Insulins physiological actions

The actions of insulin on the global human metabolism level include:

Control of cellular intake of certain substances, most prominently glucose in muscle and adipose tissue (about ⅔ of body cells).
Increase of DNA replication and protein synthesis via control of amino acid uptake.
Modification of the activity of numerous enzymes.
The actions of insulin on cells include:

Increased glycogen synthesis – insulin forces storage of glucose in liver (and muscle) cells in the form of glycogen; lowered levels of insulin cause liver cells to convert glycogen to glucose and excrete it into the blood. This is the clinical action of insulin, which is directly useful in reducing high blood glucose levels as in diabetes.
Increased fatty acid synthesis – insulin forces fat cells to take in blood lipids, which are converted to triglycerides; lack of insulin causes the reverse.
Increased esterification of fatty acids – forces adipose tissue to make fats (i.e., triglycerides) from fatty acid esters; lack of insulin causes the reverse.
Decreased proteolysis – decreasing the breakdown of protein.
Decreased lipolysis – forces reduction in conversion of fat cell lipid stores into blood fatty acids; lack of insulin causes the reverse.
Decreased gluconeogenesis – decreases production of glucose from non-sugar substrates, primarily in the liver (remember, the vast majority of endogenous insulin arriving at the liver never leaves the liver); lack of insulin causes glucose production from assorted substrates in the liver and elsewhere.
Decreased autophagy - decreased level of degradation of damaged organelles. Postprandial levels inhibit autophagy completely.[18]
Increased amino acid uptake – forces cells to absorb circulating amino acids; lack of insulin inhibits absorption.
Increased potassium uptake – forces cells to absorb serum potassium; lack of insulin inhibits absorption. Insulin's increase in cellular potassium uptake lowers potassium levels in blood.
Arterial muscle tone – forces arterial wall muscle to relax, increasing blood flow, especially in micro arteries; lack of insulin reduces flow by allowing these muscles to contract.
Increase in the secretion of hydrochloric acid by Parietal cells in the stomach.

Elevated Sodium-to-Potassium Excretion Ratio Linked to Greater Risk for CVD

Patients with elevated sodium-to-potassium excretion ratios may face increased risk for cardiovascular events, reports Archives of Internal Medicine.


In two prospective studies, some 2300 adults aged 30 to 54 and with prehypertension provided four 24-hour urine samples over 18 to 36 months, and then were followed for 10 to 15 years.


During follow-up, 8% of the participants experienced major cardiovascular events, including MI, coronary revascularization, and cardiovascular death. After adjustment for multiple confounders, the risk for cardiovascular events increased as the sodium-to-potassium excretion ratio increased. Neither sodium nor potassium excretion alone was significantly associated with cardiovascular risk.


The authors conclude that these results, taken together with previous research, suggest that "lowering dietary sodium intake, while increasing potassium consumption, at the population level might reduce the incidence of CVD."

Low-Glycemic-Index Diet Improves Glycemic Control, HDL in Type 2 Diabetes

Patients with stable type 2 diabetes can improve their glycemic control and HDL level with a low-glycemic-index diet, according to a study published in JAMA.


Roughly 200 patients taking antihyperglycemic drugs underwent randomization to either a low-glycemic-index diet or a high-cereal-fiber diet for 6 months. (The low-glycemic-index diet emphasized foods like pumpernickel bread, bulgur-and-flax breakfast cereal, and peas, lentils, and nuts; the high-cereal-fiber diet emphasized whole-grain breads and breakfast cereals, brown rice, and avoidance of starchy foods.)


By the 6-month mark, hemoglobin A1c levels decreased and HDL levels rose, both significantly, in patients on the low-glycemic-index diet.


The authors say the low-glycemic-index diet may add further glycemic control in patients on antihyperglycemic drugs.

Eating veggies shrinks the brain

MELBOURNE: Scientists have discovered that going veggie could be bad for your brain-with those on a meat-free diet six times more likely to suffer brain shrinkage.

Vegans and vegetarians are the most likely to be deficient because the best sources of the vitamin are meat, particularly liver, milk and fish. Vitamin B12 deficiency can also cause anaemia and inflammation of the nervous system. Yeast extracts are one of the few vegetarian foods which provide good levels of the vitamin.

The link was discovered by Oxford University scientists who used memory tests, physical checks and brain scans to examine 107 people between the ages of 61 and 87.

