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  1. There’s little question that fish contain environmental pollutants such as mercury and PCBs with, generally, bigger fish such as shark and tuna containing more and smaller fish like sardines containing less. That’s been common knowledge between health researchers for a while now. The real question is whether that translates into any of the major degenerative diseases in people (such as cancer or diabetes). Well, sadly, in the case of diabetes it does appear to be the case. Here’s a great video by Dr. Michael Greger summarizing the science between diabetes risk and fish consumption: https://www.youtube.com/watch?v=I60O474F_GI As he mentioned in the video, besides the pollutants, the causal link could also very well be the oxidative stress causing n-3 fatty acid content of the fish. That obviously goes against the mainstream opinion on diet but one can certainly find smart people that would support that notion and as far as I’ve seen the research on fish oil seems to be quite mixed. P.S. Is there actually a way to embed a video on this site instead of just posting a link? Thanks.
  2. I did not know that about canned tuna. http://whfoods.org/genpage.php?tname=george&dbid=97 Examples of Tuna Fish and Their Omega 3 Fat Content Type of Fish Total Omega 3 Fat EPA (unique type of Omega 3 Fat) DHA (Unique type of Omega 3 Fat) fresh bluefin tuna, baked, 6 ounces 2.5 grams 0.6 grams 1.9 grams fresh albacore tuna, baked, 6 ounces 2.6 grams 0.5 grams 1.7 grams fresh skipjack, baked, 6 ounces 2.7 grams 0.7 grams 2.0 grams Light tuna, canned in water, 6 ounces 0.46 grams 0.08 grams 0.38 grams Light tuna, canned in oil, 6 ounces 0.34 grams 0.05 grams 0.38 grams Starkist TM Albacore tuna, canned in water, 6 ounces* 1.35 grams data not available data not available Papa George Gourmet Albacore tuna, canned in olive oil, not drained, 6 ounces 8.1 grams 2.6 grams 5.5 grams *The brand name data is derived from Starkist's website and lab reports supplied by these two specialty tuna companies, see Sources below. Sources: Am J Clin Nutr, January 2000 Supplement; 71:179S-188S. USDA Nutrient Composition Database: http://www.nal.usda.gov/fnic/foodcomp/Data/index.html Food Processor for Windows, Version 7.60, Database Version December 2000, ESHA Research, Salem, OR. Simopoulos A, Kifer RR, and Martin RE (Eds). (1986). The Health Effects of Polyunsaturated Fatty Acids in Seafoods. Academic Press, New York. Starkist Tuna: www.Starkist.com Papa George Gourmet Albacore, Seattle, WA. www.PapaGeorgeTuna.com Phone: 206-255-4203. Product lab analysis provided by Food Products Laboratory, Portland, OR.
  3. All, Like we've seen for cardiovascular disease, eating fish can be a mixed blessing. The omega-3 fatty acids (DHA/EPA) are thought to be beneficial, particularly for brain function. But the mercury, PCBs and other contaminants that bioaccumulate in the fat of fish may also have harmful effects. This new study[1] (thanks to Al Pater!) looks at the association between consumption of fish, plant omega-3s, brain mercury levels and Alzheimer's disease and brain mini-strokes. What they found is a bit nuanced, but worth thinking about. They gave 550 quite elderly but initially dementia-free people in several US nursing homes a yearly dietary questionnaire to measure their weekly intake of fish, DHA/EPA and the plant-derived omega-3 Alpha Linolenic Acid (ALA) until they died. Over an average follow-up of 4.5 years, 286 of the participates died (average age 89!). These folks' brains were autopsied to measure mercury levels and to look for physical signs of Alzheimer's disease (plaques and tangles) as well as brain injuries associated with other forms of dementia, in particular macroinfarctions and microinfarctions (i.e. strokes of various sizes). Here are the highlights of what they found: The more fish meals per week a subject consumed, the higher their brain mercury level (P < 0.02). There was no correlation between intake of ALA or DHA/EPA supplements and brain mercury level. For the majority of people (77%) who weren't carriers of the APOE4 allele that increases one's susceptibility to Alzheimer's disease, neither eating fish, dietary DHA/EPA nor consuming ALA had a significant effect (one way or the other) on the risk of Alzheimer's disease. For the minority (23%) of subjects who were APOE4 carriers, eating more fish and more dietary DHA/EPA was associated with a decreased risk of Alzheimer's disease markers (P < 0.04). Neither DHA/EPA supplements nor dietary ALA impacted Alzheimer's risk in these folks. Dietary ALA, but not fish or DHA/EPA, was associated