Showing posts with label Inflammation and Degenerative Diseases. Show all posts
Showing posts with label Inflammation and Degenerative Diseases. Show all posts

Sunday, September 13, 2009

Coronary Heart Disease Is an Early Form of Scurvy

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

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

Saturday, September 12, 2009

Saturated Fat - The misunderstood nutrient

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.

Monday, January 7, 2008

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

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.

###

(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

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.

of Illinois at Urbana-Champaign (2007, June 15). Cytokine Resistance Contributes To Pathology Of Type 2 Diabetes. ScienceDaily. Retrieved January 8, 2008, from http://www.sciencedaily.com­ /releases/2007/06/070614121333.htm

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

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.

Of California - San Diego (2005, February 3). Pro-inflammatory Enzyme Linked To Diabetes; Immune System's Macrophages May Be Key To Treatment. ScienceDaily. Retrieved January 8, 2008, from http://www.sciencedaily.com­ /releases/2005/02/050201101958.htm

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

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

Sunday, January 6, 2008

Diet and Inflammation


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

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

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

  1. 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.
  2. 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.
    1. 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.
    2. Avoid all partially hydrogenated fat. These fats create inflammatory chemicals and also damage cell membrane function.
    3. 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!
    4. 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.
    5. 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.
  3. Floss - inflammation effects of periodontal disease also cause inflammation of your arteries.
  4. 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.
  5. 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…
  6. Increase Lean Muscle Mass and Reduce Body - Reducing fat helps reduce CRP.
  7. Get Fiber - Consume your recommended 20-plus grams of fiber..
  8. Practice the Friendship Solution - Social interaction helps reduce depression which helps to lower CRP.
  9. 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.
  10. 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

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.