When the volunteers were retested five years later the medics found those with the lowest levels of vitamin B12 were also the most likely to have brain shrinkage. It confirms earlier research showing a link between brain atrophy and low levels of B12.

Brain scans of more than 1,800 people found that people who downed 14 drinks or more a week had 1.6% more brain shrinkage than teetotallers. Women in their seventies were the most at risk.

Beer does less damage than wine according to a study in Alcohol and Alcoholism.

Researchers found that the hippocampus-the part of the brain that stores memories - was 10% smaller in beer drinkers than those who stuck to wine.

And being overweight or obese is linked to brain loss, Swedish researchers discovered. Scans of around 300 women found that those with brain shrink had an average body mass index of 27 And for every one point increase in their BMI the loss rose by 13 to 16%.



Read more: Eating veggies shrinks the brain - The Times of India http://timesofindia.indiatimes.com/home/science/Eating-veggies-shrinks-the-brain/articleshow/3480629.cms#ixzz17V6kv5XC

AHA Champions Omega-6 PUFAs to Counter Popular Nutrition Advice

January 28, 2009 (Dallas, Texas) — Contrary to advice from some popular diet books, people should not consider reducing their intake of omega-6 fatty acids, found in vegetable oils, in proportion to their intake of omega-3 polyunsaturated fatty acids (PUFAs), found in oily fish, a new statement from the American Heart Association (AHA) is stressing [1].

According to the science advisory released by the AHA this week, people should aim to get 5% to 10% of their daily calories from omega-6 fatty acids, primarily linoleic acid, a proportion they are likely already getting if they follow dietary recommendations from the AHA.

According to Dr Dariush Mozaffarian (Harvard University, Boston, MA) one of the advisory writing group members, the AHA has zeroed in on omega-6s to counter nutritional advice from other sources that has deemphasized the role for plant-based PUFAs.

"Although I think most scientists and clinicians generally recognize evidence demonstrating the benefit of omega-6 fatty acids, there are a minority of scientists who have vocally proposed that omega-6 fatty acids are harmful and advise reducing intake of omega-6," he told heartwire . "The goal of this advisory was to review and clarify the evidence for benefit vs harm."

Lead author for the writing group, Dr William S Harris, explained to heartwire that recommendations to reduce omega-6 intake come from a handful of scientific studies whose findings have been taken up and incorporated into popular nutrition books. One such book, cited in the AHA advisory, is the Omega Rx Zone, by Dr Barry Sears, whose wildly popular, low-glycemic-load "Zone diet" has been championed by movie stars and professional athletes since the early 21st century.

According to Harris, one of the ideas promulgated by diet and nutrition books is the idea of an optimal omega-6:3 ratio, something he says is based on an "misinterpretation of the science." The rationale for reducing linoleic-acid intake comes from research showing that it is metabolized to arachidonic acid, which is involved in the synthesis of proinflammatory molecules. But omega-6 PUFAs also have powerful anti-inflammatory properties that counteract any proinflammatory activity, say the advisory authors. "It's incorrect to view the omega-6 fatty acids as 'proinflammatory,' " Harris spells out in an AHA press release. "Eating less linoleic acid will not lower tissue levels of arachidonic acid because the body tightly regulates the synthesis of [arachidonic acid] from [linoleic acid]," he stated.

"Cardiologists, I think, have had a good feeling about vegetable oils for years and years--things like corn and saffron oil; they've been a good and healthy replacement for saturated fats in the diet since the 1970s, and the AHA has been promoting them for years," Harris told heartwire . "This paper serves as a review, pulling together the many lines of evidence in humans, to say that higher omega-6 intake is associated with better cardiovascular health. . . . We're basically not telling people to start doing something different; we're telling people not to stop eating their omega-6."

But Dr Artemis Simopoulos (Center for Genetics, Nutrition, and Health, Washington, DC), a leading proponent of reducing omega-6 intake, disputes the AHA advisory, arguing to heartwire that US and other Western diets include far too much omega-6 PUFAs, in levels far higher than intake of omega-3s (a ratio of 16:1, she says). "The studies that have been done very clearly show that [eicosapentaenoic acid] EPA and [docosahexaenoic acid] DHA are very potent anti-inflammatory agents, whereas linoleic and arachidonic acids areonly slightly so. And when you have them in high amounts as they exist in Western diets, they interfere with the incorporation and the elongation and saturation going from alpha-linolenic acid to EPA and DHA," she said. "Second, it's important to think in terms of evolution and evolutionary biology. We evolved on a diet that was never, until 150 years ago and in particular the past 50 years, so high in omega-6 fatty acids. This is an artificial way and a general experiment, being done without any scientific evidence."

