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  1. There’s little question that fish contain environmental pollutants such as mercury and PCBs with, generally, bigger fish such as shark and tuna containing more and smaller fish like sardines containing less. That’s been common knowledge between health researchers for a while now. The real question is whether that translates into any of the major degenerative diseases in people (such as cancer or diabetes). Well, sadly, in the case of diabetes it does appear to be the case. Here’s a great video by Dr. Michael Greger summarizing the science between diabetes risk and fish consumption: https://www.youtube.com/watch?v=I60O474F_GI As he mentioned in the video, besides the pollutants, the causal link could also very well be the oxidative stress causing n-3 fatty acid content of the fish. That obviously goes against the mainstream opinion on diet but one can certainly find smart people that would support that notion and as far as I’ve seen the research on fish oil seems to be quite mixed. P.S. Is there actually a way to embed a video on this site instead of just posting a link? Thanks.
  2. Here is an useful new study [1] (press release) for folks concerned about risk of impaired glucose tolerance, insulin insensitivity, and diabetes. It was a one-year randomized control trial of obese folks with metabolic syndrome, but not overt diabetes. Half the participants (the Reg-AGE group) ate their normal diet and used their normal cooking methods for the year. The other half (the Low AGE or L-AGE group) were told not to change what or how much they ate, but simply to use cooking techniques known to minimize the formation of Advanced Glycation End-products (AGEs). In particular, they were instructed as follows: L-AGE participants prepared their own food at home after being individually instructed on how to reduce dietary AGE intake by modifying the cooking time and temperature without changing the quantity, quality or composition of food. They were specifically instructed to avoid frying, baking or grilling, and they were encouraged to prepare their food by boiling, poaching, stewing or steaming. Below is a sample daily diet for both the Reg-AGE and the L-AGE diets. Note these are just examples given to the L-AGE subjects for how to model their own, self-selected low AGE diet. They were given phone calls twice per week from a dietitian to encourage and facilitate compliance: Based on diet questionnaire responses, compliance was good. The AGE intake was about 65% lower in the L-AGE group compared with the Reg-AGE group by the end of the study. Both groups lost a modest, nearly comparable amount of weight (1-3 lbs on average) - not enough to explain the following differences. Here are the dramatic main results, in graphical form (black bars represent the L-AGE group and the white bars represent the Reg-AGE group): As you can see from the first graph, insulin sensitivity (HOMA-IR - a measure of pancreatic β-cell function) improved, and fasting leptin and insulin dropped on the L-AGE diet. While glucose area-under-the-curve in response to an OGTT didn't improve, the second graph shows that the L-AGE group used dramatically less insulin to clear the same amount of glucose, indicating that their insulin sensitivity was much improved. The third graph shows that important markers of circulating AGEs and markers of systemic inflammation (e.g. TNFα) came down dramatically in the L-AGErs, but rose across the board in the Reg-AGE group. The opposite was true for pro-health and longevity markers like the level of SIRT1 and adiponectin - which went up in L-AGE folks by the end of the study, and stayed flat or dropped in the Reg-AGE group. The authors conclude the paper with: L-AGE [diet] is effective against insulin resistance in obese individuals with the metabolic syndrome. Here is more good color commentary by the authors from the popular press interview (my emphasis): The investigators believe that daily AGE consumption in the standard Western diet is at least three times higher than the safety limit for these oxidants. This could, in part, explain the changes seen in disease demographics. Dr. Vlassara cautioned, "Even though the AGEs pose a more immediate health threat to older adults, they are a similar danger for younger people, including pregnant women and children, and this needs to be addressed. AGEs are ubiquitous and addictive, since they provide flavor to foods. But they can be controlled through simple methods of cooking, such as keeping the heat down and the water content up in food and by avoiding pre-packaged and fast foods when possible. Doing so reduces AGE levels in the blood and helps the body restore its own defenses." Sorry to rain on your Labor Day cookouts, but you, your family and friends may want to skip the barbie (not to mention the fry pan, oven and toaster) to reduce your risk of impair glucose metabolism, insulin resistance, not to mention cancer [2]. --Dean ---------- [1] Diabetologia. 