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  1. Dr. Greger has authored an article today for the very popular health & wellness website Care2 titled How Does Obesity Increases Cancer Risk? The interesting part is that he focuses on the cancer promoting effects of IGF-1, and uses data from Luigi Fontana's studies (particularly [1]) of some of us long-term CR practitioners. He also mentions the CR Society by name in the article! Unfortunately, he doesn't include a link to the CR Society website , but I've included one in the comments. Here are the relevant passages: <snip> The only dietary group that comes close to the recommended BMI of 21 to 23 were those eating strictly plant-based diets, so maybe it’s the weight loss that did it [i.e. reduced IGF-1 - DP]. To put that to the test, we’d have to find a group of people that eat meat, but are still as slim as vegans. And that’s what researchers did—long-distance endurance runners, running an average of 48 miles a week for 21 years were as slim as vegans. If we run 50,000 miles we too can maintain a BMI of even a raw vegan. So what did they find? If we look at blood concentrations of cancer risk factors among the groups of study subjects, we see that only the vegans had significantly lower levels of IGF-1. That makes sense given the role animal protein plays in boosting IGF-1 levels. But the vegan group didn’t just eat less animal protein, they ate fewer calories. And in rodents at least, caloric restriction alone reduces IGF-1 levels. So maybe low IGF-1 among vegans isn’t due to their slim figures, but maybe the drop in IGF-1 in vegans is effectively due to their unintentional calorie restriction? So we’d have to compare vegans to people practicing severe calorie restriction. To do this, the researchers recruited vegans from the St. Louis Vegetarian Society, and went to the Calorie Restriction Society to find folks practicing severe caloric restriction. What did they find? Only the vegan group got a significant drop in IGF-1. These findings demonstrate that, unlike in rodents, long-term severe caloric restriction in humans does not reduce the level of this cancer-promoting hormone. It’s not how many calories we eat, but the protein intake that may be the key determinant of circulating IGF-1 levels in humans, and so reduced protein intake may become an important component of anti-cancer and anti-aging dietary interventions. The discussion of vegans having low IGF-1, but not the omnivorous (or at least high protein) CR practitioners, comes from the Fontana study [1], which we've discussed many times before. What's nice to see is that (for once) Dr. Greger doesn't (directly) promote a plant-based diets in his final analysis. Instead he focuses on the importance of keeping protein intake low as a potential key for preventing cancer. What he doesn't mention is that in [1], when the CR practitioners reduced protein from 1.67 g/kg body weight to 0.95 g/kg body weight, their IGF-1 level dropped a lot. This is one of the main reasons that many of us changed from a relatively high protein CR diet that we practiced in the early 2000s to the relatively low protein CR diet that we practice today, and why (I presume) Michael Rae modified the Megamuffin 2.0 recipe, with 28% of calories from protein to the Megamuffin 3.0 recipe, with only 15% of calories from protein. --Dean ------------- [1] Aging Cell. 2008 Oct;7(5):681-7. Long-term effects of calorie or protein restriction on serum IGF-1 and IGFBP-3 concentration in humans. Fontana L(1), Weiss EP, Villareal DT, Klein S, Holloszy JO. Author information: (1)Division of Geriatrics & Nutritional Sciences, Washington University School of Medicine, St Louis, MO 63110, USA. lfontana@dom.wustl.edu Comment in Aging Cell. 2009 Apr;8(2):214; author reply 215. Reduced function mutations in the insulin/IGF-I signaling pathway increase maximal lifespan and health span in many species. Calorie restriction (CR) decreases serum IGF-1 concentration by ~40%, protects against cancer and slows aging in rodents. However, the long-term effects of CR with adequate nutrition on circulating IGF-1 levels in humans are unknown. Here we report data from two long-term CR studies (1 and 6 years) showing that severe CR without malnutrition did not change IGF-1 and IGF-1 : IGFBP-3 ratio levels in humans. In contrast, total and free IGF-1 concentrations were significantly lower in moderately protein-restricted individuals. Reducing protein intake from an average of 1.67 g kg(-1) of body weight per day to 0.95 g kg(-1) of body weight per day for 3 weeks in six volunteers practicing CR resulted in a reduction in serum IGF-1 from 194 ng mL(-1) to 152 ng mL(-1). These findings demonstrate that, unlike in rodents, long-term severe CR does not reduce serum IGF-1 concentration and IGF-1 : IGFBP-3 ratio in humans. In addition, our data provide evidence that protein intake is a key determinant of circulating IGF-1 levels in humans, and suggest that reduced protein intake may become an important component of anticancer and anti-aging dietary interventions. PMCID: PMC2673798 PMID: 18843793
  2. Michael and Saul will be happy about this one, since I'm going to criticize Dr. Greger's latest video (embedded below), about happiness titled Which Foods Increase Happiness? I'm also curious what Sthira might have to say :-), if he's still out there...?! In the video, Dr. Greger reviews studies of the link between fruit/vegetable (FV) intake and happiness. In the first part of the video, he reviews a number of studies that have (not surprisingly) found a positive association between FV consumption and positive mood / happiness. Then, to his credit, he asks the perennial question for these kinds of observational studies, namely the direction of causality. Does FV intake increase happiness, or do happy people eat more FVs? He points to evidence for the latter. For example, study [1] found that people in a good mood are more likely than unhappy people to prefer healthy food alternatives (e.g. grapes) over unhealthy ones (e.g. M&Ms) when given the choice. But then he goes on to argue for causality in the other direction (FV intake -> happiness) as well, based in large part on study [2]. Here is where my criticism comes in. In [2], researchers tracked (via an internet questionnaire) the FV intake and mood of nearly 300 young adults (avg. age of 20), for three weeks. Affect was gauged each day by having them rate how closely their current mood matched each of 9 positive and 9 negative adjectives (e.g. relaxed, excited, happy, ... vs. depressed, anxious, sad, ...) on a 1-5 scale. The self-rated scores for the positive (and negative) adjectives were averaged together to form a positive (and negative) affect score for each subject each day. These details will be important below, in case you are wondering why I'm going into so much detail... What they found was that higher reported FV intake on a given day was associated with a better mood on the same day. No surprise there, but also no insight as to causality. To try to get at causality, they then looked at FV intake on one day vs. mood on the next day, and visa versa - mood on one day vs. FV intake on the next day. What the found was that FV intake on one day predicted better mood on the next day, but better mood on one day didn't predict more FV intake on the next. So case closed right? Doesn't this tells us that it is FV intake that causes (future) happiness? That's (more or less) Dr. Greger's conclusion. But the key comes in the last few seconds of the video, when Dr. Greger says: How many fruits and vegetables [to increase happiness]? Seems we need to consume approximately 7.2 daily servings of fruit or 8.2 servings of vegetables to notice a meaningful change. So what does that somewhat ambiguous last statement actually mean, and how does it relate to the findings in the rest of the paper? That last statement is based on this sentence from [2]: Because the typical daily consumption in our sample was 1.7 servings of fruit and 2.5 servings of vegetables, our data suggest that young adults would need to consume approximately 7.2 daily servings of fruit or 8.2 servings of vegetables to notice a meaningful change in positive affect. In other words, because of the small size of the effect, the researchers found that a person would need to eat about 5.5 extra servings of FVs per day relative to their normal intake to experience a "meaningful change" in happiness level. What do they consider a "meaningful change"? Here is the footnote from the paper on their definition: A meaningful change in positive affect was defined as an increase in 0.16 points (i.e., increasing from the mean of 2.59 –> 2.75 points on the positive affect scale). A change of 0.16 points reflects a Cohen’s d of 0.20, a small effect, which was computed by the formula 0.20 = (2.75–2.59)/0.80, where 0.80 equals the average within-person standard deviation in positive affect. So they're defining a "meaningful change" as going from 2.59 to 2.75 on a 1-5 scale. Now if you ask me, that is a pretty tiny improvement from eating an extra 5.5 helpings of FVs. I looked up the Cohen's d measure they used a metric for effects size. Interesting statistical stuff. It seems like in the same way statisticians have agreed that P < 0.05 in a student t-test is 'significant', they've also (sorta supposedly) agreed on a definition for 'small', 'medium' and 'large' effects based on this "Cohen's d" metric. The authors of [2] equated a "meaningful change" with a "small effect" as measured by Cohen's d, which is basically defined as a change in a variable by 25% of one standard deviation in its data. Below is a helpful graphic to give you a feel for what that kind of "meaningful change" would really look like: Imagine the dark grey gaussian represents the distribution of a single individual's happiness over time on a 1-5 scale - most days they felt a middling amount of happiness, but on a smaller number of days they were happier, and on a smaller number of days they were sadder. The extreme tails would represent the (very rare) best and worst days of their life. Hence the gaussian distribution. The "meaningful change" the authors are postulating that would result from eating an additional 5.5 servings of FVs per day equates to shifting the happiness gaussian from the dark grey rightward to the light blue gaussian. I may be a curmudgeon, and you can judge for yourself, but to me this seems like a pretty small shift in happiness as a result of eating a whole lot more fruits and vegetables. So while Dr. Greger's portrayal of the relationship between FV intake and happiness isn't incorrect per se, he may be tilting the interpretation of the data in favor of fruits and vegetables, sort of like the authors of the apples and mortality study may have done in favor of apples. This perspective appears to be shared by the authors of [2], as reflected in the title they gave to their paper (my emphasis): "Many apples a day keep the blues away - ..." And to their credit (the authors of [2] that is, not Dr. Greger), they do say in the discussion that they agree with the authors of the review article [3], which observed that double-blind, randomized control trials are needed to definitively determine if eating more FVs really does indeed lead to improvements in mood: Of course, inferences about causality should be considered tentative until replicated with an experiment. Although our design allowed us to conduct lagged analyses, and these analyses suggested that fruit and vegetable consumption might be influencing positive affect, we agree that future research needs to include randomized controlled trials (RCTs) evaluating the influence of high fruit and vegetable intake on affect and well-being [3]. Sadly, Dr. Greger doesn't mention the randomized trials of FV intake and mood that have been done. Although small and not double (or single) blinded, this one [4] was encouraging. It found that, among 100 students randomly assigned to eat either a piece of fruit or a serving of "chocolate/crisps" each afternoon for 10 days, the fruit-eaters reported a better mood at the end of the study. But in truly double-blind randomized control trials of various fruit juices (i.e. blueberry [5], cranberry [6] and grape [7] juice), the effect of fruit juice intake on mood was at best small and non-significant [5], or missing altogether [6][7]. This is yet another example of where careful reading of the whole published paper, and looking at its results in the context of other research findings, is important for getting a more complete understanding of the research... --Dean ----------- [1] Fedorikhin, Alexander and Patrick, Vanessa M., Positive Mood and Resistance to Temptation: The Interfering Influence of Elevated Arousal (2010). Journal of Consumer Research, Vol. 37, No. 4, 2010. Available at SSRN: http://ssrn.com/abstract=2086834 ----------- [2] Br J Health Psychol. 