She says that a ratio of 2:1 or even 1:1 omega-6 to omega-3 fatty acids is better. "Whether you look in terms of evolution, whether you look in terms of genetic variation, high amounts of omega-6 fatty acids are not consistent with health or normal development."

Authors of the AHA statement, however, respectfully disagree. According to Mozaffarian, people should focus on eating a healthy diet. "Focusing on specific ratios is not useful," he said.

In the paper, Harris discloses receiving research grants and being a consultant/advisory board member for Monsanto. Disclosures for other writing group members are listed in the paper.

1.Harris WS, Mozaffarian D, Rimm E, et al. Omega-6 fatty acids and risk for cardiovascular disease. Circulation 2009; DOI: 10.1161/CIRCULATIONAHA.108.191627. Available at: http://circ.ahajournals.org. Abstract

Elevated Resting Heart Rate Linked to Increased Cardiac Risk in Postmenopausal Women

Resting heart rate — a "low tech and inexpensive measure of autonomic tone" — independently predicts coronary risk in postmenopausal women, according to an analysis from the Women's Health Initiative published online in BMJ.


Researchers measured resting heart rate among nearly 130,000 postmenopausal women without histories of MI, stroke, or coronary revascularization. During 8 years' follow-up, 2300 coronary events (MI or coronary death) and 1900 strokes occurred.


After adjustment for confounders including age, smoking, hormone use, and physical activity, coronary risk was 26% higher among women with the highest resting heart rates (greater than 76 beats/minute) than among those with the lowest (62 beats/minute or less). Resting heart rate did not predict stroke risk.


The authors conclude that the association between resting heart rate and coronary risk "might be large enough to be clinically meaningful."

High and Low BMIs Associated with Increased Mortality Risk

Adults on the lower and higher ends of the BMI scale face increased mortality risk, according to a study published online by Lancet.


Researchers examined data from 57 prospective studies comprising nearly 900,000 adults who had their BMI measured at baseline. After deaths occurring in the first 5 years' follow-up were excluded, all-cause mortality was lowest among those with BMIs in the middle range (22.5 to 25 kg/m2).


Above 25, every 5-unit increase in BMI translated to a:


30% increased risk for all-cause mortality;
40% higher risk for death from ischemic heart disease or stroke;
60% to 120% increase in renal, hepatic, or diabetic mortality;
10% increased risk for cancer-related deaths.

Adults at the lowest end of the BMI scale (below 22.5) were also at higher risk for death, partly due to smoking-related respiratory disease.

High Intake of Red and Processed Meats Linked to Increased Mortality Risk

High intake of red and processed meats is associated with increased risk for death in older adults, while white meat may have a protective effect, reports Archives of Internal Medicine.


More than a half million adults aged 50 to 71 completed food-frequency questionnaires and then were followed for 10 years; during that time, some 48,000 men and 23,000 women died.


After adjustment for confounders including BMI and smoking status, men and women in the highest quintile of red meat intake had significantly increased risks for overall mortality, cancer-related deaths, and cardiovascular-disease–related deaths, relative to those in the lowest quintile. High intake of processed meat was also associated with increased mortality risks.


Conversely, consumption of white meat (poultry and fish) was associated with significantly decreased risks for total and cancer-related mortality.

high fat diet and parkinsons

By Ben Harder, Special for USA TODAY
For a month that tested her determination, Marilyn Deaton dined on little but fat. The recipes she prepared included eggs baked with gobs of cream cheese, small portions of fish outweighed by butter, oil and mayo, and ground beef mixed with so much heavy cream that it ran a light brown.
"I can't stand things that are soft and slimy," says Deaton, 60, of New York. She missed "crunchable stuff," such as carrots, she says.

Deaton has Parkinson's disease. The disagreeable diet was an experimental treatment prescribed by her doctors. Four other Parkinson's patients followed the same menu.

The results, which included modest improvements in balance, tremors and mood, were encouraging but too preliminary to prove an effect, says Theodore VanItallie of St. Luke?s-Roosevelt Hospital Center in New York. VanItallie and his colleagues published their findings last year in the journal Neurology.