2016 Jul 29. [Epub ahead of print] Oral AGE restriction ameliorates insulin resistance in obese individuals with the metabolic syndrome: a randomised controlled trial. Vlassara H(1,)(2), Cai W(1), Tripp E(1), Pyzik R(1), Yee K(1), Goldberg L(1), Tansman L(1), Chen X(1), Mani V(3), Fayad ZA(3), Nadkarni GN(4), Striker GE(1,)(4), He JC(4), Uribarri J(5). AIMS/HYPOTHESIS: We previously reported that obese individuals with the metabolic syndrome (at risk), compared with obese individuals without the metabolic syndrome (healthy obese), have elevated serum AGEs that strongly correlate with insulin resistance, oxidative stress and inflammation. We hypothesised that a diet low in AGEs (L-AGE) would improve components of the metabolic syndrome in obese individuals, confirming high AGEs as a new risk factor for the metabolic syndrome. METHODS: A randomised 1 year trial was conducted in obese individuals with the metabolic syndrome in two parallel groups: L-AGE diet vs a regular diet, habitually high in AGEs (Reg-AGE). Participants were allocated to each group by randomisation using random permuted blocks. At baseline and at the end of the trial, we obtained anthropometric variables, blood and urine samples, and performed OGTTs and MRI measurements of visceral and subcutaneous abdominal tissue and carotid artery. Only investigators involved in laboratory determinations were blinded to dietary assignment. Effects on insulin resistance (HOMA-IR) were the primary outcome. RESULTS: Sixty-one individuals were randomised to a Reg-AGE diet and 77 to an L-AGE diet; the data of 49 and 51, respectively, were analysed at the study end in 2014. The L-AGE diet markedly improved insulin resistance; modestly decreased body weight; lowered AGEs, oxidative stress and inflammation; and enhanced the protective factors sirtuin 1, AGE receptor 1 and glyoxalase I. The Reg-AGE diet raised AGEs and markers of insulin resistance, oxidative stress and inflammation. There were no effects on MRI-assessed measurements. No side effects from the intervention were identified. HOMA-IR came down from 3.1 ± 1.8 to 1.9 ± 1.3 (p < 0.001) in the L-AGE group, while it increased from 2.9 ± 1.2 to 3.6 ± 1.7 (p < 0.002) in the Reg-AGE group. CONCLUSIONS/INTERPRETATION: L-AGE ameliorates insulin resistance in obese people with the metabolic syndrome, and may reduce the risk of type 2 diabetes, without necessitating a major reduction in adiposity. Elevated serum AGEs may be used to diagnose and treat 'at-risk' obesity. TRIAL REGISTRATION: ClinicalTrials.gov NCT01363141 FUNDING: The study was funded by the National Institute of Diabetes and Digestive and Kidney Diseases (DK091231). DOI: 10.1007/s00125-016-4053-x PMID: 27468708 ------ [2] Diabetes Metab Syndr Obes. 2015 Sep 1;8:415-26. doi: 10.2147/DMSO.S63089. eCollection 2015. Current perspectives on the health risks associated with the consumption of advanced glycation end products: recommendations for dietary management. Palimeri S(1), Palioura E(1), Diamanti-Kandarakis E(1). Author information: (1)Endocrine Unit, Medical School University of Athens, Athens, Greece. Advanced glycation end products (AGEs) constitute a complex group of compounds produced endogenously during the aging process and under conditions of hyperglycemia and oxidative stress. AGEs also have an emerging exogenous origin. Cigarette smoke and diet are the two main exogenous sources of AGEs (glycotoxins). Modern Western diets are rich in AGEs which have been implicated in the pathogenesis of several metabolic and degenerative disorders. Accumulating evidence underlies the beneficial effect of the dietary restriction of AGEs not only in animal studies but also in patients with diabetic complications and metabolic diseases. This article reviews the evidence linking dietary glycotoxins to several disorders from diabetic complications and renal failure to liver dysfunction, female reproduction, eye and cognitive disorders as well as cancer. Furthermore, strategies for AGE reduction are discussed with a focus on dietary modification. DOI: 10.2147/DMSO.S63089 PMCID: PMC4562717 PMID: 26366100