2013 Nov;18(4):782-98. doi: 10.1111/bjhp.12021. Epub 2013 Jan 24. Many apples a day keep the blues away--daily experiences of negative and positive affect and food consumption in young adults. White BA(1), Horwath CC, Conner TS. Full text: http://sci-hub.io/10.1111/bjhp.12021 OBJECTIVES: Prior research has focused on the association between negative affect and eating behaviour, often utilizing laboratory or cross-sectional study designs. These studies have inherent limitations, and the association between positive affect and eating behaviour remains relatively unexplored. Therefore, the objective of this study was to investigate the bidirectional relationships between daily negative and positive affective experiences and food consumption in a naturalistic setting among healthy young adults. DESIGN: Daily diary study across 21 days (microlongitudinal, correlational design). METHODS: A total of 281 young adults with a mean age of 19.9 (± 1.2) years completed an Internet-based daily diary for 21 consecutive days. Each day they reported their negative and positive affect, and their consumption of five specific foods. Hierarchical linear modelling was used to test same-day associations between daily affect and food consumption, and next-day (lagged) associations to determine directionality. Moderating effects of BMI and gender were also examined in exploratory analyses. RESULTS: Analyses of same-day within-person associations revealed that on days when young adults experienced greater positive affect, they reported eating more servings of fruit (p = .002) and vegetables (p < .001). Results of lagged analysis showed that fruits and vegetables predicted improvements in positive affect the next day, suggesting that healthy foods were driving affective experiences and not vice versa. Meaningful changes in positive affect were observed with the daily consumption of approximately 7-8 servings of fruit or vegetables. CONCLUSIONS: Eating fruit and vegetables may promote emotional well-being among healthy young adults. PMID: 23347122 --------------- [3] Blanchflower, D., Oswald, A., & Stewart-Brown, S. (2012). Is psychological well-being linked to the consumption of fruit and vegetables? Social Indicators Research. Advance online publication. doi:10.1007/s11205-012-0173-y. Free full text: Abstract Humans run on a fuel called food. Yet economists and other social scientists rarely study what people eat. We provide simple evidence consistent with the existence of a link between the consumption of fruit and vegetables and high well-being. In crosssectional data, happiness and mental health rise in an approximately dose-response way with the number of daily portions of fruit and vegetables. The pattern is remarkably robust to adjustment for a large number of other demographic, social and economic variables. Well-being peaks at approximately 7 portions per day. We document this relationship in three data sets, covering approximately 80,000 randomly selected British individuals, and for seven measures of well-being (life satisfaction, WEMWBS mental well-being, GHQ mental disorders, self-reported health, happiness, nervousness, and feeling low). Reverse causality and problems of confounding remain possible. We discuss the strengths and weaknesses of our analysis, how government policy-makers might wish to react to it, and what kinds of further research -- especially randomized trials -- would be valuable. ------------ [4] Front Nutr. 2014 Jul 16;1:10. doi: 10.3389/fnut.2014.00010. eCollection 2014. Positive effects of a healthy snack (fruit) versus an unhealthy snack (chocolate/crisps) on subjective reports of mental and physical health: a preliminary intervention study. Smith AP(1), Rogers R(1). Author information: (1)School of Psychology, Cardiff University , Cardiff , UK. BACKGROUND/AIMS: Recent research has shown associations between type of snack and wellbeing. These studies have been cross-sectional and the aim of the present research was to examine this topic using an intervention study. METHODS: A between-subjects intervention study was carried out. Volunteers (100 students, mean age = 19.00 years; 27 male, 73 female) completed online questionnaires measuring anxiety and depression, fatigue, somatic symptoms, cognitive difficulties, and distress at baseline. They were then randomly assigned to one of two snacking conditions - chocolate/crisps or fruit. Volunteers consumed one snack item in the mid-afternoon each day for 10 days. At the end of the intervention, the volunteers completed the questionnaires again. RESULTS: Analyses of the baseline data confirmed that consumption of chocolate was associated with greater emotional eating and depression. Analyses of covariance, with the baseline data as covariates, were carried out on the post-intervention responses. The results showed that consumption of fruit was associated with lower anxiety, depression, and emotional distress than consumption of crisps/chocolate. Similarly, scores for somatic symptoms, cognitive difficulties, and fatigue were greater in the crisps/chocolate condition. CONCLUSION: These results extend findings from cross-sectional studies and give a clearer indication of causal effects of different types of snacks on wellbeing. PMCID: PMC4428353 PMID: 25988113 ------------ [5] J Agric Food Chem. 2010 Apr 14;58(7):3996-4000. doi: 10.1021/jf9029332. Blueberry supplementation improves memory in older adults. Krikorian R(1), Shidler MD, Nash TA, Kalt W, Vinqvist-Tymchuk MR, Shukitt-Hale B, Joseph JA. Author information: (1)Department of Psychiatry, University of Cincinnati Academic Health Center, Cincinnati, Ohio 45267-0559, USA. robert.krikorian@uc.edu The prevalence of dementia is increasing with expansion of the older adult population. In the absence of effective therapy, preventive approaches are essential to address this public health problem. Blueberries contain polyphenolic compounds, most prominently anthocyanins, which have antioxidant and anti-inflammatory effects. In addition, anthocyanins have been associated with increased neuronal signaling in brain centers, mediating memory function as well as improved glucose disposal, benefits that would be expected to mitigate neurodegeneration. This study investigated the effects of daily consumption of wild blueberry juice in a sample of nine older adults with early memory changes. At 12 weeks, improved paired associate learning (p = 0.009) and word list recall (p = 0.04) were observed. In addition, there were trends suggesting reduced depressive symptoms (p = 0.08) and lower glucose levels (p = 0.10). We also compared the memory performances of the blueberry