Showing posts from November, 2010

Reversing beta cell dysfunction

Mostly a bookmarking post, but indicates the possibility of "curing" type 2 diabetes. Genipin inhibits UCP2-mediated proton leak and acutely reverses obesity- and high glucose-induced β cell dysfunction in isolated pancreatic islets Summary Uncoupling protein 2 (UCP2) negatively regulates insulin secretion. UCP2 deficiency (by means of gene knockout) improves obesity- and high glucose-induced β cell dysfunction and consequently improves type 2 diabetes in mice. In the present study, we have discovered that the small molecule, genipin, rapidly inhibits UCP2-mediated proton leak. In isolated mitochondria, genipin inhibits UCP2-mediated proton leak. In pancreatic islet cells, genipin increases mitochondrial membrane potential, increases ATP levels, closes K ATP  channels, and stimulates insulin secretion. These actions of genipin occur in a UCP2-dependent manner. Importantly, acute addition of genipin to isolated islets reverses high glucose- and obesity-induced β cell dys

Lipogenesis v. Adipose Mass Gain ~ Fructose

A while back I posted a summary of lipid vocabulary:   Lip-ocabulary .  I had hoped to address this sooner than now. Another topic on my (rather long) list of how Taubes either misunderstands or misrepresents lipid metabolism and storage involves his use of terms related to "lipogenesis"  (e.g. fructose is the most lipogenic of carbs) to imply that it leads to fat accumulation.   In his defense, there are any number of scholarly articles and texts that use the term lipogenesis to describe the "genesis" of fat stores.  However they do so in the context of discussions of adipose tissue and do not conflate de novo lipogenesis and fat storage.  Adipogenesis may not be exactly appropriate either, as this term is most correctly attributed to the formation of new fat cells.  But at least the "adipo" implies fat tissue, thus it might loosely apply to the genesis of adipose tissue (whether by proliferation or filling of existing cells) rather than the synthesis

Happy Thanksgiving

Enjoy this thankful day with your familyand/or friends!   Eat, drink and be merry!!

Exercise & Insulin Sensitivity I ~ IR in older populations

Just wanted to share two studies I came across relating exercise and cardiac fitness to insulin sensitivity.  I'm sure to add more to this series as I come across them. I only have access to the abstracts for these studies.  If any of you have access to the full text, please consider sharing it with me via my email address in my profile.  Thanks! Study 1: Association of cardiorespiratory fitness with insulin sensitivity in overweight and obese postmenopausal women: a Montreal Ottawa New Emerging Team study The purpose of this study was to examine the relation between insulin sensitivity and cardiorespiratory fitness in overweight and obese postmenopausal women. The study population consisted of 127 overweight and obese postmenopausal women (age, 57.7 ± 4.8 years; body mass index, 32.7 ± 4.7 kg/m 2 ). Subjects were classified by dividing the entire cohort into tertiles (T) based on insulin sensitivity expressed per kilograms of lean body mass (LBM) (T1, <10.9; T2, 10.9-12.9,

Oats ... More Reader Input Requested

I'm being a bit lazy here because we're hosting Thanksgiving and stupid me decided to tackle some "spring like" cleaning and re-organizing.  So I thought I would ask for your help in answering the following question because my reading around the net has been conflicting.  Do oats contain gluten per se, or is it that most oats are contaminated by gluten from other grains processed by the same machinery or in the same facility (dust?).   Thanks in advance!

Physiological, Pharmacological, and Nutritional Regulation of Circulating Adiponectin Concentrations in Humans

Physiological, Pharmacological, and Nutritional Regulation of Circulating Adiponectin Concentrations in Humans Get this one while its free folks (until the end of the month)!  Adiponectin is an all-too-often overlooked hormone in the obesity and metabolic syndrome game.   I haven't had time to read it thoroughly but it contains a wealth of information.  The graphic below summarizes the 17 page paper content: Hmmmm... cheers everyone!  (booze is adiponectin friendly :) )

Legumes ~ Reader Input Request

I'm trying to reconcile the plethora information I keep coming across regarding the benefits of the Mediterranean Diet and similar with the shunning of legumes in the Paleo community (including peanuts and cashews).  There is a lot of info on toxic compounds in legumes. I would be interested in any and all input on this topic, links I should check out, etc.   Lately I've been upping my carb consumption slightly and have always enjoyed such foods as chili with various kidney beans, garbanzo beans (mostly in salads), and Mexican bean dishes.  I've already incorporated some of these into my diet (infrequently) to no ill effect, probably causing many of you to cringe and worry over my imminent demise.  ;-) ... or maybe not {VBG}.

