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  1. How the sugar industry sweetened research in its favor By Jacqueline Howard, CNN Updated 12:26 PM ET, Mon September 12, 2016 http://www.cnn.com/2016/09/12/health/sugar-industry-heart-disease-research/index.html Story highlights A new paper claims the sugar industry funded early heart disease research Experts compare the findings to the tobacco industry's controversial history Sugar Association: "It is challenging for us to comment on events that allegedly occurred 60 years ago" Special Communication | September 12, 2016 Sugar Industry and Coronary Heart Disease Research -- A Historical Analysis of Internal Industry Documents FREE ONLINE FIRST Cristin E. Kearns, DDS, MBA1,2; Laura A. Schmidt, PhD, MSW, MPH1,3,4; Stanton A. Glantz, PhD1,5,6,7,8 JAMA Intern Med. Published online September 12, 2016. doi:10.1001/jamainternmed.2016.5394 http://archinte.jamanetwork.com/article.aspx?articleid=2548255 Abstract Early warning signals of the coronary heart disease (CHD) risk of sugar (sucrose) emerged in the 1950s. We examined Sugar Research Foundation (SRF) internal documents, historical reports, and statements relevant to early debates about the dietary causes of CHD and assembled findings chronologically into a narrative case study. The SRF sponsored its first CHD research project in 1965, a literature review published in the New England Journal of Medicine, which singled out fat and cholesterol as the dietary causes of CHD and downplayed evidence that sucrose consumption was also a risk factor. The SRF set the review’s objective, contributed articles for inclusion, and received drafts. The SRF’s funding and role was not disclosed. Together with other recent analyses of sugar industry documents, our findings suggest the industry sponsored a research program in the 1960s and 1970s that successfully cast doubt about the hazards of sucrose while promoting fat as the dietary culprit in CHD. Policymaking committees should consider giving less weight to food industry–funded studies and include mechanistic and animal studies as well as studies appraising the effect of added sugars on multiple CHD biomarkers and disease development.
  2. There is a really interesting new meta-analysis [1] in this week's issue of The Lancet on the association between height and health/longevity. Here is a popular press article on the study, with the title Big And Tall: Nutritious Meals May Make Us Taller But They Could Also Increase Our Cancer Risk. The researchers looked at 121 epidemiological studies of over a million people that assessed the association of height with health and lifespan. The heart of the paper are these two graphs: showing how in both men and women, being taller reduces risk of coronary heart disease, but increases risk of cancer. Here is a graphical representation of the over/undernutrition-based mechanisms the authors postulate to explain the observations: The link to cancer via higher insulin in people who eat a lot (and hence grow taller) is familiar. What was a bit surprising was their suggestion that increased levels of grow factors like IGF-1 in taller people may actually improve insulin sensitivity and hence reduce diabetes and cardiovascular disease. --Dean ------------- [1] The Lancet Diabetes & Endocrinology Available online 28 January 2016 DOI: http://dx.doi.org/10.1016/S2213-8587(15)00474-X| Divergent associations of height with cardiometabolic disease and cancer: epidemiology, pathophysiology, and global implications Norbert Stefan, MD, Hans-Ulrich Häring, MD, Frank B Hu, MD, Dr Matthias B Schulze, DrPHcorrespondenceemail Full text: http://dx.doi.org.sci-hub.io/10.1016/S2213-8587(15)00474-X Summary Among chronic non-communicable diseases, cardiometabolic diseases and cancer are the most important causes of morbidity and mortality worldwide. Although high BMI and waist circumference, as estimates of total and abdominal fat mass, are now accepted as predictors of the increasing incidence of these diseases, adult height, which also predicts mortality, has been neglected. Interestingly, increasing evidence suggests that height is associated with lower cardiometabolic risk, but higher cancer risk, associations supported by mendelian randomisation studies. Understanding the complex epidemiology, biology, and pathophysiology related to height, and its association with cardiometabolic diseases and cancer, is becoming even more important because average adult height has increased substantially in many countries during recent generations. Among the mechanisms driving the increase in height and linking height with cardiometabolic diseases and cancer are insulin and insulin-like growth factor signalling pathways. These pathways are thought to be activated by overnutrition, especially increased intake of milk, dairy products, and other animal proteins during different stages of child development. Limiting overnutrition during pregnancy, early childhood, and puberty would avoid not only obesity, but also accelerated growth in children—and thus might reduce risk of cancer in adulthood.
