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Found 9 results

  1. mccoy

    Exrteme proliferation & growth

    Riccardo Piana (better known as Rich Piana) was a former bodybuilder and social media star, very well known for his youtube videos often portraying his supermassive supertatooed body. He deceased recently in August 2017. In this video, 2 years ago, he warns kids about the use of growth factors and the damage he suffered. It is very interesting to listen from a self-experimenter the dranatic deleterious effects of the use of GH, IGF-1 and insulin on organs. Proliferation and growth of muscle tissue and all internal organs, even guts. Everything we already know from teh sceintific literature stands absolutely true in the real world. https://www.youtube.com/watch?v=ssORS0QMJe0
  2. New Dr. Greger video showing how meat & dairy combined with carbs causes a compounding insulin spike effect, but plant based whole foods blunt the insulin response. https://youtu.be/AoHvkrcr6EM
  3. 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
  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. There is a really interesting new meta-analysis [1] in this week's issue of The Lancet on the association between height and health/longevity. Here is a popular press article on the study, with the title Big And Tall: Nutritious Meals May Make Us Taller But They Could Also Increase Our Cancer Risk. The researchers looked at 121 epidemiological studies of over a million people that assessed the association of height with health and lifespan. The heart of the paper are these two graphs: showing how in both men and women, being taller reduces risk of coronary heart disease, but increases risk of cancer. Here is a graphical representation of the over/undernutrition-based mechanisms the authors postulate to explain the observations: The link to cancer via higher insulin in people who eat a lot (and hence grow taller) is familiar. What was a bit surprising was their suggestion that increased levels of grow factors like IGF-1 in taller people may actually improve insulin sensitivity and hence reduce diabetes and cardiovascular disease. --Dean ------------- [1] The Lancet Diabetes & Endocrinology Available online 28 January 2016 DOI: http://dx.doi.org/10.1016/S2213-8587(15)00474-X| Divergent associations of height with cardiometabolic disease and cancer: epidemiology, pathophysiology, and global implications Norbert Stefan, MD, Hans-Ulrich Häring, MD, Frank B Hu, MD, Dr Matthias B Schulze, DrPHcorrespondenceemail Full text: http://dx.doi.org.sci-hub.io/10.1016/S2213-8587(15)00474-X Summary Among chronic non-communicable diseases, cardiometabolic diseases and cancer are the most important causes of morbidity and mortality worldwide. Although high BMI and waist circumference, as estimates of total and abdominal fat mass, are now accepted as predictors of the increasing incidence of these diseases, adult height, which also predicts mortality, has been neglected. Interestingly, increasing evidence suggests that height is associated with lower cardiometabolic risk, but higher cancer risk, associations supported by mendelian randomisation studies. Understanding the complex epidemiology, biology, and pathophysiology related to height, and its association with cardiometabolic diseases and cancer, is becoming even more important because average adult height has increased substantially in many countries during recent generations. Among the mechanisms driving the increase in height and linking height with cardiometabolic diseases and cancer are insulin and insulin-like growth factor signalling pathways. These pathways are thought to be activated by overnutrition, especially increased intake of milk, dairy products, and other animal proteins during different stages of child development. Limiting overnutrition during pregnancy, early childhood, and puberty would avoid not only obesity, but also accelerated growth in children—and thus might reduce risk of cancer in adulthood.
  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.
  8. Zeta

    Elevated fasting glucose

    Hi everyone. I have a broad question, or a series of broad questions, connected with a complicated morass of health problems I've been having for the past few years. I'm still waiting to find the right way to "go public" with a bunch of my health info in order to groupsource my health problems. For now, one question that, without the broader context of everything else that's been happening to me, might be hard to answer, but to put the question in a context-free form: Could 5 g of glycine taken at bedtime, plus 4-5 g more taken in the middle of the night, usually around 3 hours before waking, have a measurable effect on waking fasting glucose? Some of the (complicated) background: I've been on moderate CR, fairly consistently, for over 20 years. I'm in my early 50s. My waking fasting glucose was routinely, with essentially no variation, around 70 mg/dL until a few years ago. Then I noticed, around three years ago, that it was between 75 and 80. Then, a year or so ago, it was routinely 85. Now I've noticed something weird. It's still around 85 when I wake, but then, even though I don't eat for several hours after waking, it goes up to around 90 as the first hour or two of the morning progresses. I've tested many times: the change is robust, even if the absolute numbers on my meter (Accu-Chek Compact Plus) might be off. Again, the very complicated background is probably needed here, but a short version: I think I started going through a very rapid manopause a few years ago (but I don't have a pre-manopause testosterone baseline, so I can't be certain) -- I noticed loss of hair on legs, reduced libido, etc. -- and I'm guessing the increase in morning glucose is related to that, and not to a switch from lowish fat to somewhat high fat (45-50% fat by calories, mostly nuts) diet that I made around that same time. Plus, I'm pretty sure that manopause and glucose changes started before the dietary changes. (I wish I had better records on that....) I also started getting much weaker physically around that time. Anyway, my narrower question: 9-10 g of protein isn't a tiny amount. Could this be contributing to the higher morning glucose, and to the weird continued increase in fasting glucose as the morning wears on? Or might it be fat from the previous evening's meal (even though my last meal is always finished at least 4 hours before going to bed)?? (I'm still learning about the effects of dietary fat on the liver, etc.) Thanks for any help. I'm starting to think I should be on metformin. Oh, another data point. I do my pre-breakfast 7-minute 3- or 4-interval workout a few hours after waking, then measure my fasting glucose, and the workout knocks it down from 90 to 87 or so. That's all! I would expect a bigger decrease.
  9. Hi, everyone, reading some recent books and papers I've gathered some clues that not caloric restriction in general but the blood sugar control/insulin control might be the major cornerstone for longevity - so I wonder if low-carb, low-glycemic (but fructose-limited) oder even low-carb high-fat (good fats like Omega-3 rich plant oils) diets could give the same fine results like caloric restriction. Is there any recent reseach available focussing this issue? Any ideas/hints or publications are much appreciated! Thanks! Max