  3. All, Al's latest post about new CR paper contained a really interesting new study in rhesus monkeys [1], with potentially troubling implications for men practicing serious CR with (resulting) low testosterone. It was a study of middle-aged (~12 yo) male rhesus monkeys, making it more relevant to us than any of the rodent studies. Half the monkeys were orchidectomized ☹ to put the kibosh on their testosterone level, and the other half were subjected to mock surgery. After two months of recovery on a standard chow diet (15F / 27P / 59C) supplemented with fresh fruits & vegetables, both groups were made pudgy by shifting them for six months to a western style diet (WSD) that has a similar macronutrient profile to the diet many of us eat day-to-day (33F / 17P / 51C). Then, for 4 additional months, they calorie-restricted both groups by putting them back on the standard chow + F&V diet, but giving them only 70% of their individual baseline (pre-surgery) calorie intake (i.e. 30% CR). They intended to model in their rhesus monkeys the life history of men who undergo androgen deprivation therapy (ADT) for treatment of prostate cancer, so see if calorie-restriction could prevent the metabolic syndrome such treatment often induces in men. But while not perfect, the parallels with us CR folks are unmistakable - i.e. chronic CR resulting in the combination of reduced muscle mass and low testosterone. What they found appears to me to be pretty troubling, as I alluded to in the title and introduction. First, two months after the surgery, while still eating the standard, low-fat chow + F&V diet ad libidum, the orchidectomized (O) monkeys (OMs), but not the intact (I) monkeys (IMs) showed a decrease in lean mass. Not too surprising - lean mass drops with low testosterone. During the six-months of western-style diet (WSD), both groups gained fat. No surprise. But unlike the I monkeys, the O monkeys also lost additional lean mass and bone mass during the WSD period. Once again we see the negative effects of low-T on body composition. In short, the OMs became pretty classic examples of hypogonadal middle-aged men - pudgy, with little muscle mass and low testosterone. Now comes the interesting part - what happened as a result of 30% CR? Obviously both groups lost significant (and comparable) amount of fat mass. Both groups also lost lean mass. As a result, after the CR period both groups had returned to their relatively-lean baseline (pre-surgery) weight. But relatively to baseline, both groups had a higher percent body fat that they started with, and the O monkeys in particular had a lot less lean mass. The O monkeys also exhibited reduced bone mineral density as a result of CR, and effect not seen in the I monkeys. In short, low testosterone dropped the O monkey's lean mass and bone mass, and CR did nothing to counteract this effect - if anything it exacerbates it. But is that necessarily such a big deal? Maybe having low testosterone and reduced muscle mass after CR isn't a problem. In fact, without all that metabolically active muscle tissue, a CR practitioner could presumably eat fewer calories, and hence get more of the healthspan and lifespan benefits of CR, since "CR works by reducing Calorie intake -- period" a famous CR proponent once said. But so as to avoid getting myself into hot water yet again, I'll note that even he recognizes the importance of maintaining lean mass and bone mass via exercise while practicing CR... Obviously late-life sarcopenia and frailty is one concern some of us have about sacrificing too much muscle and bone mass to the CR gods. Unfortunately this short-term study didn't investigate the impact of these effects. But what they did find was even more germane to one of the negative side-effect that has been front and center in our discussions lately (discussed in depth here and here), namely impaired glucose tolerance (IGT). Not surprisingly, glucose tolerance (as measured by an OGTT) got worse in both I and O monkeys after eating the western diet for six months. But then, after 30% CR for four months, the I monkeys' glucose tolerance improved to the point where it was close to baseline again. In contrast, the poor, skinny, low-testosterone O monkeys, lacking much muscle mass, continued to show impaired glucose tolerance. The authors summarized their result as: CR improved these metabolic parameters [i.e. hyperinsulinemia and insulin resistance - DP] only in intact animals, whereas orchidectomized animals remained glucose-intolerant, despite a significant loss in fat mass. Put another way, CR coupled with low testosterone results in a precipitous drop in muscle mass, which led to impaired glucose tolerance. Note - the impaired metabolic health of the CR + Low-T monkeys was not a result of either differences in food intake or physical activity between the two groups - "... there was no significant group differences in these parameters under any of the dietary regimens studied." But they did observe an interesting effect of physical activity. At the end of the western diet period (i.e. pre-CR), across the entire population of monkeys, as well as within each group, monkeys that engaged in more physical activity had a lower percent fat mass (and by implication, a higher percent lean muscle