  3. Your mom didn't know how right she was when she told you to eat your fruits & vegetables (F/V), at least if you are a girl... This new study [1] in the journal Circulation assessed the diets of 2500 young black and white men and women (~25 years of age, 62% female) and then measured their level of artery calcification 20 years later using computed tomography - arguably the 'gold standard' for assessing artery health. It found that people eating the most F/V (highest tertile - 7-9 servings / day) were 25% less likely 20 years later to have developed calcified arteries relative to the lowest F/V eaters (2-4 servings / day). From the full text, here are a few of the highlights, including one kicker: Fruits and vegetables were about equally protective Including legumes in with the vegetable category kept the association about the same - i.e. legumes were about as good for arteries as fruits & veggies. Of course people eating lots of F/V had healthier diets in other ways as well, but the inverse association between F/V and artery calcification was still significant even after controlling for these other dietary factors. Shockingly left out of the abstract was the fact that the inverse relationship between F/V intake and artery calcification (CAC) was only observed in women! To quote the full text: [R]eported intake of F/V did not appear to be associated with prevalent CAC among men: OR (95% CI) 1.0 (ref), 0.77 (0.52-1.12), 0.89 (0.60-1.31), p-value for trend 0.67 Here was their explanation for this surprising results: The lack of association between F/V intake and CAC in men in our study may be due to a lack of power, as our study included only 935 male participants. However, a less significant association between CVD and F/V intake in men has been seen in other studies. Data from the European Prospective Investigation into Cancer and Nutrition (EPIC)-Heart study demonstrated a 15% (95% CI: 6% to 23%) lower risk for CHD mortality per 80gram/day increase in fruit and vegetable intake in women, but a non-significant 2% (95% CI: -2% to +2%) CHD mortality reduction in men (p-value for heterogeneity 0.007) [2] Similar findings were reported in a cohort of Japanese women and men.3 In the CHD risk factor study INTERHEART, the 3 lifestyle behaviors associated with a lower risk of CHD were F/V intake, exercise, and moderate alcohol consumption, and the protective effects of exercise and moderate alcohol consumption were larger in women compared to men with a trend towards F/V intake being more protective in women as well.[3] So why did the researchers leave out this surprising lack of inverse relationship between F/V intake and later artery calcification in men from both the abstract and from the popular press coverage of this study? Perhaps so as to avoid undermining the credibility of their (laudable) public health message, as summarized in the concluding sentence of the abstract: Our results reinforce the importance of establishing a high intake of F/V as part of a healthy dietary pattern early in life. Somehow I was unaware of the attenuated CVD benefits men seem to get from eating lots fruits and vegetables. --Dean ---------- [1] Circulation. 2015 Oct 26. pii: CIRCULATIONAHA.114.012562. [Epub ahead of print] The Association of Fruit and Vegetable Consumption During Early Adulthood With the Prevalence of Coronary Artery Calcium After 20 Years of Follow-Up: The CARDIA Study. Miedema MD(1), Petrone A(2), Shikany JM(3), Greenland P(4), Lewis CE(3), Pletcher MJ(5), Gaziano JM(2), Djousse L(2). Free full text: http://circ.ahajournals.org/content/early/2015/10/14/CIRCULATIONAHA.114.012562.long BACKGROUND: -The relationship between intake of fruits and vegetables (F/V) during young adulthood and coronary atherosclerosis later in life is unclear. METHODS AND RESULTS: -We studied participants of the Coronary Artery Risk Development in Young Adults (CARDIA) study, a cohort of young, healthy black and white individuals at baseline (1985-1986). Intake of F/V at baseline was assessed using a semi-quantitative interview administered diet history and CAC was measured at year 20 (2005-2006) using computed tomography. We used logistic regression to adjust for relevant variables and estimate the adjusted odds ratios (OR) and 95% confidence intervals (CI) across energy-adjusted, sex-specific tertiles of total servings of F/V per day. Among our sample (n=2,506), the mean (SD) age at baseline was 25.3 (3.5) years and 62.7% were female. After adjustment for demographics and lifestyle variables, higher intake of F/V was associated with a lower prevalence of