subjects with a demographically matched sample who consumed a berry placebo beverage in a companion trial of identical design and observed comparable results for paired associate learning. The findings of this preliminary study suggest that moderate-term blueberry supplementation can confer neurocognitive benefit and establish a basis for more comprehensive human trials to study preventive potential and neuronal mechanisms. PMCID: PMC2850944 PMID: 20047325 -------- [6] J Altern Complement Med. 2005 Apr;11(2):305-9. A double-blinded, placebo-controlled, randomized trial of the neuropsychologic efficacy of cranberry juice in a sample of cognitively intact older adults: pilot study findings. Crews WD Jr(1), Harrison DW, Griffin ML, Addison K, Yount AM, Giovenco MA, Hazell J. Author information: (1)Virginia Polytechnic Institute and State University, Blacksburg, Virginia, USA. wdcrewsjr@aol.com OBJECTIVES: The aim of this research was to conduct the first known clinical trial of the short-term (i.e., 6 weeks) efficacy of cranberry juice on the neuropsychologic functioning of cognitively intact older adults. PARTICIPANTS: Fifty (50) community-dwelling, cognitively intact volunteers, > or = 60 years old, who reported no history of dementia or significant neurocognitive impairments, participated in this study. DESIGN: A 6-week, double-blind, placebo-controlled, randomized, parallel-group, clinical trial was utilized. Participants were randomly assigned to receive either 32 ounces/day of a beverage containing 27% cranberry juice per volume (n = 25) or placebo (n = 25) for 6 weeks, and administered a series of neuropsychologic tests at both pretreatment baseline and again after 6 weeks of either cranberry juice or placebo treatment to assess treatment-related changes. OUTCOME MEASURES: Efficacy measures consisted of participants' raw scores on the following standardized neuropsychologic tests: Selective Reminding Test, Wechsler Memory Scale-III Faces I and Faces II subtests, Trail Making Test (Parts A and B), Stroop Color and Word Test, and the Wechsler Adult Intelligence Scale- III Digit Symbol-Coding subtest. A subjective Follow-up Self-report Questionnaire was also administered to participants at the conclusion of the end-of-treatment phase assessments. RESULTS: Two-factor, mixed analyses of variance (ANOVA) revealed no significant group (cranberry juice and placebo) by trial (pretreatment baseline and end-of-treatment assessments) interactions across all of the neuropsychologic tests and measures utilized in this study when a Bonferroni corrected alpha level was used to correct for multiple comparisons (i.e., .05/17 group by trial comparisons = .003). Pearson Chi-Square analyses of the groups' self-reported changes over the 6-week treatment phase in their abilities to remember, thinking processes, moods, energy levels, and overall health on the Follow-up Self-report Questionnaire revealed no significant relationships. However, a nonsignificant trend (X2(1) = 2.373, p = 0.123) was noted for participants' self-reported overall abilities to remember from pretreatment baseline to the end-of-treatment assessment. Specifically, more than twice as many participants in the cranberry group (n = 9, 37.5%) rated their overall abilities to remember by treatment end as "improved" as compared to placebo controls (n = 4, 17.4%). CONCLUSIONS: Taken together, no significant interactions were found between the cranberry and placebo groups and their pretreatment baseline and end-of-treatment phase (after 6 weeks) standardized neuropsychologic assessments. A nonsignificant trend was noted, however, on a subjective, self-report questionnaire where twice as many participants in the cranberry group rated their overall abilities to remember by treatment end as "improved" compared to placebo controls. PMID: 15865497 ----------- [7] Br J Nutr. 2010 Mar;103(5):730-4. doi: 10.1017/S0007114509992364. Epub 2009 Dec 23. Concord grape juice supplementation improves memory function in older adults with mild cognitive impairment. Krikorian R(1), Nash TA, Shidler MD, Shukitt-Hale B, Joseph JA. Author information: (1)Department of Psychiatry, University of Cincinnati Academic Health Center, Cincinnati, OH, USA. robert.krikorian@uc.edu Concord grape juice contains polyphenol compounds, which have antioxidant and anti-inflammatory properties and influence neuronal signalling. Concord grape juice supplementation has been shown to reduce inflammation, blood pressure and vascular pathology in individuals with CVD, and consumption of such flavonoid-containing foods is associated with a reduced risk for dementia. In addition, preliminary animal data have indicated improvement in memory and motor function with grape juice supplementation, suggesting potential for cognitive benefit in ageing humans. In this initial investigation of neurocognitive effects, we enrolled twelve older adults with memory decline but not dementia in a randomised, placebo-controlled, double-blind trial with Concord grape juice supplementation for 12 weeks. We observed significant improvement in a measure of verbal learning and non-significant enhancement of verbal and spatial recall. There was no appreciable effect of the intervention on depressive symptoms and no effect on weight or waist circumference. A small increase in fasting insulin was observed for those consuming grape juice. These preliminary findings suggest that supplementation with Concord grape juice may enhance cognitive function for older adults with early memory decline and establish a basis for more comprehensive investigations to evaluate potential benefit and assess mechanisms of action. PMID: 20028599
