The Carb-Sane Asylum

One more on the measurement side of things since these type posts are easier to put the finishing touches on to get out the door.  This is another older paper, and I'm trying to track down more info on newer/current analyses and their specificity.  Unlike the last discussion here , I want to focus on the secretory capacity of the  β-cell through the progression of diabetes.   Serum proinsulin levels at fasting and after oral glucose load in patients with Type 2 (non-insulin-dependent) diabetes mellitus  (1988).   40 newly diagnosed with T2 diabetes + 21 IGT -- No medications or special diet BMI < 27 in men, < 25 in women Controls were weight matched to study group participants.

In the last installment , I discussed the context of blood glucose readings over 140 mg/dL in diabetics vs. non-diabetics.  In this installment I'm going to discuss it in the context of an Oral Glucose Tolerance Test, OGTT.   The crux of this post is that the results of this study do not justify the Ruhl/Jaminet/(and I'll add Kresser) takeaway message vis a vis diabetes complications and "spikes" in blood glucose.   The fact that 50% of the neuropathy subjects to whom OGTT's were administered had 2 hr. glucose levels over 140 (e.g. diagnosed as Impaired Glucose Tolerance, IGT) simply does not support:  Nerve Damage Occurs when Blood Sugars Rise Over 140 mg/dl (7.8 mmol/L) After Meals as stated on Ruhl's site and in Perfect Health Diet (Kindle Locations 712-716).  ( This seems to have been repeated by Chris Kresser as well ). What is an OGTT?  The most common form is conducted in the fasted state, at least 8 hrs, studies seem to favor 10 or ...

direct image link As often happens, when looking for something a bit more specific, I came across this image at right, which led me to this webpage:  Laboratory Testing for Diabetes Mellitus. Curve 1 is a normal OGTT, Curve 6 is a diabetic.  The other causes are listed: Pathologic conditions causing impaired, or diabetic, glucose tolerance results: Hypercorticism - curve 5. Acromegaly - between curves 4 and 5 Hyperthyroidism - curve 4. Pheochromacytoma (or "emotional hyperglycemia") - between curves 4 and 5

This post (that is going to be a series to keep post lengths manageable) has been brewing for quite a while, but I was reminded of it because Jenny Ruhl came out with a diet book recently, and appeared recently as an "expert" on Jimmy Moore's Ask the Low Carb Experts podcast.  After listening to her previous podcast with Jimmy , I had some mixed reviews.  Jenny is certainly articulate, well-read (though I disagree, often strongly, with many of her interpretations) on the topic, and quite a bit more moderate/measured than most in her views on controlling diabetes with low carb.   But she also seems to view all diabetes through her own MODY eyes.  MODY (Mature Onset Diabetes of the Young) is a rare genetic form (there are actually several rare genetic forms classified as MODY) that is lumped quite often under the category of Type 1.5.  One of these days I need to address some other things on Jenny's website, as the site (and her book) is one of the commonly...

It's been a while since Part I of this series ... too many irons in too many fires and all that jazz.  But one research track I went down recently reminded me of this lingering series and I thought I'd finish up this second installment. We hear all the time truisms such as that the acute effects of a hormone differ from the chronic effects, and whenever a hormone is present in excess of normal levels, the term " fill in hormone here resistance" is sure to be close behind.  Now there is no doubt that hormone resistance is a very real phenomenon, but what does it mean, specifically? The concept of insulin resistance, IR, is highly complicated by the fact that insulin has varying actions in various tissues and organs.  I do intend to discuss tissue-specific IR in more depth as this series unfolds.  But for today, I am going to limit the discussion to insulin and the muscle cell.  After all, when general IR is discussed, it is usually systemic or skeletal muscle i...

I've blogged previously on the LoBAG diets for treatment of diabetes.   These diets are higher in protein that standard recommendations - 30% vs. 15% - with varying carb content (20,30 & 40% have been studied).  With both of the lower carb diets, this group has achieved good improvements in HbA1c levels in relatively short time (5-10 weeks).  In comparing their diets  they observed: Increasing the protein content of the diet from 15 to 30% resulted in an 35% increase in IGF-I regardless of whether the carbohydrate content was 40%, 20%, or 30% as in the present study. Thus the dietary protein-induced increase in IGF-I is independent of the amount of dietary carbohydrate and fat. I believe the near-OCD obsession with insulin in the LC community overshadows the vast body of research on other hormones and peptides that's out there and their role in metabolism.

Elevated plasma nonesterified fatty acids are associated with deterioration of acute insulin response in IGT but not NGT High concentrations of nonesterified fatty acids (NEFA) are a risk factor for developing type 2 diabetes in Pima Indians. In vitro and in vivo, chronic elevation of NEFA decreases glucose-stimulated insulin secretion. We hypothesized that high fasting plasma NEFA would increase the risk of type 2 diabetes by inducing a worsening of glucose-stimulated insulin secretion in Pima Indians. The subjects were 151 Pima - 107 with normal glucose tolerance (NGT) and 44 with impaired glucose tolerance (IGT) at the outset of the study.  At the outset none of the subjects had been diagnosed with frank diabetes.  These subjects were part of a study on pathogenesis of diabetes in the Pima and returned for annual visits to have various tests performed.  Of note, offspring of diabetic mothers were excluded from the analysis, thus the NGT group did not include this "at r...