with reduced prevalence of macroinfarctions (P < 0.03) and microinfarctions (P < 0.04) associated with non-Alzheimer's cognitive impairment, independent of APOE4 status. Those were the major, statistically significant findings. There is one more thing I noticed looking at the table below that appears interesting/suggestive for the majority of us who are lucky enough not have the APOE4 gene. The cells I've highlighted below represent the level of various markers of Alzheimer's disease for APOE4-negative folks. The red cells represent the level of Alzheimer's markers for people who ate the most fish (top red row), or the most dietary DHA/EPA (bottom red row). From the confidence intervals, you can see that none of them are individually significant. But also notice that all of them are positive, meaning there was a trend towards increased markers of Alzheimer's disease in APOE4-negative people who ate the most fish, especially fatty fish. In contrast, now look at the green cells, representing markers for Alzheimer's disease in APOE4-negative people who consumed the most plant-derived ALA. Notice these too are not individually significant, but all of them are negative, pointing towards a reduced risk of Alzheimer's disease with increasing ALA intake. From all this, my summary takeaway message from this study would be the following: For people with the APOE4 gene and therefore increased risk of Alzheimer's disease, eating fish is likely to reduce one's risk of Alzheimer's disease, despite increasing brain mercury levels For people without the APOE4 gene, fish consumption doesn't seem to reduce, and may even increase, one's risk of Alzheimer's disease For people without the APOE4 gene, plant-derived omega-3 ALA (e.g. from walnuts, olive oil, flax, chia) consumption may reduce one's risk of Alzheimer's disease For everyone, dietary ALA appears to reduce one's risk of brain markers for non-Alzheimer's cognitive impairment. Or more succinctly, ALA is likely to be good for everyone's brain health, and fish is likely to be good for the brain health of only the minority of people who carry the APOE4 allele. This seems like an illustration of a benefit of getting one's DNA sequenced with a company like 23andMe to determine whether one is a carrier of the APOE4 allele. --Dean ------------ [1] JAMA. 2016 Feb 2;315(5):489-97. doi: 10.1001/jama.2015.19451. Association of Seafood Consumption, Brain Mercury Level, and APOE e4 Status With Brain Neuropathology in Older Adults. Morris MC, Brockman J, Schneider JA, Wang Y, Bennett DA, Tangney CC, van de Rest O. Full text: http://jama.jamanetwork.com.sci-hub.io/article.aspx?articleID=2484683 Abstract IMPORTANCE: Seafood consumption is promoted for its many health benefits even though its contamination by mercury, a known neurotoxin, is a growing concern. OBJECTIVE: To determine whether seafood consumption is correlated with increased brain mercury levels and also whether seafood consumption or brain mercury levels are correlated with brain neuropathologies. DESIGN, SETTING, AND PARTICIPANTS: Cross-sectional analyses of deceased participants in the Memory and Aging Project clinical neuropathological cohort study, 2004-2013. Participants resided in Chicago retirement communities and subsidized housing. The study included 286 autopsied brains of 554 deceased participants (51.6%). The mean (SD) age at death was 89.9 (6.1) years, 67% (193) were women, and the mean (SD) educational attainment was 14.6 (2.7) years. EXPOSURES: Seafood intake was first measured by a food frequency questionnaire at a mean of 4.5 years before death. MAIN OUTCOMES AND MEASURES: Dementia-related pathologies assessed were Alzheimer disease, Lewy bodies, and the number of macroinfarcts and microinfarcts. Dietary consumption of seafood and n-3 fatty acids was annually assessed by a food frequency questionnaire in the years before death. Tissue concentrations of mercury and selenium were measured using instrumental neutron activation analyses. RESULTS: Among the 286 autopsied brains of 544 participants, brain mercury levels were positively correlated with the number of seafood meals consumed per week (??=?0.16; P?=?.02). In models adjusted for age, sex, education, and total energy intake, seafood consumption (=?1 meal/week) was significantly correlated with less Alzheimer disease pathology including lower density of neuritic plaques (ß?=?-0.69 score units [95% CI, -1.34 to -0.04]), less severe and widespread neurofibrillary tangles (ß?=?-0.77 score units [95% CI, -1.52 to -0.02]), and lower neuropathologically defined Alzheimer disease (ß?=?