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UK Review Affirms Omega-3s and “Med” Diet as Heart-Healthy
12/11/2006
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Review finds little evidence in favor of vitamins or low-starch diets: Cardiac value of high omega-3/omega-6 ratio questioned
by Craig Weatherby


Earlier this month, members of the UK Heart Health and Thoracic Dietitians Group undertook an informal review of the evidence on various proposed nutritional approaches to enhancing heath health.

The UK team looked at studies on the efficacy of various dietary changes for reducing the risk of heart attacks or strokes in people who have already suffered such an adverse cardiovascular event: a kind of aid called “secondary prevention”.

A group of dietitians at London’s Charing Cross Hospital gathered all of the systematic evidence reviews published prior to January, 2005, limiting their literature search to reviews that addressed the effects of diet on secondary prevention of adverse cardiovascular events (Mead A et al 2006).

Rather than a “meta-analysis”, or rigorous statistical analysis of prior studies, this was an informal review intended to help UK dietitians provide accurate preventive nutrition advice to cardiovascular patients.

Each prior study was scrutinized by two dietitians, and the group then discussed the state of the evidence for various dietary interventions and arrived at some consensus conclusions.

These were their main findings, to which we’ve added our own comments:

Dietary changes not proven to reduce risks for heart patients
  • Supplemental antioxidant vitamins (vitamins C and E). Unlike these antioxidant vitamins, the polyphenol antioxidants in tea, berries, and chocolate enhance several aspects of cardiovascular health very substantially.

  • Low-glycemic-index diets. The glycemic index of a food measures how much it raises blood sugar. Sugars and starches raise blood sugar levels rapidly and substantially, and are therefore considered “high-glycemic” foods. [This finding is surprising, since there is a good deal of evidence linking dietary sugars and starches to increases in inflammation, which is considered a risk factor for cardiovascular disease.

  • Increased intake of the B-vitamin called folate (folic acid) does not seem to yield much reduction in the risk of adverse cardiovascular events, even though folate reduces blood levels of homocysteine: a protein associated with greater risk of clogged arteries, cardiac death, stroke, and dementia.
Dietary changes that reduce risks for heart patients
  • Reduction in saturated fat intake and substitution of saturated fats with unsaturated fats. It is important to recognize that not all saturated fats are associated with adverse changes in people’s blood lipid (cholesterol and triglyceride) profiles. Stearic acid, which is abundant in cocoa butter and beef fat, neither worsens nor improves blood lipid profiles, and is not blamed for worsening cardiovascular health. Even palmitic acid, which raises cholesterol more than any other fat, is not unhealthful unless it dominates your fat intake. (Palmitic acid is most abundant in beef fat, pork fat, palm-kernel oil, coconut oil, and dairy products.)

  • Mediterranean-type diets, which are dominated by vegetables, fruits, fish, and olive oil, reduce cardiac risks.

  • Increased intake of omega-3 fatty acids from fish. Recent evidence indicates that fish oil may raise the risk of arrhythmias in patients with implanted cardiac defibrillators.
To expand on the UK team's very general characterizations, we’d like to add some points about each of the main kinds of dietary fat.

Saturated Fatty acids (SFA: meats, dairy, coconut, cocoa butter)
Studies comparing different world population groups link higher intake of saturated fat and total cholesterol with higher death rates from coronary heart disease. But the results of studies comparing people within distinct population groups are not so clear.

Higher saturated fat intakes do not raise risk of stroke.

Different kinds of saturated fatty acids (SFA) have different effects on blood lipid and cholesterol levels.
  • Stearic acid, a long-chain SFA abundant in beef, pork, and cocoa butter, does not raise “bad” forms of cholesterol, probably because it is rapidly converted to oleic acid, the MUFA abundant in olive oil. Stearic acid may lower “good” HDL cholesterol slightly in women and may increase concentrations of one undesirable form of cholesterol called lipoprotein (a).

  • Short-chain SFAs such as lauric acid (coconut oil) and myristic acid (dairy) raise total cholesterol moderately.

  • Medium-chain palmitic acid, an SFA abundant in beef, pork, palm oil, and cocoa butter, has mixed and variable effects, but generally raises total cholesterol more than the other SFAs. Even though chocolate contains cocoa butter, whose fat is about one-half palmitic acid, it does not raise "bad" LDL cholesterol. Instead, it raises "good" HDL cholesterol while reducing blood stickiness and enhancing artery health, thanks in large part to its flavanol antioxidants.
Monounsaturated fatty acids (MUFA: olives, macadamia nuts, avocadoes)
The predominant MUFA in olive, macadamia nut, and most commercial oils, called oleic acid, reduces risk of cardiac death mortality by preventing clogged arteries and dangerous clotting. Compared with the standard American diet, the traditional Mediterranean diet is much higher in MUFAs and lower in saturated meat and diary fats.