I've previously blogged on  the effects of high doses of salicylates, aka aspirin, and insulin resistance.  In summary from that paper/post: ...  high doses of salicylates reverse hyperglycemia, hyperinsulinemia, and dyslipidemia in obese rodents by sensitizing insulin signaling. So I was poking around in my Downloads folder the other day and happened across this paper: Mechanism by which high-dose aspirin improves glucose metabolism in type 2 diabetes   (I've cleaned up the excerpts from the citation #'s as I find them distracting)

Presented without comment on the content per se: Role of the Adipocyte, Free Fatty Acids, and Ectopic Fat in Pathogenesis of Type 2 Diabetes Mellitus This is probably the most exhaustively referenced review article I've ever come across on the etiology of MetS and T2 Diabetes and the role of adipose tissue.  Too extensive to quote w/o copying the whole darned thing, although I may revisit it at some point to do a bullet point summary type post.  

Dr. William Davis is touting the success of one of his patients on a No BG Rise After Eating diet.  The post is HERE . So Jack was overweight and: Try as he might, Jack could simply not stick to the diet I urged him to follow. Three days, for instance, of avoiding wheat was promptly interrupted by his wife's tempting him with a nice BLT sandwich. This triggered his appetite, with diet spiraling downward in short order.  Presumably the diet he urged was low carb.  But just going LC and trying to cut wheat lasted only three days.  So the good Dr. Davis told Jack to get a BG meter and strive for 1 hour postprandial glucose levels to be no higher than before eating.  So: If any food or combination of foods increase blood glucose more than the pre-meal value, then eliminate the culprit food or reduce the portion size. For example, if dinner consists of baked salmon, asparagus, and mashed potatoes, and pre-meal blood glucose is 115 mg/dl, post-meal 155 m...

Just some musings on carbohydrates and fats, but with a scientific basis so put it here. Personally I believe the obesity epidemic can be blamed primarily on two phenomena: 1.  The abundance of high calorie foods high in fats & carbs (I'll call them CF) in ever larger portions, and 2.  Liquid calories loaded with sugar and/or fat To prevent obesity my solution is simple:  Keep the fats and carbs separate.  If you're going to eat carbohydrate, eat it with lean protein and/or in whole form so you get sufficient fiber.  Go easy on the fat.  If you're going to eat fat, chances are it is attached to protein, forgo the carbs.  If you simply must eat CF foods, rely on portion control/calorie counting and not on satiety to determine how much you eat.  Keep the total caloric load low, perhaps in the 2-300 cal range, to keep the unnatural assault on your metabolism to a minimum.   My reasons for this are twofold: 1.  Our paleolithic ances...

The long-term effect of low-carbohydrate/high-fat diet on the development of diabetes mellitus in spontaneously diabetic rats First the disclaimers: It's a rat study The OLETF rats used are a strain that become spontaneously diabetic and mildly obese -- however to the best of my knowledge this strain was not created by genetic manipulation (e.g. it's not a "knockout").  More here . My excerpts will be from scattered around the article. The long-term effect of low-carbohydrate/high-fat diets on the development of diabetes mellitus was studied in Otsuka Long-Evans Tokushima Fatty strain (OLETF) rats. Four groups of spontaneously diabetic (type 2) male rats at 10 weeks of age were pair-fed semi-purified powder diets containing different amounts of carbohydrate (80 %, 60 %, 40 %, 20 % of total calories) for 30 weeks. The carbohydrate content was isocalorically substituted for the fat content in the diet. At the onset of experimental feeding (10 weeks...

In response to my recent post --  Can low carb cause central adiposity?  -- James Krieger posted a link to a recent study indicating I may well be on to something.  So I thought I would post this study separately (I don't have access to the full text on this one). Longitudinal adaptations to very low-carbohydrate weight-reduction diet in obese rats: body composition and glucose tolerance. Longitudinal effects of a very low-carbohydrate (VLC) and a calorie-matched high-carbohydrate (HC) weight reduction diet were compared in dietary obese Sprague-Dawley rats exhibiting impaired glucose tolerance and insulin resistance. Obese rats were divided into weight-matched groups:  (i) VLC rats consumed an energy-restricted 5% carbohydrate, 60% fat diet for 8 weeks, (ii) HC rats consumed an isocaloric 60% carbohydrate, 15% fat diet, and (iii) HF rats consumed a high-fat diet ad libitum. HC and VLC rats showed similar reductions in body fat and hepatic lipid at the midpoint of ...