  3. All, Dr. Greger has another interesting video out today (embedded below) on the benefits of vinegar (diluted acetic acid). Adding a tablespoon or so of vinegar to meals reduces the post-meal spikes in glucose, insulin and triglycerides. I've included his references (with links to the Pubmed abstracts) at the bottom. The fact that I add a little more than a tablespoon of (cider) vinegar to my salad dressing may explain in part how my glucose remains below 125 mg/dl despite eating so many calories in a single big meal per day. --Dean Dr. Greger Vinegar Video References: J B Kohn. Is vinegar an effective treatment for glycemic control or weight loss? J Acad Nutr Diet. 2015 Jul;115(7):1188. P Mitrou, E Petsiou, E Papakonstantinou, E Maratou, V Lambadiari, P Dimitriadis, F Spanoudi, S A Raptis, G Dimitriadis. Vinegar Consumption Increases Insulin-Stimulated Glucose Uptake by the Forearm Muscle in Humans with Type 2 Diabetes. J Diabetes Res. 2015;2015:175204. T Kondo, M Kishi, T Fushimi, S Ugajin, T Kaga. Vinegar intake reduces body weight, body fat mass, and serum triglyceride levels in obese Japanese subjects. Biosci Biotechnol Biochem. 2009 Aug;73(8):1837-43. J H O'Keefe, N M Gheewala, J O O'Keefe. Dietary strategies for improving post-prandial glucose, lipids, inflammation, and cardiovascular health. J Am Coll Cardiol. 2008 Jan 22;51(3):249-55. C S Johnston, A J Buller. Vinegar and peanut products as complementary foods to reduce postprandial glycemia. J Am Diet Assoc. 2005 Dec;105(12):1939-42. K Ebihara, A Nakajima. Effect of acetic acid and vinegar on blood glucose and insulin responses to orally administered sucrose and starch. May 1988. C J Panetta, Y C Jonk, A C Shapiro. Prospective randomized clinical trial evaluating the impact of vinegar on lipids in non-diabetics. World J. Cardiovas. Dis. 3, 191-196. 2013. J L Chiasson, R G Josse, R Gomis, M Hanefeld, A Karasik, M Laakso; STOP-NIDDM Trail Research Group. Acarbose for prevention of type 2 diabetes mellitus: the STOP-NIDDM randomised trial. Lancet. 2002 Jun 15;359(9323):2072-7. M Naissides, J C Mamo, A P James, S Pal. The effect of acute red wine polyphenol consumption on postprandial lipaemia in postmenopausal women. Atherosclerosis. 2004 Dec;177(2):401-8. M Hanefeld, J L Chiasson, C Koehler, E Henkel, F Schaper, T Temelkova-Kurktschiev. Acarbose slows progression of intima-media thickness of the carotid arteries in subjects with impaired glucose tolerance. Stroke. 2004 May;35(5):1073-8. Epub 2004 Apr 8. J L Chiasson, R G Josse, R Gomis, M Hanefeld, A Karasik, M Laakso; STOP-NIDDM Trial Research Group. Acarbose treatment and the risk of cardiovascular disease and hypertension in patients with impaired glucose tolerance: the STOP-NIDDM trial. JAMA. 2003 Jul 23;290(4):486-94. DECODE Study Group, the European Diabetes Epidemiology Group. Glucose tolerance and cardiovascular mortality: comparison of fasting and 2-hour diagnostic criteria. Arch Intern Med. 2001 Feb 12;161(3):397-405. A M Opperman, C S Venter, W Oosthuizen, R L Thompson, H H Vorster. Meta-analysis of the health effects of using the glycaemic index in meal-planning. Br J Nutr. 2004 Sep;92(3):367-81. "Z Beheshti, Y H Chan, H S Nia, F Hajihosseini, R Nazari, M Shaabani, M T S Omran. Influence of apple cider vinegar on blood lipids. Life Science Journal 2012;9(4). T C Wascher, I Schmoelzer, A Wiegratz, M Stuehlinger, D Mueller-Wieland, J Kotzka, M Enderle. Reduction of postchallenge hyperglycaemia prevents acute endothelial dysfunction in subjects with impaired glucose tolerance. Eur J Clin Invest. 2005 Sep;35(9):551-7. G Livesey, R Taylor, H Livesey, S Liu. Is there a dose-response relation of dietary glycemic load to risk of type 2 diabetes? Meta-analysis of prospective cohort studies. Am J Clin Nutr. 2013 Mar;97(3):584-96. J I Mann, L Te Morenga. Diet and diabetes revisited, yet again. Am J Clin Nutr. 2013 Mar;97(3):453-4. J Fan, Y Song, Y Wang, R Hui, W Zhang. Dietary glycemic index, glycemic load, and risk of coronary heart disease, stroke, and stroke mortality: a systematic review with meta-analysis. PLoS One. 2012;7(12):e52182. S H Holt, J C Miller, P Petocz. An insulin index of foods: the insulin demand generated by 1000-kJ portions of common foods. Am J Clin Nutr. 1997 Nov;66(5):1264-76. E A Gale. Lessons from the glitazones: a story of drug development. Lancet. 2001 Jun 9;357(9271):1870-5.
  4. In his latest video (embedded below), everyone's favorite ☺ nutrition expert, Dr. Michael Greger talks about a topic near and dear to my own heart - dietary diversity when it comes to plant foods. He cites several studies including [1] which found different specific fruits and vegetables were protective against the development of cancer in different regions of the colon (i.e. proximal vs. distal). Study [2] found variety of fruits & vegetables consumed (independent of quantity) was associated with reduced risk of lung cancer in smokers. But study [3] was perhaps the most interesting. Researchers followed 7000 people for 11 years to see how their reported (via 7-day food diary) dietary quantity and variety of fruits and vegetables correlated with the development of type 2 diabetes (T2D). They found eating more quantity of F&V was associated with a 21% reduced risk of subsequent T2D. But eating a greater variety of F&V trumped the benefits of quantity - being associated with a 39% reduction in subsequent risk of T2D. Every different kind of F&V a person ate per week was associated with a 4% reduction in T2D. Since I eat almost 50 different F&Vs at every meal, I should have low enough risk to protect both me and anyone standing nearby☺. Dr. G. points to the fact that the body appears to have receptors specifically (and perhaps serendipitously?) tuned to bind with specific phytochemicals in different fruits & vegetables, as an explanation for why eating a greater variety of F&V conveys health benefits. He doesn't mention the other important motivation in my book for eating a wide variety of fruits, vegetables, and other healthy plant foods. Namely, you minimize the risk of detrimental effects from eating too much of any one of them, be it a result of pesticides, contaminants, or unknown anti-nutrients. --Dean -------------- [1] J Am Diet Assoc. 2011 Oct;111(10):1479-90. doi: 10.1016/j.jada.2011.07.008. Fruit and vegetable consumption and the risk of proximal colon, distal colon, and rectal cancers in a case-control study in Western Australia. Annema N(1), Heyworth JS, McNaughton SA, Iacopetta B, Fritschi L. Author information: (1)Western Australian Institute for Medical Research, Australia. Comment in J Am Diet Assoc. 2011 Oct;111(10):1476-8. J Am Diet Assoc. 