy, Pinchas Cohen, Pak Leung, Jenny Hong-Gonzalez, Stephen J. Freedland, Jonathan Said, Dorina Gui, Navindra P. Seerum, Laura M. Popoviciu, Dilprit Bagga, David Heber, and John A. Glaspy.

Adapted from materials provided by University of California - Los Angeles.

2007-12-12T19:46:00.001-08:00

Does Omega 3 Protect Against ADHD?

ScienceDaily (Dec. 6, 2006) — A new study will provide further understanding about the effects of omega-3 fatty acids on the brain function of children with attention deficit hyperactivity disorder (ADHD).

The trial, being conducted by the Murdoch Childrens Research Institute, will study the effects of these fatty acids on the learning skills, attention span, memory, reaction time and behaviour of 150 children with ADHD over 12 weeks. The effects will also be explored in 100 children without ADHD.

Omega-3 fatty acids are found in seafood, particularly fish. There is increasing evidence that a lack of these acids may be associated with developmental problems like ADHD -- a common mental health problem which affects around 12 per cent of Australian children.

The evidence for positive effects of omega-3 fatty acids in children is mixed and the Murdoch Childrens' study will be one of the first to examine the issue in detail.

Researcher Dr Alex Collie says "ADHD is such a common disorder in Australia. This study will be an important step in validating claims that omega-3 fatty acids have a direct affect on cognition as well as behaviour."

Currently, the most commonly prescribed treatment for ADHD is stimulant medication. However in recent years parents have sought alternative treatments and researchers have noticed an increase in the use of omega-3 fatty acids.

Children taking part in the study will complete learning and behaviour tests in the first, fourth and 12th week of the study. During this time they will be given dietary supplements of either omega-3 fatty acids or placebo (supplements with no active ingredient). The children's parents and teachers will also participate, monitoring and rating the childrens' behaviour.

Adapted from materials provided by Murdoch Childrens Research Institute.

2007-12-12T19:45:00.001-08:00

Omega-3 Fatty Acids: A Way To Improve Heart Health

ScienceDaily (Aug. 13, 2007) — While a heart-healthy diet has become synonymous with plenty of fruits and vegetables and little fat and cholesterol, there’s more to the story. Omega-3 fatty acids should be part of a heart-healthy diet, too, according to the August issue of Mayo Clinic Health Letter.

Omega-3 fatty acids are a form of polyunsaturated fat important to overall health. As it pertains to heart disease, their main benefit is their ability to reduce the risk of heart rhythm problems in certain groups of people, thus reducing the risk of sudden cardiac death. In addition, omega-3s may help reduce triglycerides, lower blood pressure slightly and reduce blood clotting.

The best source of omega-3s is fatty, cold water fish such as herring, mackerel, salmon and tuna. Plant oils, such as canola and flaxseed oils, also are sources of omega-3s.

For heart disease prevention, near-maximum benefit comes from eating two 3-ounce servings of cold water fish a week. More than that doesn’t appear to offer any additional preventive benefit.

Higher amounts of two kinds of omega-3, docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), may benefit some people with established heart disease or high triglyceride levels and can have an anti-inflammatory effect for people with rheumatoid arthritis. In addition, DHA is being studied to see if it can slow the progression of Alzheimer’s disease.

For those who don’t eat fish, a fish oil supplement or an algae supplement can provide omega-3 fatty acids. However, supplements aren’t cheap, and the amount of DHA and EPA in supplements varies widely. Except for people who have established heart disease, the evidence of heart disease prevention is stronger when one eats fish instead of taking supplements. Supplements can pose risks, too. Taking more than 3 grams of fish oil a day may increase the risk of bleeding, worsen heart rhythm problems in those who have arrhythmias or cause other side effects.

Adapted from materials provided by Mayo Clinic.

2007-12-12T19:44:00.001-08:00

Fatty Fish Cuts Risk Of Death From Heart Attack In Elderly

ScienceDaily (Mar. 2, 2001) — SAN ANTONIO, Feb. 28 – Older individuals are less likely to die from a heart attack if they eat at least one serving of fatty fish per week, according to a study presented today at the American Heart Association’s 41st Annual Conference on Cardiovascular Disease Epidemiology and Prevention.

