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Dean Pomerleau posted a topic in CR PracticeAll, One of the initial motivations for studying the possible benefits of the Omega-3s PUFAs DHA & EPA came from observations that the Inuits of Greenland, whose diet contains a very high proportion of polyunsaturated fat from cold-water fish and marine mammals, suffer from relatively low rates of cardiovascular disease. But randomized control trials of the benefits of DHA / EPA supplements for (primary or secondary) prevention of cardiovascular disease have generally been disappointing (e.g. ). This new study  in Science, might suggest at least part of the explanation for this apparent paradox. That paper used population-genetic analysis of Greenland Inuits to discover regions of two chromosomes that seem to have experienced strong selection in the recent past. Those regions also happen to contain genes involved in fatty acid metabolism; and the variants of the genes that have increased in frequency in Inuits are also associated with small stature and lower weight. From the abstract: By analyzing membrane lipids, we found that the selected alleles modulate fatty acid composition, which may affect the regulation of growth hormones. Thus, the Inuit have genetic and physiological adaptations to a diet rich in PUFAs. In an accompanying commentary, there is a fascinating map of relatively recent human genetic variations and where they occur around the world (click to enlarge): The one that isn't shown that I find very interesting is the salivary amylase gene (AMY1) for digesting starch. Several studies (e.g. ) have found that the number of duplicates of the AMY1 a person has can vary from 2 to about 15 from one individual to the next. The more AMY1 copies you have, the better you are at digesting starch / carbohydrates, and the less prone you are to obesity . Study  looked at how the number of AMY1 copies varied between people of different ethnic groups and found a striking correlation between the amount of starch in their ancestral diet and the number of AMY1 copies their genome contained. Here is that result illustrated on a map (click to enlarge): In short, it appears that in cultures whose ancestral diet contained a large fraction of carbohydrates, more copies of the AMY1 gene were selected for since it helped them better process carbs. The bottom line appears to be that there is no "one size fits all" diet that is right for everyone. To some extent at least, the best diet for an individual depends on his/her genes. --Dean --------------------------------  Arch Intern Med. 2012 May 14;172(9):686-94. doi: 10.1001/archinternmed.2012.262. Efficacy of omega-3 fatty acid supplements (eicosapentaenoic acid and docosahexaenoic acid) in the secondary prevention of cardiovascular disease: a meta-analysis of randomized, double-blind, placebo-controlled trials. Kwak SM(1), Myung SK, Lee YJ, Seo HG; Korean Meta-analysis Study Group. Collaborators: Myung SK, Ju W, Oh SW, Bae JH, Kim YK, Park CH, Jeon YJ, Lee EH, Chang YJ, Park SM, Eom CS, Lee YJ, Jung HS, Kwak SM. BACKGROUND: Although previous randomized, double-blind, placebo-controlled trials reported the efficacy of omega-3 fatty acid supplements in the secondary prevention of cardiovascular disease (CVD), the evidence remains inconclusive. Using a meta-analysis, we investigated the efficacy of eicosapentaenoic acid and docosahexaenoic acid in the secondary prevention of CVD. METHODS: We searched PubMed, EMBASE, and the Cochrane Library in April 2011. Two of us independently reviewed and selected eligible randomized controlled trials. RESULTS: Of 1007 articles retrieved, 14 randomized, double-blind, placebo-controlled trials (involving 20 485 patients with a history of CVD) were included in the final analyses. Supplementation with omega-3 fatty acids did not reduce the risk of overall cardiovascular events (relative risk, 0.99; 95% CI, 0.89-1.09), all-cause mortality, sudden cardiac death, myocardial infarction, congestive heart failure, or transient ischemic attack and stroke. There was a small reduction in cardiovascular death (relative risk, 0.91; 95% CI, 0.84-0.99), which disappeared when we excluded a study with major methodological problems. Furthermore, no significant preventive effect was observed in subgroup analyses by the following: country location, inland or coastal geographic area, history of CVD, concomitant medication use, type of placebo material in the trial, methodological quality of the trial, duration of treatment, dosage of eicosapentaenoic acid or docosahexaenoic acid, or use of fish oil supplementation only as treatment. CONCLUSION: Our meta-analysis showed insufficient evidence of a secondary preventive effect of omega-3 fatty acid supplements against overall cardiovascular events among patients with a history of cardiovascular disease. PMID: 22493407 -----------------  Science. 