2011 Oct;111(10):1472-5. J Acad Nutr Diet. 2012 May;112(5):610; author reply 610-1. BACKGROUND: Fruits and vegetables (F/V) have been examined extensively in nutrition research in relation to colorectal cancer (CRC). However, their protective effect is subject to debate, possibly because of different effects on different subsites of the large bowel. OBJECTIVE: To determine whether any association between F/V consumption and risk of CRC differed by subsite of the bowel (proximal colon, distal colon, and rectum). DESIGN: The Western Australian Bowel Health Study is a population-based, case-control study conducted between June 2005 and August 2007. Complete food frequency questionnaire data were analysed from 834 CRC cases and 939 controls. Logistic regression analysis was used to estimate the effects of quartiles of F/V intake on risk of CRC at different subsites. Odds ratios (OR) and 95% confidence intervals (CI) were calculated for CRC overall and for the three separate subsites. RESULTS: Risk of proximal colon cancer and rectal cancer was not associated with intakes of total F/V, total vegetable, or total fruit. Brassica vegetable intake was inversely related with proximal colon cancer (Q4 vs Q1 OR 0.62; 95% CI 0.41 to 0.93). For distal colon cancer, significant negative trends were seen for total F/V, and total vegetable intake. Distal colon cancer risk was significantly decreased for intake of dark yellow vegetables (Q4 vs Q1 OR 0.61; 95% CI 0.41 to 0.92) and apples (Q4 vs Q1 OR 0.51; 95% CI 0.34 to 0.77). An increased risk for CRC was found to be associated with intake of fruit juice (Q4 vs Q1 OR 1.74; 95% CI 1.24 to 2.45). CONCLUSIONS: Our results suggest that different F/V may confer different risks for cancer of the proximal colon, distal colon, or rectum. Future studies might consider taking into account the location of the tumor when examining the relation between F/V consumption and risk of CRC. Copyright © 2011 American Dietetic Association. Published by Elsevier Inc. All rights reserved. PMID: 21963014 --------- [2] Cancer Epidemiol Biomarkers Prev. 2010 Sep;19(9):2278-86. doi: 10.1158/1055-9965.EPI-10-0489. Epub 2010 Aug 31. Variety in fruit and vegetable consumption and the risk of lung cancer in the European prospective investigation into cancer and nutrition. Büchner FL(1), Bueno-de-Mesquita HB, Ros MM, Overvad K, Dahm CC, Hansen L, Tjønneland A, Clavel-Chapelon F, Boutron-Ruault MC, Touillaud M, Kaaks R, Rohrmann S, Boeing H, Nöthlings U, Trichopoulou A, Zylis D, Dilis V, Palli D, Sieri S, Vineis P, Tumino R, Panico S, Peeters PH, van Gils CH, Lund E, Gram IT, Braaten T, Sánchez MJ, Agudo A, Larrañaga N, Ardanaz E, Navarro C, Argüelles MV, Manjer J, Wirfält E, Hallmans G, Rasmuson T, Key TJ, Khaw KT, Wareham N, Slimani N, Vergnaud AC, Xun WW, Kiemeney LA, Riboli E. Author information: (1)National Institute ofPublicHealth and the Environment, Bilthoven, The Netherlands. frederike.buchner@rivm.nl BACKGROUND: We investigated whether a varied consumption of vegetables and fruits is associated with lower lung cancer risk in the European Prospective Investigation into Cancer and Nutrition study. METHODS: After a mean follow-up of 8.7 years, 1,613 of 452,187 participants with complete information were diagnosed with lung cancer. Diet diversity scores (DDS) were used to quantify the variety in fruit and vegetable consumption. Multivariable proportional hazards models were used to assess the associations between DDS and lung cancer risk. All models were adjusted for smoking behavior and the total consumption of fruit and vegetables. RESULTS: With increasing variety in vegetable subgroups, risk of lung cancer decreases [hazard ratios (HR), 0.77; 95% confidence interval (CI), 0.64-0.94 highest versus lowest quartile; P trend = 0.02]. This inverse association is restricted to current smokers (HR, 0.73; 95% CI, 0.57-0.93 highest versus lowest quartile; P trend = 0.03). In continuous analyses, in current smokers, lower risks were observed for squamous cell carcinomas with more variety in fruit and vegetable products combined (HR/two products, 0.88; 95% CI, 0.82-0.95), vegetable subgroups (HR/subgroup, 0.88; 95% CI, 0.79-0.97), vegetable products (HR/two products, 0.87; 95% CI, 0.79-0.96), and fruit products (HR/two products, 0.84; 95% CI, 0.72-0.97). CONCLUSION: Variety in vegetable consumption was inversely associated with lung cancer risk among current smokers. Risk of squamous cell carcinomas was reduced with increasing variety in fruit and/or vegetable consumption, which was mainly driven by the effect in current smokers. IMPACT: Independent from quantity of consumption, variety in fruit and vegetable consumption may decrease lung cancer risk. ©2010 AACR. PMID: 20807832 ------------- [3] Diabetes Care. 2012 Jun;35(6):1293-300. doi: 10.2337/dc11-2388. Epub 2012 Apr 3. A prospective study of the association between quantity and variety of fruit and vegetable intake and incident type 2 diabetes. Cooper AJ(1), Sharp SJ, Lentjes MA, Luben RN, Khaw KT, Wareham NJ, Forouhi NG. Author information: (1)MRCEpidemiology Unit, Institute of Metabolic Science, Addenbrooke’s Hospital, Cambridge, U.K. OBJECTIVE: The association between quantity of fruit and vegetable (F&V) intake and risk of type 2 diabetes (T2D) is not clear, and the relationship with variety of intake is unknown. The current study examined the association of both quantity and variety of F&V intake and risk of T2D. RESEARCH DESIGN AND METHODS: We examined the 11-year incidence of T2D in relation to quantity and variety of fruit, vegetables, and combined F&V intake in a case-cohort study of 3,704 participants (n = 653 diabetes cases) nested within the European Prospective Investigation into Cancer and Nutrition-Norfolk study, who completed 7-day prospective food diaries. Variety of intake was derived from the total number of different items consumed in a 1-week period. Multivariable, Prentice-weighted Cox regression was used to estimate hazard ratios (HRs) and 95% CIs. RESULTS: A greater quantity of combined F&V intake was associated with 21% lower hazard of T2D (HR 0.79 [95% CI 0.62-1.00]) comparing extreme tertiles, in adjusted analyses including variety. Separately, quantity of vegetable intake (0.76 [0.60-0.97]), but not fruit, was inversely associated with T2D in adjusted analysis. Greater variety in fruit (0.70 [0.53-0.91]), vegetable (0.77 [0.61-0.98]), and combined F&V (0.61 [0.48-0.78]) intake was associated with a lower hazard of T2D, independent of known confounders and quantity of intake comparing extreme tertiles. CONCLUSIONS: These findings suggest that a diet characterized by a greater quantity of vegetables and a greater variety of both F&V intake is associated with a reduced risk of T2D. PMCID: PMC3357245 PMID: 22474042
