Nutrition

"I like palmitic acid. It causes insulin resistance. Thank goodness. Ted sent me this link. It's depressing. I'm going to discuss a thought drug. I'm going to call it Palmitofake, and it can be developed by Pfizer, no, Fort Dodge. I particularly dislike FD for anaesthesia related reasons. So what does Palmitofake do? BTW, if you didn't need any other hint you can tell this drug is going to bomb as there is neither an x, y or z in its name. Trust FD to screw up (in my mind). Palmitofake is a fluoride substituted analogue of palmitic acid which irreversibly binds to the acyl-CoA interaction site of JNK1 and so inhibits the pathway by which palmitic acid keeps GLUT4 transporters off of the cell surface membrane, whole body-wide. The logic to this is that the lipotoxin, palmitic acid (nature's second biggest mistake, the biggest was obviously cholesterol) can no longer keep glucose out of cells and metabolism can run, unimpaired by fat, for ever on glucose. Woo hoo bring on the glucose."

"We've been having an interesting discussion in the comments about a recently published paper by Dr. Stephen C. Benoit and colleagues (free full text). They showed that a butter-rich diet causes weight gain and insulin resistance in rats, compared to a low-fat diet or a diet based on olive oil. They published a thorough description of the diets' compositions, which is very much appreciated! They went on to show that infusing palmitic acid (a 16-carbon saturated fat) directly into the brain of rats also caused insulin resistance relative to oleic acid (an 18-carbon monounsaturated fat, like in olive oil). Here's a representation of palmitic acid. The COOH end is the acid end, and the squiggly line is the fatty end. Thus it's called a "fatty acid", various forms of which are the fat currency of the body."

"Peter at Hyperlipid and Stephan at Whole Health have dispelled yet again myths regarding the indictment of the 16:0 long-chained saturated fatty acid Palmitic Acid as the prime instigator of insulin resistance (IR). Researchers are always wrong -- it's... HIGH CARBS PLUS Palmitic acid. Their brilliant posts discuss below: --Sportzaid (FRUCTOSE) + Palmitate = IR RETARDNESS --High Carb Lab Chow + Palmitate = IR in the brain Yes. Such inferences applied to low carbers (LCers) is pure ridiculousness. Non-applicable. Low/no carb + Palmitic Acid = GOOD THING. All the low-carb/high saturated fat (palmitic acid) and ketosis trials by Hays JH, Volek JS, and Krauss RM have shown reductions in blood insulin, blood glucoses (BG) and peripheral tissue insulin resistance (IR). Directly contrary to the high carb animal or human studies. Palmitic acid has a special evolutionary, adaptive role in mammalian metabolism. Stephan showed that it likely 'fills in' when blood glucose starts to decline. "

Animal Pharm (drbganimalpharm) -a nutrtion blog

Hyperlipid: a nutrition blog

A nutrition blog by Dr. Ayers Inflammation is the foundation for cancer and degenerative/autoimmune diseases. Small changes in diet and exercise, e.g. omega-3 oils, vitamin D, low starch, plant antioxidants, and maintaining muscle mass, can dramatically alter predisposition to disease and aging, and minimize the negative impact of genetic risks. Based on my experience in biological research, I am trying to explain how the anti-inflammatory diet and lifestyle combat disease. Anti-Inflammatory Diet All health care starts with diet. Here are my recommendations for a basic Anti-Inflammatory Diet and Lifestyle. There are over 140 articles on diet, inflammation and disease here, and more articles by Dr. Ayers on Suite101 .

"Anti-inflammatory Diet Components of an Anti-inflammatory Diet (focus on meats, fish, eggs and leafy vegetables)"

"July 9, 2008 | Michael O'Riordan Boston, MA - The consumption of a diet containing vegetable oils rich in alpha-linolenic acid (ALA) is associated with significant reductions in the risk of nonfatal MI, a new study has shown [1]. Investigators say the protective effect of ALA is evident among individuals with low intakes, suggesting the greatest benefit might be in developing countries, where fatty-acid consumption is limited. "The potential for benefit is great when the baseline intake is low," said lead investigator Dr Hannia Campos (Harvard Medical School, Boston, MA). "In countries where people eat very little fish-and some of these countries have almost no sources of omega-3 fatty acids because they cook with corn or sunflower oils-the consumption of vegetable oils with ALA could have a major impact on heart disease." In an editorial accompanying the published study [2], Dr William Harris (University of South Dakota, Sioux Falls) said that the data are suggestive and would be good news for individuals who will not or cannot eat fish, but more studies are still needed. "If ALA were able to do the same 'heavy lifting' that [eicosapentaenoic acid] EPA and [docosahexaenoic acid] DHA do, this would be welcomed news, because the capacity to produce ALA is essentially limitless, whereas there are only so many fish in the sea," he writes. "