mass), and exhibited better glucose metabolism, as illustrated in these two graphs showing % body fat (left) and OGTT glucose area under the curve (right), as a function of how active each of the monkeys was, as measured by a collar-worn accelerometer (Open circles = O monkeys, solid circles = I monkeys): Unfortunately, they don't report correlation between physical activity and glucose metabolism after the CR period. But given the across-the-board drop in lean mass as a result of CR that they observed, it seems likely to me that the observed relationship would still-hold, and perhaps be exaggerated, post-CR. So how do the authors interpret their results? Here are some of the key passages from the discussion section: The present study demonstrates that skeletal muscle loss in testosterone-deficient [non-human primates] correlated with the development of [insulin resistance] and glucose intolerance during the [western style diet] and CR periods. Surprisingly, there was no significant effect of testosterone deficiency on diet-induced change in fat mass, including fat gain during the WSD period and fat loss during the CR period, suggesting that insulin resistance in [low-testosterone androgen deprivation therapy] patients is related to the loss of skeletal muscle, which is the primary anatomical site responsible for glucose disposal. In other words, according to the authors: low-T (with or without CR) → reduced muscle mass → impaired glucose tolerance. Thus, testosterone may play a protective role in male physiology, while its deficiency may increase the susceptibility of males to metabolic syndrome. While this study was really meant to model men who are hypogonadal as a results of android deprivation treatment for prostate cancer, it seems to me to have potentially important implications for CR folks1, many of whom exhibit low-T, low muscle mass, and impaired glucose tolerance. The silver lining may be the observation about physical activity. By staying active (particularly after meals), and eating enough to maintaining muscle mass and avoid getting too skinny, we may be able to mask (if not altogether prevent) the negative effects of impaired glucose tolerance associated with serious CR that many of us have observed. --Dean ------- 1And Todd A in particular. ------------ [1] Int J Obes (Lond). 2016 Aug 18. doi: 10.1038/ijo.2016.148. [Epub ahead of print] Perpetuating effects of androgen deficiency on insulin-resistance. Cameron JL, Jain R, Rais M, White AE, Beer TM, Kievit P, Winters-Stone K, Messaoudi I, Varlamov O. Full text: http://sci-hub.cc/10.1038/ijo.2016.148 Abstract Background/Objectives: Androgen deprivation therapy (ADT) is commonly used for treatment of prostate cancer, but is associated with side effects such as sarcopenia and insulin resistance. The role of lifestyle factors such as diet and exercise on insulin sensitivity and body composition in testosterone-deficient males is poorly understood. The aim of the present study was to examine the relationships between androgen status, diet, and insulin sensitivity. Subjects/Methods: Middle-aged (11-12-yo) intact and orchidectomized male rhesus macaques were maintained for two months on a standard chow diet, and then exposed for six months to a Western-style, high-fat/calorie-dense diet (WSD) followed by four months of caloric restriction (CR). Body composition, insulin sensitivity, physical activity, serum cytokine levels, and adipose biopsies were evaluated before and after each dietary intervention. Results: Both intact and orchidectomized animals gained similar proportions of body fat, developed visceral and subcutaneous adipocyte hypertrophy, and became insulin resistant in response to the WSD. CR reduced body fat in both groups, but reversed insulin resistance only in intact animals. Orchidectomized animals displayed progressive sarcopenia, which persisted after the switch to CR. Androgen deficiency was associated with increased levels of interleukin- 6 and macrophage-derived chemokine (CCL22), both of which were elevated during CR. Physical activity levels showed a negative correlation with body fat and insulin sensitivity. Conclusion: Androgen deficiency exacerbated the negative metabolic side effects of the WSD, such that CR alone was not sufficient to improve altered insulin sensitivity, suggesting that ADT patients will require additional interventions to reverse insulin resistance and sarcopenia. Key words: androgen deprivation therapy, hypogonadal, Western-style diet, obesity, sarcopenia. Abbreviations: ADT, androgen-deprivation therapy, CR, caloric restriction; NHP, nonhuman primate; SM, skeletal muscle; SC, subcutaneous; VIS, visceral; WAT, white adipose tissue; WSD, Western-style diet. PMID: 27534842
  4. 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.