Eating fatty fish at least once per week was associated with a 44 percent lower risk of dying from a heart attack among a group of older adults, average age 72. In contrast, eating fried fish – which is typically lean – was not associated with a lower risk of dying from a heart attack. Examples of fatty fish are tuna, salmon and mackerel; examples of lean fish are cod, catfish and snapper.

“Our findings are consistent with results of prior studies done in predominantly middle-aged adults,” says Dariush Mozaffarian, M.D., lead author of the study and fellow in cardiology and health services research at the University of Washington/Seattle Veterans Affairs Medical Center.

Fish is thought to protect against death from heart attack because it contains good fats called omega-3 (or n-3) polyunsaturated fatty acids (PUFAs). “Fatty fish are more abundant in omega-3 fatty acids, while fried fish are typically lean fish without significant omega-3 fatty acids. Because these omega-3 fatty acids may protect against dying from a heart attack, eating fatty fish may be of greater benefit than eating fried fish,” says Mozaffarian.

The researchers found that individuals with a higher intake of fatty fish had higher plasma levels of omega-3 PUFAs. There was no correlation between intake of fried fish and plasma levels of omega-3 PUFAs. Many deaths from heart disease are due to cardiac arrhythmias, or heart rhythm disturbances, and omega-3 fatty acids may reduce the risk of arrhythmias, he says.

“The study suggests that modest consumption of fatty fish at any age may be beneficial,” says David S. Siscovick, M.D., professor of medicine and epidemiology, and co-director of the University of Washington Cardiovascular Health Research Unit, and a co-author of the study. “When encouraging people to eat a healthy diet, it may be important to differentiate which types of fish are good sources of omega-3 fatty acids,” he says.

Researchers analyzed the relationship between eating fatty fish, eating fried fish and the risk of fatal heart attack and coronary heart disease deaths among nearly 4,000 men and women older than age 65 involved in the National Heart, Lung and Blood Institute’s Cardiovascular Health Study, launched in 1988 to assess the determinants of heart disease and strokes among older adults.

At the beginning of the study, all participants were free of known cardiovascular disease. Mozaffarian and his colleagues used a detailed food questionnaire to assess the participants’ usual diet. Participants were followed for an average of 6.8 years.

The researchers did not determine which specific types of fatty fish were consumed, therefore it is not possible to recommend one type of fatty fish, tuna or salmon, for example, over another.

“The study highlights the benefit of one or two servings per week of fish rich in omega-3-PUFAs, not all fish,” says Siscovick. In October 2000, the American Heart Association issued updated dietary guidelines for healthy adults, which recommend eating at least two servings of fatty fish per week. For more information on the 2000 dietary guidelines visit http://www.americanheart.org.

Co-authors of the study are Rozenn N. Lemaitre, Ph.D.; Lewis H. Kuller, M.D.; Greg Burke, M.D., Caroline Blaum, M.D., and Russell Tracy, Ph.D.

Adapted from materials provided by American Heart Association.

2007-12-12T19:42:00.001-08:00

Fatty Fish Protects Against Cancer

ScienceDaily (Sep. 20, 2006) — If you want to avoid cancer of the kidneys, a new major study from Karolinska Institutet in Sweden shows that eating salmon or other kinds of fatty fish a few times a month would be one good way to go about it.

At the end of the 1980s, 90,000 Swedish women were sent a questionnaire on their dietary habits in connection with their mammography scan. Now, with the help of another questionnaire a decade later and the cancer registry, scientists at Karolinska Institutet have concluded that women who eat fatty fish gain significant protection against renal cancer.

At least one portion of fatty fish a week during the period (1987-2004) reduced the risk of renal cancer by 74 per cent compared with those who never ate fatty fish. The group who ate fresh fish at least once a week but for whom follow-up information were unavailable, saw a 40 per cent reduction.

"This is the first time that a link between the consumption of fatty fish and renal cancer has been studied," says Professor Alicja Wolk, one of the scientists working with the study. "The reason previous studies have been unable to demonstrate a link between fish consumption and renal cancer is that they made no distinction between fatty and non-fatty fish."