Their trial and other recent studies hint that a diet nearly devoid of protein and carbohydrates might temper symptoms of several neurodegenerative disorders, including Alzheimer's and Lou Gehrig's disease, VanItallie says.

Researchers suspect that such a high-fat diet also could stall brain tumors and help patients with certain other health problems — if it doesn't cause strokes along the way.

Though such a solution may sound far-fetched, a similar diet has been used since the 1920s to treat severe epilepsy. Numerous studies, most of them in children who had exhausted other options, have since found that it reduces seizures.

There's scant clinical evidence to address whether the plan, called the ketogenic diet, has wider therapeutic promise. Researchers aren't sure how it works against epilepsy, and they hold various theories about why it might, or might not, help in other disorders.

Some of the benefits result from a shift in the brain's metabolism from blood sugar, the body's main fuel, to ketone bodies, a secondary energy source that is a byproduct of fat metabolism, says Richard Veech, a physician and biochemist with the National Institutes of Health in Bethesda, Md.

But, Veech says, "while VanItallie has shown that (the ketogenic diet) works, as a practical matter, one can't recommend it."

The obvious downside

Consequences of high fat intake, heart problems for one, could offset the diet's hypothetical benefits in some people, Veech says. In any case, the daunting challenge of maintaining the unpalatable regimen makes it unlikely to catch on.

"Most people would have a very hard time following this diet," says Cathy Non-as, the dietitian at North General Hospital in New York who designed Deaton's plan. The plan requires that 90% of the patients' calories come from fat and just 8% from protein. In the average American diet, fat makes up 33% of calories, and protein accounts for 15%.

When a person fasts or subsists mainly on fat, blood sugar declines. The liver responds by converting fatty acids into ketone bodies, which normally circulate in the blood at low levels, rising as time passes since a person's most recent meal, when glucose is abundant.

Popular low-carb diets, such as Atkins, may generate some ketone bodies, but not necessarily enough to have a therapeutic benefit, VanItallie says.

Ketone bodies can accumulate to dangerous levels, in diabetics, for example, and turn the blood acidic. But moderately elevated levels are theoretically beneficial in a range of circumstances, Veech says.

Lab studies and a few desperate medical cases lend some support to that notion. For example, when added to intravenous resuscitation fluids in place of a typical ingredient, ketone bodies also reduce organ damage after major blood loss, says hematologist C. Robert Valeri of the Naval Blood Research Laboratory in Plymouth, Mass. He and his colleagues demonstrated that in pigs.

Other teams have shown that the molecules protect mice against neurological changes linked to Parkinson's and Alzheimer's.

Last month, researchers at Mount Sinai School of Medicine in New York reported similar findings for Lou Gehrig's disease, or amyotrophic lateral sclerosis. Giulio Pasinetti of Mount Sinai says his team is launching a trial to treat patients with the disease.

In an older report, a ketogenic diet appeared to slow tumor growth in two children with inoperable brain cancer. Neurobiologist Thomas Seyfried of Boston College later demonstrated the effectiveness of that approach in mice.

Most brain tumor cells, Seyfried says, "can't burn ketones for energy," so elevating ketone levels and simultaneously reducing blood sugar may starve the tumors while nourishing healthy cells.

A 'lite' version

VanItallie and Non-as are gearing up for a new Parkinson's trial that will test a hybrid of the 90%-fat regimen and the Atkins diet. They've invited their former volunteers to participate.

Deaton says her Parkinson's symptoms improved during the original trial, which was conducted in 2003. And losing 26 pounds was a bonus, she says. But even with a more lenient menu on the table, she doesn't plan on signing up again.

She's trying a more conventional weight-loss plan. It lets her eat carrots.

fatter is better 2

May 19, 2009 (Washington, DC) — Despite being a key cause of heart disease, obesity appears to be protective in a range of cardiovascular problems, a new review concludes [1]. But that doesn't mean people shouldn't try to lose weight, lead author on the paper, Dr Carl J Lavie (Ochsner Medical Center, New Orleans, LA), told heartwire . Indeed, patients who fare the best seem to be obese patients who manage to lose some weight, he said.

"First, obesity is a very strong risk factor and increases all types of heart disease, but second, once you get heart disease, the obese patients do better, so their prognosis is not doomsday," Lavie explained. "In fact, if you have obese patients with congestive heart failure or coronary heart disease or other heart disorders, those patients actually have a pretty good prognosis if they are treated well. But third, the ones who lose weight do even better."