2015 Sep 18;349(6254):1343-1347. Greenlandic Inuit show genetic signatures of diet and climate adaptation. Fumagalli M(1), Moltke I(2), Grarup N(3), Racimo F(4), Bjerregaard P(5), Jørgensen ME(6), Korneliussen TS(7), Gerbault P(8), Skotte L(2), Linneberg A(9), Christensen C(10), Brandslund I(11), Jørgensen T(12), Huerta-Sánchez E(13), Schmidt EB(14), Pedersen O(3), Hansen T(15), Albrechtsen A(16), Nielsen R(17). The indigenous people of Greenland, the Inuit, have lived for a long time in the extreme conditions of the Arctic, including low annual temperatures, and with a specialized diet rich in protein and fatty acids, particularly omega-3 polyunsaturated fatty acids (PUFAs). A scan of Inuit genomes for signatures of adaptation revealed signals at several loci, with the strongest signal located in a cluster of fatty acid desaturases that determine PUFA levels. The selected alleles are associated with multiple metabolic and anthropometric phenotypes and have large effect sizes for weight and height, with the effect on height replicated in Europeans. By analyzing membrane lipids, we found that the selected alleles modulate fatty acid composition, which may affect the regulation of growth hormones. Thus, the Inuit have genetic and physiological adaptations to a diet rich in PUFAs. Copyright © 2015, American Association for the Advancement of Science. PMID: 26383953 -----------------  Nat Genet. 2014 May;46(5):492-7. doi: 10.1038/ng.2939. Epub 2014 Mar 30. Low copy number of the salivary amylase gene predisposes to obesity. Falchi M(1), El-Sayed Moustafa JS(2), Takousis P(3), Pesce F(4), Bonnefond A(5), Andersson-Assarsson JC(6), Sudmant PH(7), Dorajoo R(8), Al-Shafai MN(9), Bottolo L(10), Ozdemir E(3), So HC(11), Davies RW(12), Patrice A(13), Dent R(14), Mangino M(15), Hysi PG(15), Dechaume A(16), Huyvaert M(16), Skinner J(17), Pigeyre M(18), Caiazzo R(18), Raverdy V(13), Vaillant E(16), Field S(19), Balkau B(20), Marre M(21), Visvikis-Siest S(22), Weill J(23), Poulain-Godefroy O(16), Jacobson P(24), Sjostrom L(24), Hammond CJ(15), Deloukas P(25), Sham PC(11), McPherson R(26), Lee J(27), Tai ES(28), Sladek R(29), Carlsson LM(24), Walley A(30), Eichler EE(31), Pattou F(18), Spector TD(32), Froguel P(33). Comment in Nat Rev Endocrinol. 2014 Jun;10(6):312. Common multi-allelic copy number variants (CNVs) appear enriched for phenotypic associations compared to their biallelic counterparts. Here we investigated the influence of gene dosage effects on adiposity through a CNV association study of gene expression levels in adipose tissue. We identified significant association of a multi-allelic CNV encompassing the salivary amylase gene (AMY1) with body mass index (BMI) and obesity, and we replicated this finding in 6,200 subjects. Increased AMY1 copy number was positively associated with both amylase gene expression (P = 2.31 × 10(-14)) and serum enzyme levels (P < 2.20 × 10(-16)), whereas reduced AMY1 copy number was associated with increased BMI (change in BMI per estimated copy = -0.15 (0.02) kg/m(2); P = 6.93 × 10(-10)) and obesity risk (odds ratio (OR) per estimated copy = 1.19, 95% confidence interval (CI) = 1.13-1.26; P = 1.46 × 10(-10)). The OR value of 1.19 per copy of AMY1 translates into about an eightfold difference in risk of obesity between subjects in the top (copy number > 9) and bottom (copy number < 4) 10% of the copy number distribution. Our study provides a first genetic link between carbohydrate metabolism and BMI and demonstrates the power of integrated genomic approaches beyond genome-wide association studies. PMID: 24686848 -------------------------  Perry, G. H., Dominy, N. J., Claw, K. G., Lee, A. S., Fiegler, H., Redon, R., et al. (2007). Diet and the evolution of human amylase gene copy number variation. [10.1038/ng2123]. Nat Genet, 39(10), 1256-1260.