  5. [Note: This is my first thread on the new "General Health & Longevity" forum - thanks for making it!] Yet another study has found drinking a surprisingly large number of cups of coffee per day to be health promoting. This new study [1] in the Journal Circulation by Harvard researchers (press release, including a video, here) used epidemiological data from 74,890 women in the Nurses' Health Study, 93,054 women in the Nurses' Health Study 2, and 40,557 men in the Health Professionals Follow-up Study. Participants completed food questionnaires every four years during an average follow-up period of 22.5 years, providing researchers with coffee consumption data. There appeared to be a shallow, U-shaped mortality curve for coffee drinking, with the greatest reduction in non-smoker mortality (15%) among those who consumed 3-5 cups of coffee per day. Greater than 5 cups per day reduced all-cause mortality by slightly less (12%) when compared to never-drinkers. Both caffeinated and decaf coffee was found to reduce mortality. The causes of death that were significantly lower among coffee drinkers were cardiovascular disease, neurological diseases, and suicide. This Harvard study is in agreement with another large, epidemiological study [2] from earlier this year which found an even greater reduction in all-cause and cause-specific morality among a Japanese cohort of 90,000 people followed for 19 years. It too found a sweet spot around 3-4 cups per day, with a reduction in all-cause mortality of 24%. So once again, coffee is found to be good for you. But remember not to drink it too hot, and be sure to filter it, preferably with a paper filter. ---------- [1] Circulation November 16, 2015, Published online before print doi: 10.1161/CIRCULATIONAHA.115.017341 Association of Coffee Consumption with Total and Cause-Specific Mortality in Three Large Prospective Cohorts Ming Ding1; Ambika Satija1; Shilpa N. Bhupathiraju1; Yang Hu1; Qi Sun2; Jiali Han3; Esther Lopez-Garcia4; Walter Willett2; Rob M. van Dam5; Frank B. Hu2* Abstract Background—The association between consumption of caffeinated and decaffeinated coffee and risk of mortality remains inconclusive. Methods and Results—We examined the associations of consumption of total, caffeinated, and decaffeinated coffee with risk of subsequent total and cause-specific mortality among 74,890 women in the Nurses' Health Study (NHS), 93,054 women in the NHS 2, and 40,557 men in the Health Professionals Follow-up Study. Coffee consumption was assessed at baseline using a semi-quantitative food frequency questionnaire. During 4,690,072 person-years of follow-up, 19,524 women and 12,432 men died. Consumption of total, caffeinated, and decaffeinated coffee were non-linearly associated with mortality. Compared to non-drinkers, coffee consumption one to five cups/d was associated with lower risk of mortality, while coffee consumption more than five cups/d was not associated with risk of mortality. However, when restricting to never smokers, compared to non-drinkers, the HRs of mortality were 0.94 (0.89 to 0.99) for ≤ 1 cup/d, 0.92 (0.87 to 0.97) for 1.1-3 cups/d, 0.85 (0.79 to 0.92) for 3.1-5 cups/d, and 0.88 (0.78 to 0.99) for > 5 cups/d (p for non-linearity = 0.32; p for trend < 0.001). Significant inverse associations were observed for caffeinated (p for trend < 0.001) and decaffeinated coffee (p for trend = 0.022). Significant inverse associations were observed between coffee consumption and deaths due to cardiovascular disease, neurological diseases, and suicide. No significant association between coffee consumption and total cancer mortality was found. Conclusions—Higher consumption of total coffee, caffeinated coffee, and decaffeinated coffee was associated with lower risk of total mortality. PMID: 26572796 ------------ [2] Am J Clin Nutr. 2015 May;101(5):1029-37. doi: 10.3945/ajcn.114.104273. Epub 2015 Mar 11. Association of coffee intake with total and cause-specific mortality in a Japanese population: the Japan Public Health Center-based Prospective Study. Saito E(1), Inoue M(1), Sawada N(1), Shimazu T(1), Yamaji T(1), Iwasaki M(1), Sasazuki S(1), Noda M(1), Iso H(1), Tsugane S(1). BACKGROUND: Despite the rising consumption of coffee worldwide, few prospective cohort studies assessed the association of coffee intake with mortality including total and major causes of death. OBJECTIVE: We aimed to investigate the association between habitual coffee drinking and mortality from all causes, cancer, heart disease, cerebrovascular disease, respiratory disease, injuries, and other causes of death in a large-scale, population-based cohort study in Japan. DESIGN: We studied 90,914 Japanese persons aged between 40 and 69 y without a history of cancer, cerebrovascular disease, or ischemic heart disease at the time of the baseline study. Subjects were followed up for an average of 18.7 