Omega-6 polyunsaturated fatty acids (corn, soy, canola, and cottonseed oils)
The standard American diet is unnaturally high in omega-6 fatty acids that lower total cholesterol but, when consumed in excess, induce plaque-promoting oxidation of LDL cholesterol, increase blood stickiness (platelet activation), and suppress the immune system. (Dietary omega-3s also promote oxidation of LDL cholesterol, but simultaneously raise levels of "good" HDL cholesterol and decrease blood stickiness and the risk of arrhythmias, thereby reducing rates of cardiac death.)

Omega-3 polyunsaturated acids (PUFAs)
The key marine omega-3s from fish fat (EPA and DHA) work together to reduce heart attacks, strokes, and death rates from heart disease, especially in people who’ve already suffered an adverse event or diagnosis (heart attack, stroke, congestive heart failure).

As the UK dietary study group said, “Studies that have demonstrated the protective effects of fatty fish intake against myocardial infarction (heart attacks) outnumbered those that did not.” And the same is true for rates of sudden cardiac death.

The short-chain, plant-derived omega-3 called alpha linolenic acid (ALA) also reduces death rates from heart disease, but not nearly as strongly.

Marine omega-3s appear to reduce cardiovascular risks more by preventing irregular rhythms than by keeping arteries free of clogs, but the picture is probably more complex, and likely includes their anti-inflammatory effects.

Cardiac value of high omega-3/omega-6 ratio questioned
Total intake of omega-3s may matter more than the ratio of omega-3s to omega-6s in your diet, according to the results of a recent study by Harvard University’s Dariush Mozaffarian, M.D., and the conclusions of an evidence review by biochemist and heart researcher William Harris, Ph.D., Professor of Medicine at the University of Missouri - Kansas City.

(We heard Drs. Harris and Mozaffarian speak forcefully in favor of fishy diets at the government-sponsored Seafood & Health ’05 conference in Washington D.C.)

This finding is surprising, given the competition between dietary omega-3s and omega-6s for entry into key metabolic pathways through which both types of PUFAs exert their distinct influences. (The only exceptions are the one in 20 people with a specific genetic variation, in whom omega-6s increase the thickness of the inner two layers of the wall of the carotid artery.)

Among other distinctions, omega-3s tend to yield anti-inflammatory effects, while omega-6s are generally pro-inflammatory. However, as Dr. Harris notes, the available evidence suggests that omega-6 PUFAs do not inhibit the anti-inflammatory effects of omega-3s while relatively high intake of both types of PUFAs is associated with the lowest levels of inflammation.

His case seems reasonably well supported by the evidence, which includes a recent study by Harvard University’s Dariush Mozaffarian, M.D.

Dr. Mozaffarian analyzed data from the Health Professionals Follow Up Study (HPFS) to see whether higher omega-6 intakes blunted the cardiovascular-risk-reducing effects of higher omega-3 intakes. As Dr. Harris said in his review, “These findings, which derive from data from over 51,000 men followed for 14 years, are not consistent with the view that the omega-6/omega-3 ratio has clinical relevance …”.

In other words, Dr. Mozaffarian's analysis of HPFS data indicates that decreasing your intake of omega-6s does not enhance heart health nearly as much as increasing intake your of omega-3s.

Still, the results of Dr. Harris’ evidence review should not be viewed as a license to over-consume the omega-6 fatty acids abundant in our most commonly consumed vegetable oils (corn, soy, cottonseed, canola) and in grain-fed beef, pork, and chicken, if only because high intake of omega-6s appears to promote cancer growth.


Sources
  • Harris WS, Assaad B, Poston WC.Tissue omega-6/omega-3 fatty acid ratio and risk for coronary artery disease. Am J Cardiol. 2006 Aug 21;98(4A):19i-26i. Epub 2006 May 30. Review.
  • Harris WS. The omega-6/omega-3 ratio and cardiovascular disease risk: uses and abuses. Curr Atheroscler Rep. 2006 Nov;8(6):453-9.
  • Khor GL. Dietary fat quality: a nutritional epidemiologist's view. Asia Pac J Clin Nutr. 2004 Aug;13(Suppl):S22.
  • Mead A, Atkinson G, Albin D, Alphey D, Baic S, Boyd O, Cadigan L, Clutton L, Craig L, Flanagan C, Greene P, Griffiths E, Lee NJ, Li M, McKechnie L, Ottaway J, Paterson K, Perrin L, Rigby P, Stone D, Vine R, Whitehead J, Wray L, Hooper L; on behalf of the UK Heart Health and Thoracic Dietitians Interest Group (Specialist group of the British Dietetic Association). Dietetic guidelines on food and nutrition in the secondary prevention of cardiovascular disease - evidence from systematic reviews of randomized controlled trials (second update, January 2006). J Hum Nutr Diet. 2006 Dec;19(6):401-19.
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