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
Monday, January 7, 2008
Smoking Doubles Risk Of Degenerative Eye Condition
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
The findings are based on a representative sample of over 4,000 people, aged 75 and older, from 49 general practices across
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
"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
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,
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
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
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
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
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.
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
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,
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
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
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
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
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.
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Adapted from materials provided by Eleanor Roosevelt Institute.
Sunday, January 6, 2008
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
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
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
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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
- 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
- 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
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
ScienceDaily (Jan. 22, 2001 ) — BUFFALO , N.Y. Buffalo
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
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
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
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
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
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
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
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
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
"Many people can fight type II diabetes through diet and exercise alone," said John Thyfault, professor in the MU
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
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.
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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
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.
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