Alpha-linolenic acid and risk of nonfatal acute myocardial infarction. Campos H, Baylin A, Willett WC. Circulation. 2008 Jul 22;118(4):339-45. Epub 2008 Jul 7. Erratum in: Circulation. 2008 Sep 16;118(12):e492. PMID: 18606916 doi: 10.1161/CIRCULATIONAHA.107.762419 Conclusions - Consumption of vegetable oils rich in {alpha}-linolenic acid could confer important cardiovascular protection. The apparent protective effect of {alpha}-linolenic acid is most evident among subjects with low intakes.

Cardiovascular risk and alpha-linolenic acid: can Costa Rica clarify? Harris WS. Circulation. 2008 Jul 22;118(4):323-4. Epub 2008 Jul 7. Review. PMID: 18606912 doi: 10.1161/CIRCULATIONAHA.108.791467

Relationship of dietary linoleic acid to blood pressure. The International Study of Macro-Micronutrients and Blood Pressure Study [corrected] Miura K, Stamler J, Nakagawa H, Elliott P, Ueshima H, Chan Q, Brown IJ, Tzoulaki I, Saitoh S, Dyer AR, Daviglus ML, Kesteloot H, Okayama A, Curb JD, Rodriguez BL, Elmer PJ, Steffen LM, Robertson C, Zhao L; International Study of Macro-Micronutrients and Blood Pressure Research Group. Hypertension. 2008 Aug;52(2):408-14. Epub 2008 Jul 7. Erratum in: Hypertension. 2008 Sep;52(3):e29. PMID: 18606902 doi: 10.1161/HYPERTENSIONAHA.108.112383 Dietary linoleic acid intake may contribute to prevention and control of adverse blood pressure levels in general populations

"June 21, 2006 | Michael O'Riordan Rome, Italy - One of the possible ways in which long-chain omega-3 fatty acids play a role in decreasing cardiovascular events is by entering advanced atherosclerotic plaques. According to the results of a new study, investigators were able to show that the incorporation of eicosapentaenoic acid (EPA) into advanced plaque was associated with a decreased expression of various matrix metalloproteinases (MMPs) involved in causing plaque instability, as well as with decreased plaque inflammation. These are results of the Omacor Carotid Endarterectomy Intervention (OCEAN) study, presented here this week at the International Symposium on Atherosclerosis by Dr Philip Calder (University of Southampton, UK). "By increasing the availability of omega-3 fatty acids, they appear in advanced atherosclerotic plaques, indicated in this study by the carotid artery, and this results in lower numbers of macrophages, foam cells, and T cells, as well as the lower expression of inflammatory markers," said Calder. "Histologically, this results in a plaque that appears to be less inflamed and more stable. This may contribute to reduced mortality in patients consuming omega-3 fatty acids, for example, in the GISSI Prevenzione trial.""

Association of n-3 polyunsaturated fatty acids with stability of atherosclerotic plaques: a randomised controlled trial. Thies F, Garry JM, Yaqoob P, Rerkasem K, Williams J, Shearman CP, Gallagher PJ, Calder PC, Grimble RF. Lancet. 2003 Feb 8;361(9356):477-85. PMID: 12583947 doi:10.1016/S0140-6736(03)12468-3 Interpretation Atherosclerotic plaques readily incorporate n-3 PUFAs from fish-oil supplementation, inducing changes that can enhance stability of atherosclerotic plaques. By contrast, increased consumption of n-6 PUFAs does not affect carotid plaque fatty-acid composition or stability over the time course studied here. Stability of plaques could explain reductions in non-fatal and fatal cardiovascular events associated with increased n-3 PUFA intake

n-3 Fatty acids and cardiovascular disease: actions and molecular mechanisms. Torrejon C, Jung UJ, Deckelbaum RJ. Prostaglandins Leukot Essent Fatty Acids. 2007 Nov-Dec;77(5-6):319-26. Epub 2007 Dec 3. Review. Erratum in: Prostaglandins Leukot Essent Fatty Acids. 2008 Feb;78(2):157. PMID: 18060753 In conclusion, a growing body of evidence, encompassing human to cellular and molecular studies are defining the roles for n-3 FA as bioactive agents for reducing the risks of and treating CVD.