One significant difference between oily and non-fatty fish lies in how much omega-3 fatty acids and vitamin D they contain -- substances that, according to earlier cell studies, seem to protect against cancer. Fatty fish contains more omega-3 fatty acids than non-oily fish, and 3 to 5 times as much vitamin D. As fatty fish, the study included salmon, raw herring, sardines and mackerel; as non-fatty, cod and tuna (amongst other kinds).

The study is to be published in the Journal of the American Medical Association (JAMA) on 20 September.

Adapted from materials provided by Karolinska Institutet.

2007-12-12T19:40:00.001-08:00

Eating Oily Fish May Reduce Inflammation

ScienceDaily (Mar. 14, 2005) — A new study explains how a diet high in oily fish like salmon and mackerel improves inflammatory conditions, particularly in combination with low doses of aspirin. In a study in the March 7 issue of The Journal of Experimental Medicine, Arita and colleagues identify an anti-inflammatory lipid in humans that is derived from an essential fatty acid in fish oil.

Fatty fish contain large amounts of omega-3 fatty acids--diet-derived essential fatty acids known to benefit patients with cardiovascular disease and arthritis. This research group recently identified a new class of aspirin-triggered bioactive lipids, called resolvins, the activity of which may in part explain the beneficial effects of omega-3 fatty acids. Resolvins are made from the omega-3 fatty acids by cellular enzymes and can reduce inflammation in mice. The main bioactive component of this class of lipids was identified in mice and named resolvin E1.

The researchers have now identified this lipid in plasma taken from volunteers given omega-3 fatty acids and aspirin. Human resolvin E1, the authors show, inhibits both the migration of inflammatory cells to sites of inflammation and the turning on of other inflammatory cells.

This study also reveals a potential pitfall of COX-2 inhibitors, drugs designed to block inflammation, which have been shown to have negative cardiovascular side effects. COX-2 is involved in making resolvin E1 and the authors suggest that inhibition of vascular COX-2 by these inhibitors might block the synthesis of resolvin E1, which would eliminate an important anti-inflammatory pathway. The experiment to prove this idea, however, has yet to be done.

Adapted from materials provided by Journal Of Experimental Medicine.

2007-12-12T19:38:00.001-08:00

Anti-inflammatory Effects Of Omega 3 Fatty Acid In Fish Oil Linked To Lowering Of Prostaglandin

ScienceDaily (Apr. 4, 2006) — Omega 3 fatty acids in dietary fish oil are reported to have anti-inflammatory and anti-thrombogenic and anti-arrhythmic effects in humans, but the biochemical basis for these beneficial health effects is not well understood. Now a University of Michigan biochemist reports that fish oil significantly diminishes the production and effectiveness of various prostaglandins, naturally occurring hormone-like substances that can accentuate inflammation and thrombosis.

Dr. William L. Smith described his findings on April 4 at Experimental Biology 2006 in San Francisco. His presentation was part of the scientific program of the American Society for Biochemistry and Molecular Biology (ASBMB).

Dietary fish oil causes its prostaglandin-lowering effects through three different mechanisms, says Dr. Smith.

First, the much fewer prostaglandins are made from omega 3 fatty acids as compared to the other class of fatty acids in the body, the omega 6 family of fatty acids that originate in the diet from leafy vegetables and other plant sources.

Second, the omega 3 fatty acids compete with omega 6 fatty acids for the same binding site on the COX 1 enzyme that converts the omega 6 fatty acids to prostaglandin (which is why the COX 1 enzyme and its COX 2 cousin are the targets of anti-inflammatory drugs like ibuprofen). The more omega 3 fatty acids present to block the binding sites, the fewer omega 6 fatty acids are able to be converted to prostaglandin.

Third, although omega 3 fatty acids also are converted to prostaglandins, the prostaglandins formed from omega 3 are generally 2 to 50 times less active than those formed from the omega 6 fatty acids from dietary plants.

The biochemical basis of other benefits of dietary fish oil -- for example, omega 3 fatty acids' impact on neuronal development and visual acuity -- are probably due to effects on biochemical pathways regulating nerve transmission. Understanding the different pathways through which omega 3 works to convert prostaglandin helps explain why the plant-based omega 6 fatty acids don't simply provide the same benefits. Because of omega 3 fatty acids' known benefits to health, especially cardiovascular health, Dr. Smith's advice is simple: eat more fish.

Adapted from materials provided by Federation of American Societies for Experimental Biology.