CAC: OR (95% CI) =1.00 (reference), 0.78 (0.59-1.02), and 0.74 (0.56-0.99), from the lowest to the highest tertile of F/V, p-value for trend <0.001. There was attenuation of the association between F/V and CAC after adjustment for other dietary variables but the trend remained significant: OR (95% CI): 1.00 (reference), 0.84 (0.63-1.11), and 0.92 (0.67-1.26), p-value for trend <0.002]. CONCLUSIONS: -In this longitudinal cohort study, higher intake of F/V during young adulthood was associated with lower odds of prevalent CAC after 20 years of follow-up. Our results reinforce the importance of establishing a high intake of F/V as part of a healthy dietary pattern early in life. PMID: 26503880 ------------ [2] Eur Heart J. 2011;32:1235–1243. Fruit and vegetable intake and mortality from ischaemic heart disease: results from the European Prospective Investigation into Cancer and Nutrition (EPIC)-Heart study. Crowe FL, Roddam AW, Key TJ, Appleby PN, Overvad K, Jakobsen MU, Tjønneland A, Hansen L, Boeing H, Weikert C, Linseisen J, Kaaks R, Trichopoulou A, Misirli G, Lagiou P, Sacerdote C, Pala V, Palli D, Tumino R, Panico S, Bueno-de-Mesquita HB, Boer J, van Gils CH, Beulens JW, Barricarte A, Rodríguez L, Larrañaga N, Sánchez MJ, Tormo MJ, Buckland G, Lund E, Hedblad B, Melander O, Jansson JH, Wennberg P, Wareham NJ, Slimani N, Romieu I, Jenab M, Danesh J, Gallo V, Norat T, Riboli E; ------------ [3] Yusuf S, Hawken S, Ounpuu S, Dans T, Avezum A, Lanas F, McQueen M, Budaj A, Pais P, Varigos J, Lisheng L; INTERHEART Study Investigators. Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): casecontrol study. Lancet. 2004;364:937–952.
  4. Dean Pomerleau

    Total Cholesterol and Heart Attacks

    [Another one for the "non-CR diet and health" forum. If such a forum ever gets created, I promise I'll use my moderator super-powers to move all these threads to the new forum!] Dr. Greger's latest video titled Everything in Moderation? Even Heart Disease? has this interesting graph from [1] of cardiovascular disease and heart attacks as a function of total serum cholesterol level (click to enlarge): It shows that 35 percent of heart attacks occur in people with total serum cholesterol between 150 and 200 mg/dL. I had no idea it was that high. And virtually no heart attacks occur in people with cholesterol below 150 mg/dL, which is why many people (including me) have said it makes you virtually "heart attack proof". But then I started thinking, wait a minute. Couldn't this simply be a reflection of population statistics, and not reflect a causal relationship between cholesterol level and heart attacks? To understand this possibility, consider a similar plot of height vs. # of heart attacks. Assuming heart attacks are totally independent of height, you'd still see a similar bell curve of the number of heart attacks plotted against height, for the simple reason that height is distributed along a bell curve. So 50% of heart attacks would occur in men below the median height of 5'10" in the US, and furthermore only a tiny fraction of heart attacks (~3%) would occur in men shorter than 5'2", which is two standard deviations below the median. Does that mean that having a very short stature makes you heart attack proof? Of course not, it just means that there aren't many men shorter than 5'2" to contribute to the heart attack statistics. As an admirer of both Dr. Greger's work, I am sometimes disappointed when he uses potentially misleading statistics like this one to advance his perspective on diet and health (i.e. the value of following a plant-based diet - which I very much agree with). So what is the more accurate picture of the relationship between cholesterol and heart attack risk? Here is a graph, from [2], which BTW has a very good overview of various blood markers, including cholesterol sub-components and their association with CHD: As you can see from the graph on the right, CHD mortality rate (as opposed to total # of heart attacks) appears to be pretty asymptotic below 200 mg/dL. It's only when you get up to a total cholesterol of about 225 mg/dL that you see CHD mortality rate rising significantly, above which it goes through the roof. This is what's called evidence-based medicine, and it is why the American Heart Association and European equivalent (the European Societies for Cardiology, Hypertension and Diabetes) recommend keeping total cholesterol below 190-200, rather than necessarily trying to push it below 150 using diet or statins. With the latter, you might end up like this guy : So despite what Dr. Greger suggests, keeping one's