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Omega-6/Omega-3 Imbalance Pushes Heart/Diabetes Perils
8/27/2007
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Clinical and animal studies from Europe lend urgency to experts’ call for a swift shift in Americans’ omega-3/omega-6 intake ratio

by Craig Weatherby


Some 50 million Americans have all the signs of “metabolic syndrome” (MetS), and the increased risks of developing cardiovascular disease, stroke, and type 2 diabetes associated with this deadly cluster of physical conditions.


The relative amounts of omega-3 and omega-6 fatty acids people consume plays a key role in promoting or discouraging development of the defining characteristics of MetS.


Key Points
  • Clinical trial shows higher-than-average omega-3/omega-6 intake ratio raises levels of hormone (adiponection) that stimulates fat-burning and discourages diabetes, inflammation, and heart disease.
  • Mouse study provides similar, supportive results.

This is largely because “silent” inflammation underlies five of the six defining components of metabolic syndrome, and the body makes make hormone-like pro-inflammatory compoundscalled eicosanoidsfrom omega-6s.


In contrast, the body makes inflammation-moderating eicosanoids from omega-3s. Thus, the ratio of the two classes of omega fatty acids in cell membranes influences your body's average level of inflammation.


Metabolic syndrome is defined as having three or more of a half-dozen metabolic risk factors:

  1. Abdominal obesity (excessive fat tissue in and around the abdomen).
  2. Imbalanced blood lipids: High blood triglycerides, low HDL cholesterol and high LDL cholesterol: a state that fosters plaque buildups in artery walls.
  3. Insulin resistance/glucose intolerance (the body can’t handle blood sugar properly).
  4. “Sticky” blood, which promotes dangerous clots.
  5. Pro-inflammatory state in the body, signaled by elevated C-reactive protein levels in the blood)
  6. Elevated blood pressure.

The results of two research reports from Europe add more urgency to efforts to educate people about the dangers of the grossly imbalanced omega-3/omega-6 intake ratio typical of Americans’ diets, which are heavily skewed toward pro-inflammatory omega-6 fatty acids.


Researchers agree that people should consume no more than 3-4 omega-6 molecules for every omega-3 molecule, but most Americans ingest 20 to 40 omega-6s for every omega-3 molecule.


This why we are urged to consume more omega-3s. Ideally, many of these omega-3s should be the long-chain kind from fish (EPA and DHA), which the body uses much more efficiently than the short-chain plant form (ALA), which predominates only in leafy greens and flax seeds. (ALA also occurs in eggs from chickens fed fish or flax meal, in grass-fed meats and poultry, and in foods fortified with it.)


But we also need to cut back on omega-6 fatty acids. (See "Sources of omega-6s", below.)


Clinical trial finds healthy “omega ratio” promotes anti-diabetic hormone

Scientists’ understanding of the interplay of various hormones is expanding rapidly, and it’s becoming apparent that they play important roles in promoting or discouraging three key elements in metabolic syndrome:

  • Abdominal obesity (excessive fat tissue in and around the abdomen).
  • Insulin resistance or glucose intolerance (the body can’t use insulin or handle blood sugar properly).
  • Pro-inflammatory state.

In addition being the precursor to adult onset diabetes, insulin resistance syndrome is an important risk factor for atherosclerosis (clogged, stiff arteries) and its cardiovascular complications.


Sources of omega-6s
Most of the excess dietary omega-6 fatty acids in Americans’ diets come from common vegetable oils
corn, soy, canola, sunflower, safflower, and cottonseedwhich predominate in home cooking and in packaged and restaurant foods.


(Soy and canola oils are the major sources of omega-3s in the diets of most Americans, but these oils are much higher in omega-6s, so they are far from ideal sources.)


This is why researchers recommend using oils low in omega-6s, such as olive oil, macadamia nut oil, and “hi-oleic” versions of safflower or sunflower oil.


Americans also get lots of omega-6 fat from factory-farmed cattle, pigs, and poultry, which are fed grain-heavy diets high in omega-6s and low in omega-3s (Farmed salmon are also quite high in omega-6s, while wild salmon have much lower levels).

Abdominal fat acts like a gland. Its fat cells secrete hormones that exert strong effects on appetite, inflammation, and metabolism, and influence whether fats and carbohydrates in foods are burned or stored as belly fat.


Among the various belly-fat-generated hormones, only onecalled adiponectin— discourages insulin resistance, inflammation, and atherosclerosis, with substantially lower levels of adiponectin found in people suffering from obesity, insulin resistance, and atherosclerosis (Abbasi F et al 2004; Haluzikova D et al 2007).


Researchers at France’s University of Lyon conducted a novel study designed to test the effects of different omega-3/omega-6 intake ratios on volunteer’s levels of blood fats, hormones and inflammatory markers (Guebre-Egziabher F et al 2007).


They recruited 17 people10 men and seven women; average age 27and instructed them to eat diets low in omega-6s and high in omega-3s for 10 weeks.


A higher-than-average omega-3 to omega-6 intake ratio was achieved in the volunteers by having the participants use olive and canola oil in place of oils higher in omega-6s (corn, soy, sesame, safflower, sunflower, etc.), and by eating fish three times a week (3.5 oz of salmon, tuna, mackerel, herring and/or sardines) in place of meat.


Before and during the study, the participants were reminded how to avoid foods high in omega-6 fatty acids, including most packaged and prepared foods.


The results were encouraging and much as expected, based on animal studies, such as the one summarized below.

  • Levels of adiponectin rose 17 percent
  • Burning of body fat (fasting lipid oxidation) rose 28 percent
  • Levels of the pro-inflammatory protein TNF-alpha fell 32 percent
  • Levels of LDL cholesterol fell by eight percent

Body weight and composition and insulin sensitivity remained unchanged, as was expected from such a short trial. (It takes time for these markers to change in response to a fatty acid shift.)