According to Lavie, there is solid evidence to suggest that being overweight or obese may improve survival, not just in heart failure, but also in diseases like hypertension, coronary artery disease, and peripheral artery disease.

"There are a large number of cardiologists who don't even recognize that this is the case, and they are confused about it, too. It is honestly a confusing topic because if obesity is so bad, and it contributes to all cardiovascular risk factors and markedly increases the prevalence of developing heart disease of almost every type, then why, once they get it, do obese patients do better?"

The new review appears in the May 26, 2009 issue of the Journal of the American College of Cardiology (JACC) [1].

Obesity Likely Protects Through Various Mechanisms

The protective effects of excess weight have been best documented in heart-failure patients, where patients with higher body weight or percent body fat have demonstrated better event-free survival. In this setting, says Lavie, extra weight may function much the same way it does with cancer and other chronic diseases, by providing the body with additional fuel to help fight the disease.

Less well known is the relationship between obesity and hypertension, Lavie et al note. While people who are obese do have more hypertension, five papers spanning almost 20 years also point to the fact that obese people with hypertension seem to have lower mortality and/or lower stroke risk, despite less effective blood-pressure control, than do normal-weight people. In this setting, obese patients "may have a better prognosis in part because of having lower systemic vascular resistance and plasma renin activity compared with more lean hypertensive patients," Lavie et al write.

Also incompletely understood is the paradoxical relationship of obesity and coronary and peripheral artery diseases. Obesity is believed to play a causal role in the development of a number of major risk factors for arterial disease, among them hypertension, dyslipidemia, and diabetes, and is believed to be, in and of itself, a risk factor for atherosclerosis. But according to the JACC authors, there is also literature to suggest that overweight and obese coronary heart disease patients have a lower risk for mortality compared with under- and normal-weight coronary heart disease patients who have undergone revascularization procedures. A similar contradictory relationship has been seen in patients with peripheral artery disease.

Speaking with heartwire , Lavie emphasized that the protective effects of excess weight and excess fat likely function in different ways in different diseases. "We know that fat cells do a lot of bad things, but it's certainly conceivable that in advanced disease, the fat cell could have some beneficial effects. There's still a lot that needs to be known about this process."

Weight Loss Still Key

A key new piece of the puzzle that emerged in Lavie et al's review, however, is that weight loss, often touted as a way to reduce cardiovascular risk, appears to be a good thing in spite of the protective effects of extra weight.

"For people who follow this field, these kinds of findings have led them to question whether weight loss is good for heart-disease patients. . . . We found that the patients who do the best are the obese patients who lose weight."

This additional contradiction may be explained in part by the theory that heart disease in obese patients is likely "a different disease" than heart disease in lean people, in whom genetic factors are probably more important. "It may be that the obese person wouldn't have even gotten blocked arteries if [he] hadn't gained 70 pounds over a 30-year period," Lavie said. "The thin person who gets blocked arteries or congestive heart failure or high blood pressure is probably different from the obese patient who got the disease from becoming obese."

For now, he says, it's important particularly for the general public to appreciate that the "protective" effects of obesity in no way provide a rationale for weight gain. "Very clearly," he said, "if no one in our country became overweight or obese, heart-disease rates would go down dramatically."

For physicians, the data today are sufficiently comprehensive for them to encourage their overweight and obese patients to stay motivated to reduce their risk factors. That wasn't always the case, he added. "When people were finding this in their data, five and six years ago, they probably had some trouble getting their papers published, because it didn't make any sense."

References
1.Lavie CJ, Milani RV, Ventura HO. Obesity and cardiovascular disease. Risk factor, paradox, and impact of weight loss. J Am Coll Cardiol 2009; 53:1925–1932.

Low-Carb or Low-Fat Diet May Similarly Affect Weight, A1C in Patients With Type 2 Diabetes

July 21, 2009 — A low-carbohydrate diet may have effects similar to those of a low-fat diet on weight and hemoglobin A1C (A1C) levels in patients with type 2 diabetes, but patients following the low-carbohydrate diet have a greater increase in high-density lipoprotein (HDL) cholesterol levels after 1 year, according to the results of a randomized clinical trial reported in the July issue of Diabetes Care.