total cholesterol below 150 mg/dL, as opposed to somewhere in the range of 150-200 mg/dL, doesn't appear to provide a dramatic benefit in terms of heart attack risk. To be fair, Dr. Greger has another video on the optimal cholesterol level for heart health that does seem to get the science better. It ignores total cholesterol level, and instead looks at all the randomized control trials of cholesterol lowering drugs, which suggest that an LDL level below 70 mg/dL (about 1/2 the average LDL level in US adults, 130 mg/dL) does make one virtually "heart attack proof". But then again, the relevance of results from people who are taking statins, not to mention the relevance for us of statin-induced LDL reduction or other positive effects of statins, make it far from certain that these results apply to people keeping LDL cholesterol low through diet and lifestyle choices. --Dean --------------- [1] Atherosclerosis. 1996 Jul;124 Suppl:S1-9. Lipids, risk factors and ischaemic heart disease. Castelli WP(1). Author information: (1)Framingham Cardiovascular Institute, MA 01701-9167, USA. Over 200 risk factors for cardiovascular disease (CVD) have now been identified. Among these, the three most important are (1) abnormal lipids, including the fact that there are more than 15 types of cholesterol-containing lipoproteins and four different types of triglyceride-rich particles, some of which are very atherogenic, (2) high blood pressure, and (3) cigarette smoking. In addition, many other factors including diabetes, haemostatic factors such as fibrinogen, factor VII, plasminogen activator inhibitors, and new factors such as apolipoprotein E4 and homocysteine, are known to increase the risk of developing clinical CVD. A low risk for CVD requires that these various factors are present in the circulation in the correct proportions. Two simple tests for determining plasma lipid levels can be used to identify those individuals with an atherogenic lipid profile and who are, therefore, at increased risk for CVD. Firstly, the ratio of total cholesterol to high density cholesterol (HDL cholesterol) should be determined, followed by measurement of plasma triglyceride concentrations. This will allow differentiation of whether the low density lipoproteins (LDL), HDL cholesterol or triglyceride-rich particles such as the small dense beta-very low density lipoproteins (VLDL) are the major cause for concern. Once identified, those individuals with a high lipid risk profile should be treated before, rather than after, experiencing coronary heart disease (CHD). PMID: 8831910 ------------------- [2] The Journal of the International Federation of Clinical Chemistry and Laboratory Medicine Vol 13:2 (2003) THE ROLE OF LIPIDS IN THE DEVELOPMENT OF ATHEROSCLEROSIS AND CORONARY HEART DISEASE: GUIDELINES FOR DIAGNOSIS AND TREATMENT Victor Blaton Department of Clinical Chemistry, Hospital AZ Sint-Jan AV, Brugge, Belgium pdf: http://www.ifcc.org/ifccfiles/docs/140206200306.pdf
  5. [Another one for the "Non-CR Health forum"...] Recently there has been much hype in the popular press, including a Time Magazine story, with this provocative cover: that claim we've been wrong about saturated fat (like butter) all along. These stories have been based on meta-analyses like this one [1], that purport to find no association between saturated fat and chronic diseases, even cardiovascular disease. One of my favorite nutrition bloggers, PlantPositive, did a thorough debunking of the Time story and the people & studies it uses as sources. Among other faults of these previous meta-analyses outlined in PlantPositive's post, some of the biggest problems include: Over correction by factoring out serum cholesterol in the analysis - which is elevated by saturate fat intake and so shouldn't be controlled for. Failing to factor out the low cholesterol of saturated fat eaters who take statins to control their cholesterol. Failing to account for the health effects of what people choose to eat instead when they don't eat saturated fat-rich foods. As I recall (but an unable to verify due to the archives being down... ), we talked about all these studies and their shortcomings on the CR email list before. But now, we have something even better than critical analysis of flawed studies. We have a new prospective cohort study [2] of some of the best data available on diet, lifestyle and health from the Health Professionals and Nurses Health Studies. It appears to do a much better job, particularly with respect to the third confounder - food substitution effects. Here is popular press coverage of the