  5. All, In today's video (embedded below), Dr. Greger highlights an ex vivo study [1] of almond consumption and bone health, which I thought was pretty cool and promising, despite it being sponsored by the Almond Board of California. Ex vivo you say? I've heard of in vivo and in vitro, but what is ex vivo? It's when you treat a subject, in this case by feeding them a handful of almonds, wait a few hours, and then draw some of their blood in order to drip it on something outside the body (e.g. cancer cells) to see how the cells reacts (hence ex vivo - latin for "outside the living"). In this case they took the blood of almond-consuming subjects and dripped it on osteoclast cells, the cells in our bones whose job it is to break down bone cells, and whose activity is an important contributor to osteoporosis. They found osteoclast proliferation and activity was markedly reduced (a good thing) by the blood of the almond consumers relative to the blood of controls, suggesting almonds should have a positive effect on maintaining bone health by reducing bone tissue breakdown. This jibes with at least one population study [2], which found almonds to be one of foods associated with reduced osteoporosis. As we all know, the problems with population studies are many, including relying of dubious food frequency questionnaires, and being confounded by many lifestyle differences between the participants that could have been responsible for the observed effect (reduced osteoporosis), rather than the almonds. The sort of ex vivo experiment done in [1] gets the best of both worlds. It has the advantage of studying real people eating and importantly, digesting and assimilating known reasonable quantities of real whole foods, rather than just dripping purified almond extracts directly onto osteoclasts in a petri dish. But at the same time it allows researchers to look at the details of the mechanisms involved, without invasive procedures, which in this case would have entailed a dangerous and painful bone marrow biopsy, which no IRB would allow in a human study. Anyway, pretty cool, and seemingly reasonable evidence that almonds (and probably other nuts) may be beneficial for preventing bone loss. --Dean --------- [1] Metabolism. 2011 Jul;60(7):923-9. doi: 10.1016/j.metabol.2010.08.012. Epub 2010 Oct 13. Postprandial effects of almond consumption on human osteoclast precursors--an ex vivo study. Platt ID(1), Josse AR, Kendall CW, Jenkins DJ, El-Sohemy A. Author information: (1)Department of Nutritional Sciences, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada. Consumption of almonds has been associated with increased bone mineral density, but the direct effects of almonds on bone cells are not known. We determined whether serum obtained following the consumption of a meal containing 60 g of almonds affects human osteoclast formation, function, and gene expression in vitro. Human osteoclast precursors were cultured in medium containing 10% serum obtained from 14 healthy subjects at baseline and 4 hours following the consumption of 3 test meals containing almonds, potatoes, and rice and balanced for macronutrient composition. Osteoclast formation was determined by the number of tartrate-resistant acid phosphatase (TRAP)(+) multinucleated cells, and osteoclast function was assessed by measuring TRAP activity in the culture medium and calcium released from OsteoAssay (Lonza Walkersville, Walkersville, MD, USA) plates. The expression of cathepsin K, receptor activator of nuclear factor kB, and matrix metalloproteinase-9 genes was measured by real-time reverse transcriptase-polymerase chain reaction. Compared with serum obtained at baseline, serum obtained 4 hours following the consumption of the almond meal reduced osteoclast formation by approximately 20%, TRAP activity by approximately 15%, calcium release by approximately 65%, and the expression of cathepsin K, receptor activator of nuclear factor kB, and matrix metalloproteinase-9 by 13% to 23%. No effects were observed with serum obtained from the other test meals. Serum obtained 4 hours following the consumption of an almond meal inhibits osteoclast formation, function, and gene expression in cultured human osteoclast precursors, and provides evidence for a positive effect of almonds on bone health. Copyright © 2011 Elsevier Inc. All rights reserved. PMID: 20947104 ------------- [2] BMC Musculoskelet Disord. 2008 Feb 27;9:28. doi: 10.1186/1471-2474-9-28. The assessment of osteoporosis risk factors in Iranian women compared with Indian women. Keramat A(1), Patwardhan B, Larijani B, Chopra A, Mithal A, Chakravarty D, Adibi H, Khosravi A. Author information: (1)Shahroud University of Medical Sciences, Hafte Tir Avenue, Shahroud, Iran. keramat1@yahoo.com BACKGROUND: Osteoporosis is an important public health problem in older adults. It is more common in postmenopausal women and not only gives rise to morbidity but also markedly diminishes the quality of life in this population. There is lack of information about the risk factor of osteoporosis in developing countries. In this study we aimed to assess the risk factors for osteoporosis in postmenopausal women from selected BMD centers of two developing Asian countries (Iran and India). METHODS: This study is a multicenter interview-based study conducted in selected hospitals and health centers from urban areas in Iran and India. The case group included postmenopausal osteoporotic women who were identified as patients with bone density higher than 2.5 SD below average of young normal bone density (in L1-L4) spine region interest and/or total femoral region) by using DEXA method. The controls were chosen from postmenopausal women with normal bone density (in L1-L4 spine and total femoral regions using DEXA method) matching in age groups was strategy of choice.The sample sizes included from Iran a total of 363 subjects (178 osteoporotic and 185 normal) and from India a total of 354 subjects (203 osteoporotic and 151 normal). RESULTS: The significant (p < 0.05) risk factors in present study population with their Odds Ratios (in parenthesis, respectively in Iran and India) were as follow:Lower education defined as less than class 12 or nil college (2.1) (2.7), duration of menopause greater than 5 years: (2.2) (1.4), Menarche age (after 14 years): (1.9) (1.6), Menopause age (before 45 years): (1.1) (2), Parity more than 3: (1.1) (1), Bone and joint problem (2.3) (2.2). Calcium supplementation (0.6) and HRT (0.4) were shown as protective factors and steroid therapy (3.3) was found as a risk factor in Iran. Calcium supplementation more than 1 year (0.3) was shown as a protective factor in India.Pure vegetarianism: (2.2) and Red meat consumption more than 4 times per week (1.4) was shown as a risk factor in Indian and Iranian subjects respectively. Regular consumption of Soya (0.3), almond (0.5), fish (0.5), fruits (0.4) and milk tea 4 cups per day and more (0.4) appeared to be significant protective factors in India. Regular consumption of cheese (0.5), milk (0.5), chicken (0.4), egg (0.6), fruit (0.4), tea 7 cups per day and more (0.3) were found to be significant protective factors in Iran. Exercises were shown as protective factor in Iran (0.4) and India (0.4). There were no significant differences in association of risk factors and osteoporosis between Iranian and Indian subjects. CONCLUSION: Osteoporosis in Iranian and Indian subjects also appears to be associated with several known risk factors that well described in the literature. There were no significant differences in association of risk factors and osteoporosis between Iranian and Indian subjects. It was shown a protective role of certain nutritional dietary components and also exercises in both populations and can be exploited in preventive educational strategies on osteoporosis in these populations. PMCID: PMC2289820 PMID: 18304358