-0.53 score units [95% CI, -0.96 to -0.10]) but only among apolipoprotein E (APOE e4) carriers. Higher intake levels of a-linolenic acid (18:3 n-3) were correlated with lower odds of cerebral macroinfarctions (odds ratio for tertiles 3 vs 1, 0.51 [95% CI, 0.27 to 0.94]). Fish oil supplementation had no statistically significant correlation with any neuropathologic marker. Higher brain concentrations of mercury were not significantly correlated with increased levels of brain neuropathology. CONCLUSIONS AND RELEVANCE: In cross-sectional analyses, moderate seafood consumption was correlated with lesser Alzheimer disease neuropathology. Although seafood consumption was also correlated with higher brain levels of mercury, these levels were not correlated with brain neuropathology. PMID: 26836731
  4. All, I'm not a big proponent of eating fish, being a vegan myself. But in the interest of presenting the fact, here is a new meta-analysis [1] from Al (thanks Al!) that seems to show eating more fish is associated with reduced all-cause mortality. Specifically, among the almost 700,000 subjects across 12 prospective cohort studies, those who ate the most fish were 6% less likely to die during the follow-up period than those who ate the least fish (RR=0.94, 95% confidence interval (CI): 0.90, 0.98; I(2)=39.1%, P=0.06). Here from the full text is the forest plot of mortality risk across the 12 studies: As you can see, for most of the studies the confidence interval spans the centerline, and several are actually right of center (higher death risk for fish eating). Nevertheless, the center of mass is left of center - meaning reduced mortality risk when the studies are all combined together. Before you get too excited Saul and other fish-eating enthusiasts, consider the following.The authors did several additional sensitivity analyses to see how much the apparent benefits of eating fish depended on various factors. I think what they found was telling. Here is the table with the results, with a few items highlighted: What these sensitivity analyses show is that the mortality benefit of eating fish was attenuated to the point of being non-significant in: The six studies that were large (40,000+ subjects) The six studies that had long follow-up periods (12+ years) The four studies that compensated for differences in red meat intake between fish eaters and fish abstainers The eight studies that compensated for differences in fruit and veggie intake between fish eaters and fish abstainers Given the small (6%) benefit to start with, coupled with all these attenuating factors, it appears to me that the purported benefits of eating fish for all-cause mortality are probably marginal at best. --Dean ----------- [1] Eur J Clin Nutr. 2016 Feb;70(2):155-61. doi: 10.1038/ejcn.2015.72. Epub 2015 May 13. Fish consumption and all-cause mortality: a meta-analysis of cohort studies. Zhao LG, Sun JW, Yang Y, Ma X, Wang YY, Xiang YB. full text: http://www.nature.com.sci-hub.io/ejcn/journal/v70/n2/full/ejcn201572a.html Abstract12 BACKGROUND/OBJECTIVES: Although fish consumption may have an influence on specific mortality of major chronic diseases, the relationship between fish consumption and all-cause mortality remains inconsistent. SUBJECTS/METHODS: We performed a systematic search of publications using PubMed and Web of science up to 31 December 2014. Summary relative risk (RR) for the highest versus lowest category of fish consumption on risk of all-cause mortality was calculated by using a random effects model. Potential nonlinear relation was tested by modeling fish intake using restricted cubic splines with three knots at fixed percentiles of the distribution. RESULTS: Twelve prospective cohort studies with 672 389 participants and 57 641 deaths were included in this meta-analysis. Compared with the lowest category, the highest category of fish intake was associated with about a 6% significantly lower risk of all-cause mortality (RR=0.94, 95% confidence interval (CI): 0.90, 0.98; I(2)=39.1%, P=0.06). The dose-response analysis indicated a nonlinear relationship between fish consumption and all-cause mortality. Compared with never consumers, consumption of 60 g of fish per day was associated with a 12% reduction (RR=0.88, 95% CI: 0.83, 0.93) in risk of total death. CONCLUSIONS: These results imply that fish consumption was associated with a reduced risk of all-cause mortality. PMID: 25969396