new study. The Harvard researchers have followed these two cohorts of 42K men and 84K women for over 30 years, assessing their diet, lifestyle and health repeatedly during that time. This study looked at their fat consumption habits, and in particular changes in those habits over time and how those changes relate to coronary heart disease (CHD). In a nutshell, they found that: Replacing 5% of energy intake from saturated fats with equivalent energy intake from PUFAs, monounsaturated fatty acids, or carbohydrates from whole grains was associated with a 25%, 15%, and 9% lower risk of CHD, respectively (PUFAs, HR: 0.75, 95% CI: 0.67 to 0.84; p < 0.0001; monounsaturated fatty acids, HR: 0.85, 95% CI: 0.74 to 0.97; p = 0.02; carbohydrates from whole grains, HR: 0.91, 95% CI: 0.85 to 0.98; p = 0.01). Replacing saturated fats with carbohydrates from refined starches/added sugars was not significantly associated with CHD risk (p > 0.10). Here is a graphical depiction of these results: As you can see, trans fat is toxic relative to any other foods, including saturate fat - no surprise. More interestingly, it is about a wash to substitute saturated fat with refined carbohydrates when it comes to heart disease risk. But substituting any of the following for saturated fat results in significantly reduced CHD risk - MUFA, PUFA and whole grain carbohydrates. PUFAs appear particularly protective. Unfortunately the study did not address other healthy carbohydrate sources besides whole grains, like fruits, vegetables or legumes (which I willing to bet would do at least as well as whole grains at reducing CHD risk relative to saturated fat). They also didn't discriminate between the health effects of different types of saturated fats, some of which might not be as bad as others (i.e. those found in plants vs. animal sources). One concern is that when people clean up their diet by eliminating saturated fat, they might also undertake other health promoting lifestyle changes, making it appear that reducing saturated fat was beneficial when it actually was the other changes that made the difference. The authors addressed this potential problem by controlling for a host of other factors in their analysis, including: The multivariable model was adjusted for total energy intake, the energy contribution from protein, cholesterol intake, alcohol intake, smoking status, body mass index, physical activity, use of vitamins and aspirin, family history of myocardial infarction and diabetes, and presence of baseline hypercholesterolemia and hypertension. These results confirm what I think most people have believed all along - that saturated fat is detrimental to heart health, but probably no more so than what people will normally eat instead, crappy carbs. This explains those previous studies that found lower saturated fat intake was often not associated with lower risk of heart disease - people who ate less saturated fat were eating more refined carbs instead, and so weren't any better off. But when you replace saturated fat-rich foods with healthy fats or healthy carbs, you reduce your risk of heart disease dramatically. --Dean --------------- [1] BMJ. 2015 Aug 11;351:h3978. doi: 10.1136/bmj.h3978. Intake of saturated and trans unsaturated fatty acids and risk of all cause mortality, cardiovascular disease, and type 2 diabetes: systematic review and meta-analysis of observational studies. de Souza RJ(1), Mente A(2), Maroleanu A(3), Cozma AI(4), Ha V(5), Kishibe T(6), Uleryk E(7), Budylowski P(8), Schünemann H(9), Beyene J(10), Anand SS(11). OBJECTIVE: To systematically review associations between intake of saturated fat and trans unsaturated fat and all cause mortality, cardiovascular disease (CVD) and associated mortality, coronary heart disease (CHD) and associated mortality, ischemic stroke, and type 2 diabetes. DESIGN: Systematic review and meta-analysis. DATA SOURCES: Medline, Embase, Cochrane Central Registry of Controlled Trials, Evidence-Based Medicine Reviews, and CINAHL from inception to 1 May 2015, supplemented by bibliographies of retrieved articles and previous reviews. ELIGIBILITY CRITERIA FOR SELECTING STUDIES: Observational studies reporting associations of saturated fat and/or trans unsaturated fat (total, industrially manufactured, or from ruminant animals) with all cause mortality, CHD/CVD mortality, total CHD, ischemic stroke, or type 2 diabetes. DATA EXTRACTION AND SYNTHESIS: Two reviewers independently extracted data and assessed study risks of bias. Multivariable relative risks were pooled. Heterogeneity was assessed and quantified. Potential