y, during which 12,874 total deaths were reported. The association between coffee intake and risk of total and cause-specific mortality was assessed by using a Cox proportional hazards regression model with adjustment for potential confounders. RESULTS: We showed an inverse association between coffee intake and total mortality in both men and women. HRs (95% CIs) for total death in subjects who consumed coffee compared with those who never drank coffee were 0.91 (0.86-0.95) for <1 cup/d, 0.85 (0.81-0.90) for 1-2 cups/d, 0.76 (0.70-0.83) for 3-4 cups/d, and 0.85 (0.75-0.98) for >5 cups/d (P-trend < 0.001). Coffee was inversely associated with mortality from heart disease, cerebrovascular disease, and respiratory disease. CONCLUSION: With this prospective study, we suggest that the habitual intake of coffee is associated with lower risk of total mortality and 3 leading causes of death in Japan. © 2015 American Society for Nutrition. PMID: 25762807
  6. Antibiotic Use Linked to Higher Diabetes Risk Note: I'm starting a new generic thread about diabetes prevention with a rather narrowly focused post about diabetes and antibiotics, because I thought the study was interesting and suggested a link I hadn't heard about before. Over time I hope we'll build up posts on this thread dealing with other means of avoiding this important cause of morbidity and mortality. With that background, I thought this recent observational study [1] of a possible link between antibiotic use and subsequent development of type 2 diabetes was quite interesting and potentially relevant for CR Practitioners. It found quite a clear and dramatic dose-response relationship between the number of antibiotic prescriptions a person fills, and their subsequent risk of developing type 2 diabetes, among 5.6 million Danish people tracked for 12 years. Here is the kicker graph from the full text of the paper: As you can see from the graph, 2-4 courses of an antibiotic raised one's risk of developing diabetes by about 20%, and 5-8 courses raised it by about 40%. The authors suggest (warn) that there are two possible ways to interpret this association: There are two competing interpretations of our findings: 1) patients with type 2 diabetes are more prone to develop infections many years before they become diagnosed with type 2 diabetes and therefore have increased demand for antibiotics and 2) antibiotics increase the risk of type 2 diabetes. They suggest it may be a combination of both, but that there is definitely evidence that messing up one's gut microbiome via antibiotics can lead to weight gain, glucose intolerance, etc. So a causal link that goes as follows: antibiotics -> gut dysbiosis -> metabolic syndrome -> Type 2 diabetes seems quite plausible. I'm personally thankful that I haven't needed antibiotics in many, many years, and would be reluctant to take them now unless there was a significant danger of serious health consequences from not doing so. --Dean ---------- [1] J Clin Endocrinol Metab. 2015 Oct;100(10):3633-40. doi: 10.1210/jc.2015-2696. Epub 2015 Aug 27. Use of Antibiotics and Risk of Type 2 Diabetes: A Population-Based Case-Control Study. Mikkelsen KH(1), Knop FK(1), Frost M(1), Hallas J(1), Pottegård A(1). CONTEXT AND OBJECTIVE: Evidence that bacteria in the human gut may influence nutrient metabolism is accumulating. We investigated whether use of antibiotics influences the risk of developing type 2 diabetes and whether the effect can be attributed to specific types of antibiotics. METHODS: We conducted a population-based case-control study of incident type 2 diabetes cases in Denmark (population 5.6 million) between January 1, 2000, and December 31, 2012. Data from the Danish National Registry of Patients, the Danish National Prescription Registry, and the Danish Person Registry were combined. RESULTS: The odds ratio (OR) associating type 2 diabetes with exposure to antibiotics of any type was 1.53 (95% confidence interval 1.50-1.55) with redemption of more than or equal to 5 versus 0-1 prescriptions. Although no individual group of antibiotics was specifically associated with type 2 diabetes risk, slightly higher ORs for type 2 diabetes were seen with narrow-spectrum and bactericidal antibiotics (OR 1.55 and 1.48) compared to broad-spectrum and bacteriostatic types of antibiotics (OR 1.31 and 1.39), respectively. A clear dose-response effect was seen with increasing cumulative load of antibiotics. The increased use of antibiotics in patients with type 2 diabetes was found up to 15 years before diagnosis of type 2 diabetes as well as after the diagnosis. CONCLUSIONS: Our results could support the possibility that antibiotics exposure increases type 2 diabetes risk. However, the findings may also represent an increased demand for antibiotics from increased risk of infections in patients with yet-undiagnosed diabetes. PMCID: PMC4596043 PMID: 26312581