"Optimal weight loss strategies in patients with type 2 diabetes continue to be debated, and the best dietary strategy to achieve both weight loss and glycemic control in type 2 diabetes is unclear," write Nichola J. Davis, MD, MS, from the Albert Einstein College of Medicine of Yeshiva University, Bronx, New York, and colleagues. "Prior studies, done primarily in patients without diabetes, demonstrated weight loss outcomes with low carbohydrate diets comparable to that with other diets. Based on the effectiveness of low-carbohydrate diets for weight loss, recent guidelines from the American Diabetes Association state that for short-term weight loss either a low carbohydrate or low-fat calorie-restricted diet may be effective."

The goal of this study was to compare the effects during 1 year of a low-carbohydrate diet and a low-fat diet on weight loss and glycemic control in 105 overweight adults with type 2 diabetes. The main endpoints of the study were weight and A1C levels, and secondary endpoints were blood pressure and lipid profile, measured at 3, 6, and 12 months.

Weight loss occurred faster in the low-carbohydrate group vs the low-fat group (P = .005), with the greatest decrease in weight and A1C levels occurring during the first 3 months. However, both dietary groups had a similar 3.4% weight loss at 1 year, and neither group had a significant change in A1C levels at this time point. Blood pressure was unaffected. Compared with the low-fat dietary group, the low-carbohydrate group had a greater increase in HDL cholesterol levels (P = .002).

"The most relevant point is that there were increases in HDL cholesterol with the low carbohydrate diet," Maria-Luz Fernandez, PhD, a professor of nutritional sciences at the University of Connecticut, told Medscape Diabetes & Endocrinology when asked for independent comment. "This is a very consistent finding in low-carb interventions. HDL cholesterol is most of the time very low in diabetic people so this is a very important clinical implication."

Limitations of this study include greater baseline weight in the low-fat group vs the low-carbohydrate group, possible bias caused by use of single-day dietary recall or a single-day food record to evaluate dietary intake, and lack of objective measures of physical activity.

"Among overweight patients with type 2 diabetes, there was no significant difference in the weight or A1C change in participants after a low carbohydrate compared with a low-fat diet for 12 months," the study authors write. "Participants in both arms achieved an average 3.4% weight reduction but did not reduce A1C. Differences in the short-term effects of each diet were not sustained."

When asked about clinical caveats or recommendations regarding low-carbohydrate diets, Dr. Fernandez said: "Low-carb diets are difficult to follow if the carbohydrate is very low, but a 25% carbohydrate diet is not difficult to follow and it can be very useful for diabetic patients."

In additional research, Dr. Fernandez recommends studies to evaluate whether there are sex responses or if the responses vary depending on low HDL cholesterol levels at baseline.

This study was supported by research grants through the Robert C. Atkins Foundation (a nonprofit foundation not affiliated with Atkins Nutritionals) and the Diabetes Research and Training Center and by a Clinical and Translational Science Award. The investigators thanked Bayer Pharmaceuticals and sanofi-aventis for their donations and have disclosed no other relevant financial relationships.

Dr. Fernandez has received research funding from the American Egg Board and from the United Arab Emirates Embassy.

Diabetes Care. 2009;32:1147-1152.

New Review Endorses CV Benefits of Fish Oil

y discuss the results for each specific cardiovascular condition in turn. For CHF, three large randomized trials — the Diet and Reinfarction Trial (DART), the Gruppo Italiano per lo Studio della Sopravvivenza nell' Infarto Miocardico (GISSI)-Prevenzione, and the Japan EPA Lipid Intervention Study (JELIS) — have indicated that omega-3 PUFAs lower CV risk in both the primary- and secondary-prevention settings, they note.

Lavie elaborated to heartwire : "The benefit is different in different studies but can be as much as 30%." The effects are seen on total mortality, sudden death, CHD mortality, and cardiovascular mortality.

But there are some studies that have not shown favorable results, although there are generally methodological reasons for this, they say. However, they do flag the most recent study of post-MI patients, OMEGA, which suggests there may not be additional short-term benefit of omega-3 PUFAs in low-risk patients already receiving optimal modern therapy.

Dr. Lavie has been a consultant and speaker for Reliant, Pfizer, Bristol-Myers Squibb, and Sanofi-Aventis and is a speaker receiving honoraria from and on the speaker's bureau of GlaxoSmithKline, Abbott, and Solvay. Disclosures for the coauthors are listed in the article.

References
1.Lavie CJ, Milani RV, Mehra MR, et al. Omega-3 polyunsaturated fatty acids and cardiovascular disease. J Am Coll Cardiol 2009; 54: 585-594. Available at: http://content.onlinejacc.org.