publication bias was assessed and subgroup analyses were undertaken. The GRADE approach was used to evaluate quality of evidence and certainty of conclusions. RESULTS: For saturated fat, three to 12 prospective cohort studies for each association were pooled (five to 17 comparisons with 90 501-339 090 participants). Saturated fat intake was not associated with all cause mortality (relative risk 0.99, 95% confidence interval 0.91 to 1.09), CVD mortality (0.97, 0.84 to 1.12), total CHD (1.06, 0.95 to 1.17), ischemic stroke (1.02, 0.90 to 1.15), or type 2 diabetes (0.95, 0.88 to 1.03). There was no convincing lack of association between saturated fat and CHD mortality (1.15, 0.97 to 1.36; P=0.10). For trans fats, one to six prospective cohort studies for each association were pooled (two to seven comparisons with 12 942-230 135 participants). Total trans fat intake was associated with all cause mortality (1.34, 1.16 to 1.56), CHD mortality (1.28, 1.09 to 1.50), and total CHD (1.21, 1.10 to 1.33) but not ischemic stroke (1.07, 0.88 to 1.28) or type 2 diabetes (1.10, 0.95 to 1.27). Industrial, but not ruminant, trans fats were associated with CHD mortality (1.18 (1.04 to 1.33) v 1.01 (0.71 to 1.43)) and CHD (1.42 (1.05 to 1.92) v 0.93 (0.73 to 1.18)). Ruminant trans-palmitoleic acid was inversely associated with type 2 diabetes (0.58, 0.46 to 0.74). The certainty of associations between saturated fat and all outcomes was "very low." The certainty of associations of trans fat with CHD outcomes was "moderate" and "very low" to "low" for other associations. CONCLUSIONS: Saturated fats are not associated with all cause mortality, CVD, CHD, ischemic stroke, or type 2 diabetes, but the evidence is heterogeneous with methodological limitations. Trans fats are associated with all cause mortality, total CHD, and CHD mortality, probably because of higher levels of intake of industrial trans fats than ruminant trans fats. Dietary guidelines must carefully consider the health effects of recommendations for alternative macronutrients to replace trans fats and saturated fats. © de Souza et al 2015. PMCID: PMC4532752 PMID: 26268692 ------------ [2] J Am Coll Cardiol. 2015 Oct 6;66(14):1538-48. doi: 10.1016/j.jacc.2015.07.055. Saturated Fats Compared With Unsaturated Fats and Sources of Carbohydrates in Relation to Risk of Coronary Heart Disease: A Prospective Cohort Study. Li Y(1), Hruby A(1), Bernstein AM(2), Ley SH(1), Wang DD(1), Chiuve SE(3), Sampson L(1), Rexrode KM(4), Rimm EB(5), Willett WC(5), Hu FB(6). BACKGROUND: The associations between dietary saturated fats and the risk of coronary heart disease (CHD) remain controversial, but few studies have compared saturated with unsaturated fats and sources of carbohydrates in relation to CHD risk. OBJECTIVES: This study sought to investigate associations of saturated fats compared with unsaturated fats and different sources of carbohydrates in relation to CHD risk. METHODS: We followed 84,628 women (Nurses' Health Study, 1980 to 2010), and 42,908 men (Health Professionals Follow-up Study, 1986 to 2010) who were free of diabetes, cardiovascular disease, and cancer at baseline. Diet was assessed by a semiquantitative food frequency questionnaire every 4 years. RESULTS: During 24 to 30 years of follow-up, we documented 7,667 incident cases of CHD. Higher intakes of polyunsaturated fatty acids (PUFAs) and carbohydrates from whole grains were significantly associated with a lower risk of CHD comparing the highest with lowest quintile for PUFAs (hazard ratio : 0.80, 95% confidence interval [CI]: 0.73 to 0.88; p trend <0.0001) and for carbohydrates from whole grains (HR: 0.90, 95% CI: 0.83 to 0.98; p trend = 0.003). In contrast, carbohydrates from refined starches/added sugars were positively associated with a risk of CHD (HR: 1.10, 95% CI: 1.00 to 1.21; p trend = 0.04). Replacing 5% of energy intake from saturated fats with equivalent energy intake from PUFAs, monounsaturated fatty acids, or carbohydrates from whole grains was associated with a 25%, 15%, and 9% lower risk of CHD, respectively (PUFAs, HR: 0.75, 95% CI: 0.67 to 0.84; p < 0.0001; monounsaturated fatty acids, HR: 0.85, 95% CI: 0.74 to 0.97; p = 0.02; carbohydrates from whole grains, HR: 0.91, 95% CI: 0.85 to 0.98; p = 0.01). Replacing saturated fats with carbohydrates from refined starches/added sugars was not significantly associated with CHD risk (p > 0.10). CONCLUSIONS: Our findings indicate that unsaturated fats, especially PUFAs, and/or high-quality carbohydrates can be used to replace saturated fats to reduce CHD risk. Copyright © 2015 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved. PMCID: PMC4593072 [Available on 2016-10-06] PMID: 26429077