n-3 Fatty acids and cardiovascular disease: evidence explained and mechanisms explored. Calder PC. Clin Sci (Lond). 2004 Jul;107(1):1-11. Review. PMID: 15132735 DIETARY RECOMMENDATIONS FOR INTAKE OF LONG-CHAIN n-3 PUFAS It is clear from the forgoing discussion that long-chain n-3 fatty acids have been proven to be effective in secondary prevention of MI, with a particularly marked effect on sudden death. Thus it would be prudent to advise post-MI patients to increase long-chain n-3 PUFA consumption. Epidemiological studies, studies investigating effects on classic and emerging risk factors and mechanistic studies indicate that long-chain n-3 fatty acids also play a key role in primary prevention. This is supported by studies in animal models, including monkeys. Thus long-chain n-3 fatty acid consumption should be promoted for all individuals especially those at risk of developing cardiovascular disease. This is the reason why a number of organizations have now made recommendations relating to the intake of fatty fish (for example [3]) and of long-chain n-3 PUFAs (Table 6). It is clear that there is a wide gap between current intakes of long-chain n-3 PUFAs and many of these recommendations (Table 6). To meet these recommendations strategies other than increased consumption of fatty fish may be required.

October 17, 2006 | Steve Stiles Boston, MA - A review of the literature on the health effects of dietary fish or fish-oil intake has a reassuring message for seafood lovers, anyone eating fish for health reasons, and perhaps most everyone else [1]. Levels of mercury and other contaminants in commercially bought fish are low, and their potential risks are overwhelmed by likely reductions in cardiovascular mortality, according to a report in the October 18, 2006 issue of the Journal of the American Medical Association. "The main message is really that everybody should be eating one or two servings of fish or seafood per week for their health," Dr Dariush Mozaffarian (Harvard School of Public Health, Boston, MA) told heartwire. In his analysis, coauthored with Dr Eric B Rimm (Brigham and Women's Hospital, Boston, MA), regular "modest" intake of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), the two long-chain n-3 polyunsaturated fatty acids (PUFAs) abundant in finfish and shellfish (collectively referred to as "fish" in the article), is associated with a 36% drop in coronary disease mortality (p Those potential benefits are immense compared with the highly publicized but apparently low health risks associated with methylmercury, dioxins, and polychlorinated biphenyls (PCBs) that have been found in some fish species, they write. The evidence suggests a potential for neurodevelopmental deficits from early exposure to methylmercury, but the risk is likely diminished by limiting intake of fish with high methylmercur

"Researchers at Johns Hopkins are reporting what is believed to be the first conclusive evidence in men that the long-term ill effects of vitamin D deficiency are amplified by lower levels of the key sex hormone estrogen, but not testosterone. In a national study in 1010 men, to be presented Nov. 15 at the American Heart Association's (AHA) annual Scientific Sessions in Orlando, researchers say the new findings build on previous studies showing that deficiencies in vitamin D and low levels of estrogen, found naturally in differing amounts in men and women, were independent risk factors for hardened and narrowed arteries and weakened bones. Vitamin D is an essential part to keeping the body healthy, and can be obtained from fortified foods, such as milk and cereals, and by exposure to sunlight.

Long-term vitamin D3 supplementation may have adverse effects on serum lipids during postmenopausal hormone replacement therapy. Heikkinen AM, Tuppurainen MT, Niskanen L, Komulainen M, Penttilä I, Saarikoski S. Eur J Endocrinol. 1997 Nov;137(5):495-502. PMID: 9405029 CONCLUSIONS: Our results confirm the positive long-term effect of HRT with sequential estradiol valerate and cyproterone acetate on serum lipid concentrations. In addition, the results suggest that vitamin D3 supplementation may have unfavorable effects on lipids in postmenopausal women. Pure vitamin D3 treatment was associated with increased serum LDL cholesterol. Furthermore, the beneficial effects of HRT on serum LDL cholesterol content were reduced when estradiol valerate was combined with vitamin D3. However, the relevance of these associations to cardiovascular morbidity remains to be established.

Vitamin D association with estradiol and progesterone in young women. Knight JA, Wong J, Blackmore KM, Raboud JM, Vieth R. Cancer Causes Control. 2009 Nov 15. [Epub ahead of print] PMID: 19916051 Conclusions Higher levels of vitamin D may reduce progesterone and estradiol, providing a potential mechanism for reduction in breast cancer risk from increased vitamin D exposure in young women

Coenzyme Q10 in the treatment of hypertension: a meta-analysis of the clinical trials. Rosenfeldt FL, Haas SJ, Krum H, Hadj A, Ng K, Leong JY, Watts GF. J Hum Hypertens. 2007 Apr;21(4):297-306. Epub 2007 Feb 8. PMID: 17287847 We conclude that coenzyme Q10 has the potential in hypertensive patients to lower systolic blood pressure by up to 17 mm Hg and diastolic blood pressure by up to 10 mm Hg without significant side effects.