Mouse study provides more support for higher omega-3/0mega-6 intake ratio

The French trial was preceded by a similar study in mice, conducted at the Medical University of Vienna, Austria, whose results echo its findings in favor of higher omega-3/omega-6 ratios (Todoric J et al 2006).


The researchers started with two groups of mice:

  • Diabetic mice
  • Lean non-diabetic mice

They then divided the Diabetic and Non-Diabetic mice into 4 groups, each fed a different diet.

  1. Low-Fat Diet (LF)
  2. High-Fat Diet rich in Saturated and Monounsaturated fatty acids (HF/SM)
  3. High-Fat Diet rich in Omega-6 fatty acids (HF/6)
  4. High-Fat Diet rich in Omega-3 fatty acids (HF/3)

And the results support the value of diets with balanced omega-3 to omega-6 ratios:

  • The HF/3 (omega-3-rich) diet completely prevented the pro-inflammatory changes induced in the diabetic mice by all of the other high-fat diets, despite unreduced body weight.
  • The HF/3 (omega-3-rich) diet was the only one that did not reduce blood levels of adiponectin: the hormone that seems to discourage inflammation, insulin resistance, and atherosclerosis.
  • Compared with the LF group, the mice in the HF/SM diet group showed increases in expression of many pro-inflammatory genes, and infiltration of their adipose tissue by macrophage cells: developments that promote inflammation, insulin resistance, diabetes, and atherosclerosis, and may encourage obesity.
  • Compared with the HF/SM group, the HF/6 group showed only marginal rises in adipose tissue inflammation.

As the authors wrote:


“[High-fat diets rich in omega-3s] …prevent adipose tissue inflammation induced by high-fat diet in obese diabetic mice, thereby dissecting obesity from adipose tissue inflammation.”


“These data suggest that beneficial effects of [omega-3s] on diabetes development could be mediated by their effect on adipose tissue inflammation” (Todoric J et al 2006).


These results support the findings of the French clinical trial, and further strengthen the case for increasing American’s omega-3 intake and reducing their omega-6 intake.


For more background to today’s report, see “Omega-3s Seen to Fight Metabolic Syndrome”.



Sources

  • Abbasi F, Chu JW, Lamendola C, McLaughlin T, Hayden J, Reaven GM, Reaven PD. Discrimination between obesity and insulin resistance in the relationship with adiponectin. Diabetes. 2004 Mar;53(3):585-90.
  • Guebre-Egziabher F, Rabasa-Lhoret R, Bonnet F, Bastard JP, Desage M, Skilton MR, Vidal H, Laville M. Nutritional intervention to reduce the n-6/n-3 fatty acid ratio increases adiponectin concentration and fatty acid oxidation in healthy subjects. Eur J Clin Nutr. 2007 Aug 15; [Epub ahead of print]
  • Haluzikova D, Roubicek T, Haluzik M.  [Adiponectin and atherosclerosis] Vnitr Lek. 2007 Apr;53(4):359-63. Review. Czech.
  • Haugen F, Drevon CA.  Activation of Nuclear Factor-{kappa}B by High Molecular Weight and Globular Adiponectin. Endocrinology. 2007 Aug 16; [Epub ahead of print]
  • Huang XF, Xin X, McLennan P, Storlien L. Role of fat amount and type in ameliorating diet-induced obesity: insights at the level of hypothalamic arcuate nucleus leptin receptor, neuropeptide Y and pro-opiomelanocortin mRNA expression. Diabetes Obes Metab. 2004 Jan;6(1):35-44.
  • Huber J, Loffler M, Bilban M, Reimers M, Kadl A, Todoric J, Zeyda M, Geyeregger R, Schreiner M, Weichhart T, Leitinger N, Waldhausl W, Stulnig TM. Prevention of high-fat diet-induced adipose tissue remodeling in obese diabetic mice by n-3 polyunsaturated fatty acids. Int J Obes (Lond). 2007 Jun;31(6):1004-13. Epub 2006 Nov 28.
  • Kim JY, van de Wall E, Laplante M, Azzara A, Trujillo ME, Hofmann SM, Schraw T, Durand JL, Li H, Li G, Jelicks LA, Mehler MF, Hui DY, Deshaies Y, Shulman GI, Schwartz GJ, Scherer PE. Obesity-associated improvements in metabolic profile through expansion of adipose tissue. J Clin Invest. 2007 Aug 23; [Epub ahead of print]
  • Magkos F, Sidossis LS. Recent advances in the measurement of adiponectin isoform distribution. Curr Opin Clin Nutr Metab Care. 2007 Sep;10(5):571-5.
  • Marcus Y, Stern N. Fat cell-derived modulators of vascular cell pathophysiology: the list keeps growing. J Cardiometab Syndr. 2006 Spring;1(2):121-4. Review.
  • Todoric J, Loffler M, Huber J, Bilban M, Reimers M, Kadl A, Zeyda M, Waldhausl W, Stulnig TM. Adipose tissue inflammation induced by high-fat diet in obese diabetic mice is prevented by n-3 polyunsaturated fatty acids. Diabetologia. 2006 Sep;49(9):2109-19. Epub 2006 Jun 17.
  • Todoric J, Loffler M, Huber J, Bilban M, Reimers M, Kadl A, Zeyda M, Waldhausl W, Stulnig TM. Adipose tissue inflammation induced by high-fat diet in obese diabetic mice is prevented by n-3 polyunsaturated fatty acids. Diabetologia. 2006 Sep;49(9):2109-19. Epub 2006 Jun 17.

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