  6. In my exploration of nutrigenomics, I came across this interesting recent study [1] that looked at the interaction between a particular gene polymorphism (rs4977574 - available on 23andMe) and cardiovascular disease (CVD), as mediated by consumption of either vegetables or wine. The researchers followed 24,000 people for 15 years, during which time about 3000 of them developed cardiovascular disease. So it was a pretty big cohort, with lots of people experiencing the outcome in question - cardiovascular disease. Across the entire population, eating more veggies and drinking more wine resulted in less CVD - not too surprising given previous research on the health benefits of these foods. Things got more interesting when the researchers looked at polymorphisms of SNP rs4977574. Having one or two of the risk alleles (G worse than A) for this SNP on chromosome 9 has been previously shown to be associated with an increased risk of CVD [2]. For example, study [3] found for every G allele one carries, one has about a 13% increased risk of CVD. Study [2] was similar - in the 20-25% of the population that carry two G alleles for this SNP, risk of CVD was increased 30-40% relative to people with AA for rs4977574. This new study [1] found something very similar - for each additional G allele at rs4977574, people were 16% more likely to develop CVD. And these polymorphisms are quite common, ~30% of the study population were AA for rs4977574, 50% were AG, and 20% were GG. But things got really interesting when they looked at how vegetable and wine consumption influenced with the link between this polymorphism and CVD. For people with two 'normal' alleles for rs4977574 (AA), increasing vegetable intake was associated with lower CVD, just like in the population as a whole - no surprise. But for people with either one or two G's for rs4977574, higher vegetable intake didn't help! In other words, compared with high consumers of vegetables who carried two A's for rs4977574 (the reference group), people with AG for rs4977574 were 20-30% more likely to develop CVD, and people with GG for rs4977574 were 40-50% more likely to develop CVD, regardless of how many vegetables they ate! The opposite was true for wine. Wine didn't help reduce risk of CVD in AA carriers for rs4977574, but it did reduce risk in AG and GG carriers, by ~30% and ~40% respectively! In fact, drinking wine appeared to nearly entirely counteract the baseline increased risk of CVD in AG and GG carriers, relative to AA carriers. Here is the relevant table of results from the paper for those interested in the precise details: In summary, this study suggests that if you have one or (especially) two G alleles for rs4977574, you are at higher risk for cardiovascular disease, and that consuming wine, but not vegetables, can help lower your risk. FYI, 23andMe shows I've got one G allele for rs4977574 - which is a bummer since I love veggies and don't drink alcohol. :( Of course its only one study, and one gene locus, so the results should be taken with a grain of salt. I don't plan to eat fewer veggies or take up drinking as a result of this study, particularly since alcoholism runs in my family. I figure my good cholesterol numbers and healthy diet/lifestyle make it unlikely I'll die of CVD anyway. But it seems like another interesting example how genes and diet/lifestyle can interact to influence health in significant and sometimes surprising ways. --Dean ------------------------------------------- [1] BMC Med Genet. 2014 Dec 31;15(1):1220. [Epub ahead of print] The chromosome 9p21 variant interacts with vegetable and wine intake to influence the risk of cardiovascular disease: a population based cohort study. Hindy G, Ericson U, Hamrefors V, Drake I, Wirfält E, Melander O, Orho-Melander M. Full Text: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4331503/pdf/12881_2014_Article_138.pdf AbstractBackgroundChromosome 9p21 variants are associated with cardiovascular disease (CVD) but not with any of its known risk markers. However, recent studies have suggested that the risk associated with 9p21 variation is modified by a prudent dietary pattern and smoking. We tested if the increased risk of CVD by the 9p21 single nucleotide polymorphism rs4977574 is modified by intakes of vegetables, fruits, alcohol, or wine, and if rs4977574 interacts with environmental factors on known CVD risk markers.MethodsMultivariable Cox regression analyses were performed in 23,949 