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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
First, apropo nothing whatsoever (except that I happened upon it in a search for [ chia ] here in the forums), I hope everyone has read MIchael's Nutrition and Supplementation for Veg(etari)ans. Now, my question: I hear and read much about people getting their omega-3 needs met by flax seeds or flax seed oil, or, for some of us, fish, others, supplements, but I don't hear much about chia seeds. Is there some problem with them I haven't seen? I created an Excel spreadsheet with 250 calorie amounts of nuts, a few seeds, and a few other fatty items in order to help guide my fatty food choice, and was amazed at how nutritious chia seeds are! They're bland-tasting, to be sure -- is that why people don't get excited about them? Otherwise, lots of minerals, but no scary amounts of Cu or Mn (though not really low Mn), far more vitamins than most nuts or seeds, even a lot of carotenoids. Fairly low SFA, to boot. And then all that ALA. Is there some hidden danger? Zeta
Dean Pomerleau posted a topic in General Health and LongevityAll, 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 (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 ------------  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
All, In another apparent micronutrient synergy involving DHA for improved brain health (see Curcumin Elevates DHA in the Brain thread for the other), this new randomized control trial  found that supplementing for two years with three B-vitamins (folic acid, B6 and B12) slowed the cognitive decline that often leads from mild cognitive impairment (MCI) to Alzheimer's Disease (AD), but only if the person had "high normal" levels of serum DHA at baseline: When omega-3 fatty acid concentrations are low, B vitamin treatment has no effect on cognitive decline in MCI, but when omega-3 levels are in the upper normal range, B vitamins interact to slow cognitive decline. A clinical trial of B vitamins combined with omega-3 fatty acids is needed to see whether it is possible to slow the conversion from MCI to AD. Michael warns against CRers supplementing with DHA, but for brain health it seems that adequate DHA may be important. Curcumin might help increase DHA in the brain by boosting ALA->DHA conversion, but he's also dissed curcumin, so I'm wondering what he thinks of all this... --Dean ----------  J Alzheimers Dis. 2016 Jan 6. [Epub ahead of print] Omega-3 Fatty Acid Status Enhances the Prevention of Cognitive Decline by B Vitamins in Mild Cognitive Impairment. Oulhaj A(1), Jernerén F(2), Refsum H(2,)(3), David Smith A(2), de Jager CA(4). Free full text: http://content.iospress.com/articles/journal-of-alzheimers-disease/jad150777 A randomized trial (VITACOG) in people with mild cognitive impairment (MCI) found that B vitamin treatment to lower homocysteine slowed the rate of cognitive and clinical decline. We have used data from this trial to see whether baseline omega-3 fatty acid status interacts with the effects of B vitamin treatment. 266 participants with MCI aged ≥70 years were randomized to B vitamins (folic acid, vitamins B6 and B12) or placebo for 2 years. Baseline cognitive test performance, clinical dementia rating (CDR) scale, and plasma concentrations of total homocysteine, total docosahexaenoic and eicosapentaenoic acids (omega-3 fatty acids) were measured. Final scores for verbal delayed recall, global cognition, and CDR sum-of-boxes were better in the B vitamin-treated group according to increasing baseline concentrations of omega-3 fatty acids, whereas scores in the placebo group were similar across these concentrations. Among those with good omega-3 status, 33% of those on B vitamin treatment had global CDR scores >0 compared with 59% among those on placebo. For all three outcome measures, higher concentrations of docosahexaenoic acid alone significantly enhanced the cognitive effects of B vitamins, while eicosapentaenoic acid appeared less effective. When omega-3 fatty acid concentrations are low, B vitamin treatment has no effect on cognitive decline in MCI, but when omega-3 levels are in the upper normal range, B vitamins interact to slow cognitive decline. A clinical trial of B vitamins combined with omega-3 fatty acids is needed to see whether it is possible to slow the conversion from MCI to AD. PMID: 26757190