  7. There has been some concern over the years among CR practitioners about the possibility of diabetes, largely based on observations that some of us don't do very well on an oral glucose tolerance test (OGTT). But by-and-large we are highly sensitive to insulin (unlike type 2 diabetics and pre-diabetics). Some of us suspect our poor OGTT response may simply be a result of our pancreas being 'out of practice' - not having to pump out that much insulin on a regular basis, because of our low glycemic index / glycemic load diet, and because we eat fewer calories than most people. But others have a lingering worry that for whatever reason (perhaps related to the idea of 'use it or lose it'?), insulin producing beta-cells in our pancreas may be dying or atrophying, potentially making us susceptible to diabetes somewhere down the line... Anyway, with that background, I found this new study [1], discussed in Science Daily, to be both very interesting and potentially comforting for us skinny folk. It found that weight loss following gastric bypass surgery resulted not just in normal (visceral and subcutaneous) fat loss. It found that loss of fat accumulations in the pancreas also occurred, but only in the type II diabetics they were studying, not in the obese, but otherwise metabolically healthy, controls. The authors claim it was the loss of pancreatic fat that caused the reversal of the glucose intolerance in the diabetics via a reversal of their attenuated first-phase insulin response. At least in the Science Daily coverage, the authors are suggesting that fat 'clogging' the pancreas may in fact be the underlying cause of Type 2 diabetes: Previous work by Professor Taylor and his team highlighted the importance of weight loss through diet in reversing Type 2 diabetes. This work in 2011 transformed the thinking in diabetes as it was the first time that it had been demonstrated that diet could remove fat clogging up the pancreas allowing normal insulin secretion to be restored. Professor Taylor adds: "This new research demonstrates that the change in level of fat in the pancreas is related to the presence of Type 2 diabetes in a patient. The decrease in pancreas fat is not simply related to the weight loss itself. It is not something that might happen to anyone whether or not they had diabetes. It is specific to Type 2 diabetes. "What is interesting is that regardless of your present body weight and how you lose weight, the critical factor in reversing your Type 2 diabetes is losing that 1 gram of fat from the pancreas." Since it would seem unlikely that we CR folks would be accumulating fat in our pancreas (since we don't accumulate it anywhere else), we should be safe from this apparent cause of Type 2 diabetes at least. --Dean -------- [1] Diabetes Care, December 2015 DOI: 10.2337/dc15-0750 Sarah Steven, Kieren G. Hollingsworth, Peter K. Small, Sean A. Woodcock, Andrea Pucci, Benjamin Aribisala, Ahmad Al-Mrabeh, Ann K. Daly, Rachel L. Batterham, and Roy Taylor. Weight Loss Decreases Excess Pancreatic Triacylglycerol Specifically in Type 2 Diabetes. Abstract OBJECTIVE This study determined whether the decrease in pancreatic triacylglycerol during weight loss in type 2 diabetes mellitus (T2DM) is simply reflective of whole-body fat or specific to diabetes and associated with the simultaneous recovery of insulin secretory function. RESEARCH DESIGN AND METHODS Individuals listed for gastric bypass surgery who had T2DM or normal glucose tolerance (NGT) matched for age, weight, and sex were studied before and 8 weeks after surgery. Pancreas and liver triacylglycerol were quantified using in-phase, out-of-phase MRI. Also measured were the first-phase insulin response to a stepped intravenous glucose infusion, hepatic insulin sensitivity, and glycemic and incretin responses to a semisolid test meal. RESULTS Weight loss after surgery was similar (NGT: 12.8 ± 0.8% and T2DM: 13.6 ± 0.7%) as was the change in fat mass (56.7 ± 3.3 to 45.4 ± 2.3 vs. 56.6 ± 2.4 to 43.0 ± 2.4 kg). Pancreatic triacylglycerol did not change in NGT (5.1 ± 0.2 to 5.5 ± 0.4%) but decreased in the group with T2DM (6.6 ± 0.5 to 5.4 ± 0.4%; P = 0.007). First-phase insulin response to a stepped intravenous glucose infusion did not change in NGT (0.24 [0.13–0.46] to 0.23 [0.19–0.37] nmol ⋅ min−1 ⋅ m−2) but normalized in T2DM (0.08 [−0.01 to –0.10] to 0.22 [0.07–0.30]) nmol ⋅ min−1 ⋅ m−2 at week 8 (P = 0.005). No differential effect of incretin secretion was observed after gastric bypass, with more rapid glucose absorption bringing about equivalently enhanced glucagon-like peptide 1 secretion in the two groups. CONCLUSIONS The fall in intrapancreatic triacylglycerol in T2DM, which occurs during weight loss, is associated with the condition itself rather than decreased total body fat.
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