individuals from the population-based prospective Malmö Diet and Cancer Study (MDCS), of whom 3,164 developed CVD during 15 years of follow-up. The rs4977574 variant (major allele: A; minor allele: G) was genotyped using TaqMan® Assay Design probes. Dietary data were collected at baseline using a modified diet history method. Cross-sectional analyses were performed in 4,828 MDCS participants with fasting blood levels of circulating risk factors measured at baseline.ResultsEach rs4977574 G allele was associated with a 16% increased incidence of CVD (95% confidence interval (CI), 1.10¿1.22). Higher vegetable intake (hazard ratio (HR), 0.95 [CI: 0.91¿0.996]), wine intake (HR, 0.91 [CI: 0.86¿0.96]), and total alcohol consumption (HR, 0.92 [CI: 0.86¿0.98]) were associated with lower CVD incidence. The increased CVD incidence by the G allele was restricted to individuals with medium or high vegetable intake (Pinteraction¿=¿0.043), and to non- and low consumers of wine (Pinteraction¿=¿0.029). Although rs4977574 did not associate with any known risk markers, stratification by vegetable intake and smoking suggested an interaction with rs4977574 on glycated hemoglobin and high-density lipoprotein cholesterol (Pinteraction¿=¿0.015 and 0.049, respectively).ConclusionsOur results indicate that rs4977574 interacts with vegetable and wine intake to affect the incidence of CVD, and suggest that an interaction may exist between environmental risk factors and rs4977574 on known risk markers of CVD. PMID: 25551366 --------------------- [2] Science. 2007 Jun 8;316(5830):1488-91. Epub 2007 May 3. A common allele on chromosome 9 associated with coronary heart disease. McPherson R1, Pertsemlidis A, Kavaslar N, Stewart A, Roberts R, Cox DR, Hinds DA, Pennacchio LA, Tybjaerg-Hansen A, Folsom AR, Boerwinkle E, Hobbs HH, Cohen JC. Author information AbstractCoronary heart disease (CHD) is a major cause of death in Western countries. We used genome-wide association scanning to identify a 58-kilobase interval on chromosome 9p21 that was consistently associated with CHD in six independent samples (more than 23,000 participants) from four Caucasian populations. This interval, which is located near the CDKN2A and CDKN2B genes, contains no annotated genes and is not associated with established CHD risk factors such as plasma lipoproteins, hypertension, or diabetes. Homozygotes for the risk allele make up 20 to 25% of Caucasians and have a approximately 30 to 40% increased risk of CHD. PMID: 17478681 --------------------------------- [3] J Intern Med. 2013 Sep;274(3):233-40. doi: 10.1111/joim.12063. Epub 2013 Mar 25. Chromosome 9p21 genetic variation explains 13% of cardiovascular disease incidence but does not improve risk prediction. Gränsbo K1, Almgren P, Sjögren M, Smith JG, Engström G, Hedblad B, Melander O. Author information AbstractOBJECTIVES:To evaluate the proportion of cardiovascular disease (CVD) incidence that is explained by genetic variation at chromosome 9p21 and to test whether such variation adds incremental information with regard to CVD prediction, beyond traditional risk factors. DESIGN, SETTING AND PARTICIPANTS:rs4977574 on chromosome 9p21 was genotyped in 24 777 subjects from the Malmö Diet and Cancer study who were free from CVD prior to the baseline examination. Association between genotype and incident CVD (n = 2668) during a median follow-up of 11.7 years was evaluated in multivariate Cox proportional hazard models. Analyses were performed in quartiles of baseline age, and linear trends in effect size across age groups were estimated in logistic regression models. RESULTS:In additive models, chromosome 9p21 significantly predicted CVD in the entire population (hazard ratio 1.17 per G allele, 95% confidence interval 1.11-1.23, P < 0.001). Effect estimates increased from the highest (Q4) to the lowest quartile (Q1) of baseline age, but this trend was not significant. The overall population attributable risk conferred by chromosome 9p21 in fully adjusted models was 13%, ranging from 17% in Q1 to 11% in Q4. Addition of chromosome 9p21 to traditional risk factors only marginally improved predictive accuracy. CONCLUSION:The high population attributable risk conferred by chromosome 9p21 suggests that future interventions interfering with downstream mechanisms of the genetic variation may affect CVD incidence over a broad range of ages. However, variation of chromosome 9p21 alone does not add clinically meaningful information in terms of CVD prediction beyond traditional risk factors at any age.
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