  6. For those Dr. Greger fans out there , his new book How Not to Die comes out today. He posted a video today about the book. It sounds really good, and I've requested the first copy from my local public library when it becomes available. At 50min, he talks about dietary cholesterol and heart disease, and the tactics the egg industry uses to obscure the link - e.g. exploiting the "saturation effect" on cholesterol intake. Apparently in the first half of the book he addresses the science of how to avoid dying from the 15 leading killers (heart disease, various cancers, etc.) through diet, nutrition and exercise. In the second half, he pulls it all together into specific recommendations about what to eat and what not to eat to stay healthy. He presents the concept of the Daily Dozen, the 12 foods he tries to eat every day, and how many servings of each. I screen captured this frame from the video, which is figure from the book, that appears to summarize his Daily Dozen: He appears to be covering all the usual suspects that most of us CR practitioners try to eat / drink every day. In the "beverages" category I presume from his videos he means tea and/or coffee. Its interesting that "flaxseeds" is the only food he calls out specifically, and separately from the "Nuts & Seeds" category which he also includes. He was on one of my favorite podcasts (Rich Roll Podcast) today as well discussing the book. Here is the link to the episode. He talks about confirmation bias @ 23min - a topic many here criticize him about. Frankly he doesn't say much, except you've got to be an unbiased follower of the science. He gives an anecdote @25min where he changed his mind and his recommendations based on recent science - that of the danger of lead in tea leaves, particularly coming from China where they apparently only recently got rid of leaded gasoline. He says this isn't a problem if you are brewing tea leaves, since the lead stays with the leaves - supporting my similar conclusion about brewing cacao to avoid the heavy metal contaminants in chocolate products. But he says up until recently he was recommending putting the tea leaves in smoothies - figuring by throwing out the leaves you're losing some of the plant goodness. He's changed his tune on this, and now recommends brewing tea and discarding the leaves. At 50min, he talks about the link between dietary cholesterol, serum cholesterol and cardiovascular disease, and the tactics the egg industry uses to obscure the linkage - e.g. exploiting the "saturation effect" for dietary cholesterol. At 53min he talks about the excitement he and the scientific community have about the gut microbiome, but doesn't talk about it in too much detail except his recent video (which we discussed here) on how our immune system interprets low butyrate levels as a sign of being under attack, thereby increasing inflammation and autoimmune reactions. At 58min he talks about organic vs. conventional. He says in terms of nutrition, organic is slightly better (e.g. 20%) for phytonutrients, but probably not worth the extra expense. He says organic may be worth it to avoid heavy metals like cadmium, which are high in conventional fertilizers, and therefore higher in conventionally grown produce. He says he recommends choosing organic whenever possible, but not to let fear prevent us from eating more plants, even conventional plants. The net benefits of extra conventional fruits/vegetables far outweighs the risk. As evidence, he quotes a modeling study that found that if everyone in the US ate one more serving of fruits/vegetables per day, it would prevent 20,000 cancer deaths, but at the same time cause 10 additional cancer deaths from the extra exposure to pesticides - so lopsided are the benefits vs. the risks. At 1:01, he talks about GMOs - saying extra use of pesticides (e.g. glyphosate / Roundup) directly on the plants is the real issue with GMO foods, and there is some legitimate concern there. At 1:09 he talks about how he sees the state of nutrition science and public health recommendations as analogous to our understanding of the effects of smoking in the mid-50s. Evidence was starting to build at that time that smoking was bad for you, but powerful forces, including the American Medical Association, were still saying smoking was good for you. See this video about the shocking historic evidence for the influence the tobacco industry had on health recommendations, and how it parallels the influence and tactics of the processed food industry today. He's optimistic that, like the tide turned on tobacco, we'll see the same thing happen with processed food. At 1:13 he talks about the cognitive dissonance doctors are experiencing around diet - eating crappy themselves prevents them from wholeheartedly endorsing healthy diets for their patients. Plus the perverse incentives of the medical / pharmaceutical industry rewards doctors for prescribing pills and procedures, rather than focusing on keeping their patients health. He hopes for growth of wellness programs sponsored by corporations to make their employees healthier and thereby saving themselves money on health insurance premiums/payouts. Whatever you say about him, you've got to admit he's sincere and passionate in his beliefs and in his determination to help people live healthier lives through improved diet. The proceeds from his book (and all his speaking engagements) go to the 501c3 non-profit that funds the NutritionFacts.org website. He now has a team of 14 people that help him conduct his research, so that's a lot of mouths to feed. --Dean
  7. 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