All, This new study  published today in JAMA (popular press account) seems to suggest Omega-6 PUFA is the type of fat associated with the lowest all-cause mortality. If followed the 80K women and 40K men in the Nurses/Health Professionals Studies checking their dietary intake of fats through food frequency questionnaires every couple years. During the followup period of 1980-2012, 33K of them died. Interestingly, being in the quintile that ate the most fat and the least carbs was associated with a 16% reduction in total mortality compared with the other extreme. Just goes to show how crappy the carbs are that the average American eats... Regarding the association of specific fats and mortality, here was the ordering of most-healthy to least-healthy: Omega-6 PUFA > MUFA > Omega-3 PUFA > Saturated Fat > Trans-fat. Here are the mortality hazard ratios (95% CI) associated with being in the top (vs. bottom) quintile for consumption of each fat type, after controlling for "known & suspected risk factors": ω-6 PUFA 0.81 (0.78-0.84) MUFA 0.89 (0.84-0.94) ω-3 PUFA 0.96 (0.93-1.00) Saturated 1.08 (1.03-1.14) Trans-fat 1.13 (1.07-1.18) I don't have the full text yet, so I haven't looked at the details, but it is interesting to see that omega-6 PUFA came out on top as the healthiest fat to consume. This seem to contradict the conventional (folk?) wisdom that Omega-6 PUFA is pro-inflammatory and so we shouldn't eat very much of it, at least without balancing it with sufficient Omega-3 fats (e.g. in a 3:1 ratio). Some interesting quotes from the popular press interview with one of the authors: f people replaced a mere 5% of their calorie intake from "bad" fats with polyunsaturated fats, they could reduce their risk of death by 27%. If those calories came from monounsaturated fats, the risk of mortality dropped by 13%. One reason MUFA may not have done better is the fact that a large fraction of the MUFA in the average American diet comes from animal products, which contain saturated fat along with other unhealthy components, which the researchers couldn't entirely control for: "A large proportion of food sources of monounsaturated fat in the typical American diet are animal-sourced, such as dairy and red meats," Hu said, pointing out that those are also major sources of saturated fats. "Therefore, current analysis may not be able to completely distinguish the benefits of monounsaturated fat from the effects of food source and saturated fats." The Omega-6 PUFA that was protective was, not surprisingly linoleic acid: One polyunsaturated fat, an omega-6 fatty acid called linoleic acid, was shown in the Harvard study to be especially protective against death by cancer and coronary artery disease, Hu said. Prior studies showed linoleic acid to reduce total and bad cholesterol, and to be associated with better blood pressure and insulin sensitivity. Though some studies have connected too much omega-6 with inflammation in the body, others find no such link. Linoleic acid is found in sunflower, soybean and safflower oils, as well as nuts and seeds. Walnuts, Brazil nuts and peanuts are excellent sources, as are safflower, pumpkin and squash seeds. Omega-3 Alpha-linolenic acid (e.g. from flax seeds and walnuts) wasn't protective against all-cause mortality, but does appear to be healthy for the brain, as other studies have found: Another key polyunsaturated fat, the omega-3 fatty acid called alpha-linolenic, was not associated with "all-cause mortality," Hu said, but "interestingly, we found that alpha-linolenic acid was protective against death due to neurodegenerative disease." I'd be really interested to hear Michael's take on this one, particularly the Omega-6 vs. Omega-3 finding - even if it's just an off-the-cuff remark. As Sthira mentioned yesterday in the olive oil thread, a little of Michael's insight is better than an in-depth report from him that he never has time to finish to his own satisfaction... --Dean -----------  JAMA Intern Med. Published online July 05, 2016. doi:10.1001/jamainternmed.2016.2417 Association of Specific Dietary Fats With Total and Cause-Specific Mortality Dong D. Wang, MD, MSc1,3; Yanping Li, PhD1; Stephanie E. Chiuve, ScD1,2; Meir J. Stampfer, MD, DrPH1,2,3,4; JoAnn E. Manson, MD, DrPH2,3,4; Eric