  5. All, Anyone who has been following discussions around here will realize that I've been criticizing salmon as a healthy food, and Saul has been vehemently defending it, which has lead to some amusing exchanges, e.g. here, here and especially here, where Saul wrote: Well, the evidence just keeps piling up against Saul's sacred cow, er, fish. Background Summary: PCBs are bad sh*t. PCBs (or polychlorinated biphenyls) are man-made organic chemicals widely manufactured and used in a variety of industries, but mostly for cooling and insulating fluid for electrical devices, all over the world up until 1979 when they were banned. Unfortunately, PCBs are very persistent, remaining in the water and soil for many years, and bioaccumulating the in flesh (mostly fat) of animals. Fish, especially fatty fish, seems to be the food in the human diet where the most PCBs bioaccumulate, as illustrated by this graph (data from [2]) of PCB content in 12,000+ food samples from around Europe: Notice that fish oil is off the chart, but people typically only consume a gram or two of FO per day, and this graph represents micrograms per kilograms. Fish itself (all types) was about 5x higher than any other animal products. Fruit, vegetables and cereals had close to zero PCBs. Interestingly though, most exposure in North America comes from beef, dairy and other animal flesh rather than fish, since we eat so much more of them than fish: So how bad are PCBs? Pretty bad across the board, including causing cancer, endocrine disruption, reproductive and neurological effects. See here for more details about all the bad effects PCBs have on human health. With that background, this new study [1] posted by Al (thanks Al!) looked at dietary PCBs levels based on self-reported food-frequency questionnaires from ~36,000 elderly Swedish women, and then followed them for an average of 12 years to see how heart attack risk related to dietary PCB exposure. First, off a helpful chart of demographics of study participants by quartile of dietary PCB intake: As you can see from my highlights, the dietary PCB (and mercury) levels in these women was strongly correlated with fish and long-chain omega-3 intake. Women who ate the most fish had almost 3x the level of PCBs of those who ate the least. So what about heart attacks? Here is what the authors' found: Women in the highest quartile of dietary PCB exposure (median 286 ng/day) had a multivariable-adjusted RR of myocardial infarction of 1.21 (95% confidence interval [CI], 1.01–1.45) compared to the lowest quartile (median 101 ng/day) before, and 1.58 (95% CI, 1.10–2.25) after adjusting for EPA-DHA. Stratification by low and high EPADHA intake, resulted in RRs 2.20 (95% CI, 1.18–4.12) and 1.73 (95% CI, 0.81–3.69), respectively comparing highest PCB tertile with lowest. The intake of dietary EPA-DHA was inversely associated with risk of myocardial infarction after but not before adjusting for dietary PCB. In other words, having the highest intake of PCBs (mostly from fish) was associated with a 21% increase in the risk of heart attack relative to being in the lowest PCB intake group. But it was only a 21% increase because EPA/DHA was pulling the other way, helping to prevent heart attacks. If you statistically factor out the EPA/DHA benefits, PCBs alone would raise heart attack risk by 58% in the top vs. bottom quartile group. Analyzed the other way, EPA/DHA intake wasn't associated with fewer heart attacks, largely because of the PCBs that typically accompany them, it would appear. In fact, those in the highest quartile of DHA/EPA intake had a (non-significant) 11% increase in risk of heart attack. But when they statistically factored out the PCBs, DHA/EPA was (weakly and non-significantly) associated with a 26% reduction in heart attack risk. The relevant data is summarized in this table with my highlights, for anyone who wants to see the details: To summarize, it looks like if you can get DHA/EPA without the accompanying PCBs, it may be a slight win for heart attack risk. But when the DHA/EPA comes as a package deal with PCBs (would you like fries with that?), as it did for these fish-eating Swedish women, it's bad news. And its looks it might be even worse for us skinny folks, since they found: In a stratified analysis, we observed a higher RR [of high dietary PCBs] (2.39; 95% CI, 1.15–4.96) among lean women (waist circumference b80 cm) than among those with abdominal adiposity, however the interaction was not statistically significant (p value = 0.18) and the confidence interval was wide. ... Our results indicate a stronger association between PCB and risk of myocardial infarction among lean women meanwhile no association among women with abdominal adiposity. One likely explanation behind the observation is the higher concentrations of circulating PCBs in blood and lower dilution of PCBs in adipose tissue of lean than of obese woman [22]. Fortunately, it is possible to ensure one gets DHA/EPA without the PCBs, by choosing an algae source of DHA/EPA, like this one, rather than taking one's chances eating fish what one hopes is low in contaminants like PCBs, but which can often be mislabelled. --Dean ------------ [1] Int J Cardiol. 