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Found 9 results

  1. I hope everyone here is doing well and having a great summer. Recently I had an episode where low blood-glucose nearly caused me a big problem. Several days ago I underwent a vasectomy (my kids are getting older now and I'm happy to end my chances of further procreation). The procedure itself went well and was relatively uneventful - I was happy to see that Dr. Greger recommends it as his preferred form of birth control. Immediately after the procedure, you are kept in a holding room to see how you are feeling and I was doing great. Smiling, laughing, chatting with the hospital staff, and so forth. My BP and HR were taken and were great (110/70 HR 60, which considering I have white coat syndrome is good). They also commented on how lean I was and I said I "must be a runner." Which is somewhat true, but not anywhere to the extent to which I actually am. My leanness is probably 80% due to diet, not exercise. They come to offer me some juice and cookies and inform me that people routinely faint from this procedure. I kindly inform them that I don't consume processed food. The doctor says, "at least drink the juice - I've seen too many people faint from this." So I drink about 200ml of juice and don't touch the cookies. Feeling great, my wife drives me home, I sit on the couch, and proceed to faint! Fortunately, she was there to catch me bring me some orange juice and a big bowl of dates and instant oatmeal. I actually lost consciousness for 30-60 seconds according to her. While I follow a low glucose lifestyle with post-prandial exercise after most meals, this may have been a time when low glucose was a bad idea. If I fainted, fell and hurt myself, the outcome could have been much worse. Just thought I would share my experience here! It reminds me of how Dr. McDougall fell this past year and was injured after contracting a viral illness. Medical instances may be a time for forgetting about low glucose!
  2. 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.
  3. Anyone out there use, or has tried, Dexcom's continuous glucose monitor? From another forum, about one of their products: I'm intrigued. Summary of the pluses and minuses of continuous monitoring: http://www.diabetesselfmanagement.com/blog/is-continuous-glucose-monitoring-worth-it/ And I like the idea of a collective purchase. Would be easiest if the group were in the same area. Anyone in or near Boston interested in a collective purchase? Zeta
  4. What is the relationship between glucose levels and nitric oxide production? I had read that as glucose levels falls, NO production increases, and that this is the mechanism by which CR induces such great blood pressure (or at least one of the mechanisms). Yet when I googled it, high glucose seemed to be associated with increased NO production. Thoughts? And hello!
  5. I'm curious, from an anti-aging / disease-preventative stance, what's an ideal target range for post-prandial glucose (45m-1hr post-meal spike in blood sugar) and post-prandial elevated triglycerides?
  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. I stumbled across an new paper [1] which contrasts the impact of calorie restriction vs. protein restriction (PR) in C57BL/6 mice. Interestingly, and contrary to some other studies I've seen (e.g. see Dr. Greger's video on CR vs. PR), it didn't find that PR induced the same kind of changes to hormone levels (e.g. < IGF-1) or improvements in glucose regulation as CR. The protein restricted mice were restricted to get the same percent of calories from protein from their diet as the CR mice, but their absolute level of protein intake (i.e. grams of protein) was nonetheless a lot higher than the CR mice, because the PR mice were eating an ad lib number of calories (and as a result didn't lose weight). Plus, the percent of protein wasn't all that low (the PR groups were 16%, 14% and 12% protein vs. 20% protein for control diet). Plus the protein in the chow fed to all the rats was all casein, which is high in the two amino acids thought to be inversely related to the CR-effect - methionine and cysteine. Not only that, but the mice chow used in the study had additional cystine, which is in very closely related to cysteine (in fact metabolically interchangeable to some extent). So it seems to me this wasn't a very good test of the hypothesis that restricting specific amino acids (methionine and cysteine) has similar effects on health markers (and lifespan) as CR. But I thought it was an interesting study nonetheless. It would seem to bolster the hypothesis (as outlined in Dr. Greger's video) that it is restriction in protein high in these two amino acids (i.e. animal products), and not protein restriction in general, that could mimic CR. Go vegan :) . --Dean ----------------------------------------------- [1] The effects of graded levels of calorie restriction: II. Impact of short term calorie and protein restriction on circulating hormone levels, glucose homeostasis and oxidative stress in male C57BL/6 mice Sharon E. Mitchell1, Camille Delville1, Penelope Konstantopedos1, Jane Hurst2, Davina Derous1, Cara Green1, Luonan Chen3, Jackie J.D. Han4, Yingchun Wang5, Daniel E.L. Promislow6, David Lusseau1, Alex Douglas1, John R. Speakman1,5 Keywords: calorie restriction, protein restriction, glucose homeostasis, oxidative stress, adipokines Received: April 01, 2015 Accepted: May 20, 2015 Published: June 01, 2015 Link: http://www.researchgate.net/profile/David_Lusseau/publication/277688862_The_effects_of_graded_levels_of_calorie_restriction_II._Impact_of_short_term_calorie_and_protein_restriction_on_circulating_hormone_levels_glucose_homeostasis_and_oxidative_stress_in_male_C57BL6_mice/links/5572be2c08ae75215868be71.pdf ABSTRACT Limiting food intake attenuates many of the deleterious effects of aging, impacting upon healthspan and leading to an increased lifespan. Whether it is the overall restriction of calories (calorie restriction: CR) or the incidental reduction in macronutrients such as protein (protein restriction: PR) that mediate these effects is unclear. The impact of 3 month CR or PR, (10 to 40%), on C57BL/6 mice was compared to controls fed ad libitum. Reductions in circulating leptin, tumor necrosis factor-α and insulin-like growth factor-1 (IGF-1) were relative to the level of CR and individually associated with morphological changes but remained unchanged following PR. Glucose tolerance and insulin sensitivity were improved following CR but not affected by PR. There was no indication that CR had an effect on oxidative damage, however CR lowered antioxidant activity. No biomarkers of oxidative stress were altered by PR. CR significantly reduced levels of major urinary proteins suggesting lowered investment in reproduction. Results here support the idea that reduced adipokine levels, improved insulin/IGF-1 signaling and reduced reproductive investment play important roles in the beneficial effects of CR while, in the short-term, attenuation of oxidative damage is not applicable. None of the positive effects were replicated with PR.
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