B. Rimm, ScD1,3,4; Walter C. Willett, MD, DrPH1,3,4; Frank B. Hu, MD, PhD1,3,4 ABSTRACT Importance Previous studies have shown distinct associations between specific dietary fat and cardiovascular disease. However, evidence on specific dietary fat and mortality remains limited and inconsistent. Objective To examine the associations of specific dietary fats with total and cause-specific mortality in 2 large ongoing cohort studies. Design, Setting, and Participants This cohort study investigated 83 349 women from the Nurses’ Health Study (July 1, 1980, to June 30, 2012) and 42 884 men from the Health Professionals Follow-up Study (February 1, 1986, to January 31, 2012) who were free of cardiovascular disease, cancer, and types 1 and 2 diabetes at baseline. Dietary fat intake was assessed at baseline and updated every 2 to 4 years. Information on mortality was obtained from systematic searches of the vital records of states and the National Death Index, supplemented by reports from family members or postal authorities. Data were analyzed from September 18, 2014, to March 27, 2016. Main Outcomes and Measures Total and cause-specific mortality. Results During 3 439 954 person-years of follow-up, 33 304 deaths were documented. After adjustment for known and suspected risk factors, dietary total fat compared with total carbohydrates was inversely associated with total mortality (hazard ratio (HR) comparing extreme quintiles, 0.84; 95% CI, 0.81-0.88; P < .001 for trend). The HRs of total mortality comparing extreme quintiles of specific dietary fats were 1.08 (95% CI, 1.03-1.14) for saturated fat, 0.81 (95% CI, 0.78-0.84) for polyunsaturated fatty acid (PUFA), 0.89 (95% CI, 0.84-0.94) for monounsaturated fatty acid (MUFA), and 1.13 (95% CI, 1.07-1.18) for trans-fat (P < .001 for trend for all). Replacing 5% of energy from saturated fats with equivalent energy from PUFA and MUFA was associated with estimated reductions in total mortality of 27% (HR, 0.73; 95% CI, 0.70-0.77) and 13% (HR, 0.87; 95% CI, 0.82-0.93), respectively. The HR for total mortality comparing extreme quintiles of ω-6 PUFA intake was 0.85 (95% CI, 0.81-0.89; P < .001 for trend). Intake of ω-6 PUFA, especially linoleic acid, was inversely associated with mortality owing to most major causes, whereas marine ω-3 PUFA intake was associated with a modestly lower total mortality (HR comparing extreme quintiles, 0.96; 95% CI, 0.93-1.00; P = .002 for trend). Conclusions and Relevance Different types of dietary fats have divergent associations with total and cause-specific mortality. These findings support current dietary recommendations to replace saturated fat and trans-fat with unsaturated fats. PMID: 27379574
biohacked posted a topic in General Health and LongevityFor anyone who’s looked into and reasearched the health effects of different omega-6 containing vegetable oils, you’ll quickly find that there’s a strong connection between all of them and the major degenerative diseases such as diabetes, cancer, heart disease, alzheimer’s and even obesity. Here are a couple of excerpts from the full text studies that I found particularily interesting: On obesity from https://www.ncbi.nlm.nih.gov/pubmed/23249760: ‘Recent studies have emphasized the proadipogenic properties of the omega-6 PUFA, and provided evidence that rodents fed on diets with omega-6 PUFA contents similar to the typical US diet (6–8% energy) have an increased fat mass. Importantly, recent studies have shown that perinatal exposure to a high omega-6 PUFA diet results in a progressive accumulation of body fat across generations.’ On chronic disease from https://www.ncbi.nlm.nih.gov/pubmed/18408140: ‘Excessive amounts of omega-6 polyunsaturated fatty acids (PUFA) and a very high omega-6/omega-3 ratio, as is found in today’s Western diets, promote the pathogenesis of many diseases, including cardiovascular disease, cancer, and inflammatory and autoimmune diseases...’ On chronic disease from https://www.ncbi.nlm.nih.gov/pubmed/22570770: ‘...high intake of n-6 PUFA, along with low intakes of n-3 PUFA, shifts the physiological state to one that is proinflammatory and prothrombotic with increases in vasospasm, vasoconstriction, and blood viscosity and the development of diseases associated with these conditions.’ So if you HAVE to cook with oil (which I don’ t recommend) using something like MCT oil or adding olive oil to salad might be less harmful compared to n-6 oils. Even then, fats in general, also those in olive oil have been connected to diabetes and MCT oil/coconut oil has some pretty potent cholesterol raising effects. This is certainly common knowledge around here but I find that researching these connections on my own gives me a more complete understanding rather than just taking somebody’s word for it. I find it’s also easier to stay on a diet and avoid the harmful foods if you are constantly reading studies and seeing evidence everywhere on their negative effects yourself. If you have more reaserch to add, I’d appreciate it.
All, I'm not sure if many people around here still do dairy, especially high fat dairy. But if you do, you might want to think again, and not just for the sake of the animals, but for the sake of your heart. This new study  analyzed the data from over 200K people in the Health Care Professionals and Nurses Health Studies followed for 20-30 years. The good news? Dairy fat intake was associated with a slightly lower cardiovascular disease risk than other forms of animal fat. The bad news? Replacing 5% of energy from PUFA for 5% more dairy fat resulted in a 24% increase in your risk of cardiovascular disease. Replacing dairy with whole grains was even better (28% lower risk of CVD). Here is a graph showing the estimated impact of substituting various other foods in place of dairy fat on risk of cardiovascular disease overall (A), as well as broken down by coronary heart disease (B) vs. stroke (C ): The authors summarize as follows: To our knowledge, this is the first large-scale prospective study to examine dairy fat intake and its replacement with other types of fat in relation to CVD risk... These results support current recommendations to replace animal fats, including dairy fat, with vegetable sources of fats and polyunsaturated fat (both n–6 and n–3) in the prevention of CVD. Sorry to be the bearer of bad news, cheese lovers. Whom I kidding, no I'm not... --Dean ------------  Am J Clin Nutr. 2016 Aug 24. pii: ajcn134460. [Epub ahead of print] Dairy fat and risk of cardiovascular disease in 3 cohorts of US adults. Chen M(1), Li Y(2), Sun Q(3), Pan A(4), Manson JE(5), Rexrode KM(5), Willett WC(6), Rimm EB(6), Hu FB(7). Full text: http://sci-hub.cc/10.3945/ajcn.116.134460 BACKGROUND: Few prospective studies have examined dairy fat in relation to cardiovascular disease (CVD). OBJECTIVE: We aimed to evaluate the association between dairy fat and incident CVD in US adults. DESIGN: We followed 43,652 men in the Health Professionals Follow-Up Study (1986-2010), 87,907 women in the Nurses' Health Study (1980-2012), and 90,675 women in the Nurses' Health Study II (1991-2011). Dairy fat and other fat intakes were assessed every 4 y with the use of validated food-frequency questionnaires. RESULTS: During 5,158,337 person-years of follow-up, we documented 14,815 incident CVD cases including 8974 coronary heart disease cases (nonfatal myocardial infarction or fatal coronary disease) and 5841 stroke cases. In multivariate analyses, compared with an equivalent amount of energy from carbohydrates (excluding fruit and vegetables), dairy fat intake was not significantly related to risk of total CVD (for a 5% increase in energy from dairy fat, the RR was 1.02; 95% CI: 0.98, 1.05), coronary heart disease (RR: 1.03; 95% CI: 0.98, 1.09), or stroke (RR: 0.99; 95% CI: 0.93, 1.05) (P > 0.05 for all). In models in which we estimated the effects of exchanging different fat sources, the replacement of 5% of energy intake from dairy fat with equivalent energy intake from polyunsaturated fatty acid (PUFA) or vegetable fat was associated with 24% (RR: 0.76; 95% CI: 0.71, 0.81) and 10% (RR: 0.90; 95% CI: 0.87, 0.93) lower risk of CVD, respectively, whereas the 5% energy intake substitution of other animal fat with dairy fat was associated with 6% increased CVD risk (RR: 1.06; 95% CI: 1.02, 1.09). CONCLUSIONS: The replacement of animal fats, including dairy fat, with vegetable sources of fats and PUFAs may reduce risk of CVD. Whether the food matrix may modify the effect of dairy fat on health outcomes warrants further investigation. © 2016 American Society for Nutrition. DOI: 10.3945/ajcn.116.134460 PMID: 27557656