2015 Mar 15;183:242-8. doi: 10.1016/j.ijcard.2015.01.055. Epub 2015 Jan 27. Dietary exposure to polychlorinated biphenyls and risk of myocardial infarction - a population-based prospective cohort study. Bergkvist C(1), Berglund M(2), Glynn A(3), Wolk A(1), Åkesson A(4). Sci-hub.io full text: http://www.sciencedirect.com.sci-hub.io/science/article/pii/S0167527315000820 BACKGROUND: Fish consumption may promote cardiovascular health. The role of major food contaminants, such as polychlorinated biphenyls (PCBs) common in fatty fish, is unclear. We assessed the association between dietary PCB exposure and risk of myocardial infarction taking into account the intake of long-chain omega-3 fish fatty acids. METHODS: In the prospective population-based Swedish Mammography Cohort, 33,446 middle-aged and elderly women, free from cardiovascular disease, cancer and diabetes at baseline (1997) were followed-up for 12 years. Validated estimates of dietary PCB exposure and intake of fish fatty acids (eicosapentaenoic acid and docosahexaenoic acid; EPA-DHA) were obtained via a food frequency questionnaire at baseline. RESULTS: During follow-up 1386 incident cases of myocardial infarction were ascertained through register-linkage. Women in the highest quartile of dietary PCB exposure (median 286 ng/day) had a multivariable-adjusted RR of myocardial infarction of 1.21 (95% confidence interval [CI], 1.01-1.45) compared to the lowest quartile (median 101 ng/day) before, and 1.58 (95% CI, 1.10-2.25) after adjusting for EPA-DHA. Stratification by low and high EPA-DHA intake, resulted in RRs 2.20 (95% CI, 1.18-4.12) and 1.73 (95% CI, 0.81-3.69), respectively comparing highest PCB tertile with lowest. The intake of dietary EPA-DHA was inversely associated with risk of myocardial infarction after but not before adjusting for dietary PCB. CONCLUSION: Exposure to PCBs was associated with increased risk of myocardial infarction, while some beneficial effect was associated with increasing EPA and DHA intake. To increase the net benefits of fish consumption, PCB contamination should be reduced to a minimum. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved. PMID: 25679993 ------------ [2] EFSA Journal 2010; 8(7):1701. [35 pp.]. doi:10.2903/j.efsa.2010.1701. European Food Safety Authority; Results of the monitoring of non dioxin-like PCBs in food and feed. Free Full text: http://www.efsa.europa.eu/sites/default/files/scientific_output/files/main_documents/1701.pdf ABSTRACT Non dioxin-like polychlorinated biphenyls (NDL-PCBs) are persistent organic chemicals that accumulate in the environment and humans and are associated with a broad spectrum of health effects. Processing and distribution of PCBs has been prohibited in almost all industrial countries since the late 1980s but they still can be released into the environment from electrical appliances, building paint and sealants and waste sites that contain PCBs. In 2002 the European Commission prescribed a list of actions to be taken to reduce the presence of dioxins and PCBs in food and feed and Member States were recommended to monitor the situation. A total of 12,563 food and feed samples collected in the period 1995 - 2008 from 18 EU Member States, Iceland and Norway were retained for a detailed analysis of the occurrence of the six indicator NDL-PCBs (# 28, 52, 101, 138, 153, and 180). Overall, 18.8% of the results for single congeners were below the limit of quantification (LOQ) but their distribution varied highly between food and feed groups. PCB-153 and PCB-138 were the most commonly detected congeners. In food, the highest mean contamination level was observed in fish and fish derived products followed by eggs, milk and their products, and meat and meat products from terrestrial animals. The lowest contamination was observed in foods of plant origin. A similar pattern was observed in feed where high contamination was reported in feed containing fish derived products and comparatively very low levels in feed of plant or mineral origin. The sum of the six NDL-PCBs was on average close to five times higher than the sum of the 12 dioxin-like PCBs. This relationship varied across food groups and is presumably related to the origin of samples and the contamination source. Country-specific clustering has been observed in several food and feed groups.
  6. All, As discussed in this thread, evidence suggests ALA may be beneficial for brain health in most people, while DHA/EPA may be a mixed blessing - only helpful for avoid Alzheimer's disease (but not other forms of dementia) in those with the APOE4 allele. And as discussed in this thread, fatty fish high in DHA/EPA may be detrimental for cardiovascular health if contaminated with PCBs, as was the case in several studies of Swedish fish eaters. But this new study [1] shared by Al Pater (thanks Al!) found in another population of fish eaters, this time from Spain, dietary DHA/EPA may in fact be beneficial for avoiding cardiovascular mortality. But dietary DHA/EPA was not significantly beneficial for all-cause mortality. For dietary Alpha Linolenic Acid (ALA) which is an omega-3 from plants (e.g. walnuts, olive oil, flax, chia seeds) the opposite was the case. Namely, dietary ALA reduced all-cause mortality, but not cardiovascular mortality risk. Putting the two together, people who met the dietary recommendations for both DHA/EPA and ALA had the lowest all-cause mortality risk - 37% lower than those who didn't meet either recommendation. Perhaps the fish from Spain have less PCBs than Swedish fish (no - I don't mean the candy :-) ). The full text of the study did not address DHA/EPA supplements - DHA/EPA intake was assessed solely from dietary sources. So it is not clear if a similar beneficial effect could be achieved through a combination of ALA from plant sources and DHA/EPA supplements as fish oil or algae oil, both of which are less likely to be contaminated with mercury or PCBs than the flesh of whole fish. --Dean ------ [1] J Am Heart Assoc. 2016 Jan 26;5(1). pii: e002543. doi: 10.1161/JAHA.115.002543. Dietary Alpha-Linolenic Acid, Marine Omega-3 Fatty Acids, and Mortality in a Population With High Fish Consumption: Findings From the PREvención con DIeta MEDiterránea (PREDIMED) Study. Sala-Vila A, Guasch-Ferré M, Hu FB, et al. http://jaha.ahajournals.org/content/5/1/e002543.long http://jaha.ahajournals.org/content/5/1/e002543.full.pdf+html Abstract BACKGROUND: Epidemiological evidence suggests a cardioprotective role of Alpha-linolenic acid (ALA), a plant-derived Omega-3 fatty acid. It is unclear whether ALA is beneficial in a background of high marine Omega-3 fatty acids (long-chain n-3 polyunsaturated fatty acids) intake. In persons at high cardiovascular risk from Spain, a country in which fish consumption is customarily high, we investigated whether meeting the International Society for the Study of Fatty Acids and Lipids recommendation for dietary ALA (0.7% of total energy) at baseline was related to all-cause and cardiovascular disease mortality. We also examined the effect of meeting the society's recommendation for long-chain n-3 polyunsaturated fatty acids (=/>500 mg/day). METHODS AND RESULTS: We longitudinally evaluated 7202 participants in the PREvención con DIeta MEDiterránea (PREDIMED) trial. Multivariable-adjusted Cox regression models were fitted to estimate hazard ratios. ALA intake correlated to walnut consumption (r=0.94). During a 5.9-y follow-up, 431 deaths occurred (104 cardiovascular disease, 55 coronary heart disease, 32 sudden cardiac death, 25 stroke). The hazard ratios for meeting ALA recommendation (n=1615, 22.4%) were 0.72 (95% CI 0.56-0.92) for all-cause mortality and 0.95 (95% CI 0.58-1.57) for fatal cardiovascular disease. The hazard ratios for meeting the recommendation for long-chain n-3 polyunsaturated fatty acids (n=5452, 75.7%) were 0.84 (95% CI 0.67-1.05) for all-cause mortality, 0.61 (95% CI 0.39-0.96) for fatal cardiovascular disease, 0.54 (95% CI 0.29-0.99) for fatal coronary heart disease, and 0.49 (95% CI 0.22-1.01) for sudden cardiac death. The highest reduction in all-cause mortality occurred in participants meeting both recommendations (hazard ratio 0.63 [95% CI 0.45-0.87]). CONCLUSIONS: In participants without prior cardiovascular disease and high fish consumption, dietary ALA, supplied mainly by walnuts and olive oil, relates inversely to all-cause mortality, whereas protection from cardiac mortality is limited to fish-derived long-chain n-3 polyunsaturated fatty acids. KEYWORDS: fatty acid; nutrition; sudden cardiac death PMID: 26813890
  7. All, 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. [1]). This new study [2] 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. [3]) 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 [3]. Study [4] 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 -------------------------------- [1] 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 ----------------- [2] 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 ----------------- [3] 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 ------------------------- [4] 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.
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