Insulin Is an Anti-inflammatory and Anti-atherosclerotic Hormone

Insulin Is an Anti-inflammatory and Anti-atherosclerotic Hormone   (full text free until end of the month) Fasting hyperinsulinemia is associated with an increased risk of atherosclerotic complications of heart attack and stroke. This has resulted in the concept that insulin may promote atherosclerosis in spite of the absence of any evidence that insulin is atherogenic either in the human or in experimental models. Recent evidence shows that insulin exerts vasodilatory, anti-platelet and anti-inflammatory effects at the cellular level in vitro and in the human in vivo. Since atherosclerosis is a chronic inflammatory process of the arterial wall, insulin may be potentially anti-atherosclerotic in the long term. More recent data on experimental atherosclerosis in the mouse shows that (1) insulin administration reduces the number and the size of atherosclerotic lesions in apo E null mice and (2) in IRS-2 null mice, the interruption in insulin signal transduction results in enhanced a

Caffeine and Insulin Sensitivity

Caffeine and Insulin Sensitivity   (full text PDF free till end of the month) A number of reports have observed that acute caffeine ingestion decreases glucose tolerance and insulin sensitivity, and have raised the question whether its increased consumption throughout the world in the form of coffee and cola beverages might be of public health concern in the development of type 2 diabetes. Although some epidemiologic studies have found strong associations between coffee intake and detrimental lifestyle factors that favor obesity and diabetes, it is interesting that in spite of this, they have demonstrated that increased coffee consumption is associated with a decreased risk of developing type 2 diabetes.   When lifestyle confounders are taken into account, individuals consuming 6 cups coffee per day have at least 50% less risk of developing type 2 diabetes than those consuming 2 cups per day . Although it is perhaps premature to recommend increased coffee or caffeine intake to pre

Aspirin for Insulin Resistance? Part II: Not so fast

A follow-up post to a post a while back:   Aspirin for Insulin Resistance? I just came across the following article that has me thinking "not so fast":    The effect of salicylates on insulin sensitivity Although the carefully performed study by Kim et al. provides new insight into the mechanisms of fat-induced insulin resistance, we would like to caution against the preliminary conclusion concerning beneficial effects of salicylates on insulin resistance. First of all, in contrast to the findings of Kim et al. in the triglyceride (TG) infusion model in the rat, earlier studies in human volunteers using hyperglycemic clamp techniques reported increased insulin resistance by salicylate compounds ( 3 , 4 ). These findings suggest that the effects of salicylates may depend on the experimental model, and possibly on the species studied..... The schematic below summarizes the various actions and possible impact on insulin sensitivity for salicylates, the text under this is the l

Hyperinsulinemia and Anorexia?

In the course of a discussion over at Jimmy Moore's forum I came across something I did not know.  Anorexics -- the thinnest among us! -- can also become hyperinsulinemic!!!!   How can that be??   If it's all about the insulin causing fat accumulation, one would think this condition would result in any dietary intake getting trapped in the fat tissues, making it unavailable to the anorexic for fat-burning, resulting in voracious hunger.   But we would expect the anorexic to have very low postprandially-induced insulin levels.  No matter what they eat, they don't eat much.  So, where is this insulin coming from?   It would seem to be, yet again, a defense mechanism of our bodies.  I've come across quite a bit of contradictory observations on this. For example, in this article, anorexics had lower postprandial insulin responses and higher metabolic rates of insulin clearance  and describe anorexia as being associated with improved insulin sensitivity.  They also have

GCBC Reference Check ~ Part III of ? ~ Is glycerol phosphate rate-limiting?

In his most recent interview with Jimmy Moore , Gary Taubes did a bit of a mea culpa on the notion that dietary carbs are required to store fat.   He offers up a rather weak description of how he got it wrong for so long in his lectures ("skewed") and claims this wasn't something from the book but rather the lectures. Originally my post here stated that strictly speaking this was true, but upon rereading those sections of GCBC it is quite obviously not.  One could even go so far as to say it is the lynchpin of his hypothesis, but that is open to interpretation.  Still, Taubes repeated in the interview that G3P is "rate limiting" in the esterification process, a claim he made unequivocally  in GCBC.   Here's the relevant paragraph: A single molecule plays the pivotal role in the system.  It goes by a number of names, the simplest being glycerol phosphate.  This glycerol-phosphate molecule is produced from glucose when it is used for fuel in the fat cells

GCBC Reference Check ~ Part II of ? ~ Insulin Resistance (again)

I have previously discussed the fact that in 2001, Keith Frayn laid out a progression of insulin resistance diametrically opposed to that proposed by Taubes in GCBC.  (See:   Insulin Resistance ~ Taubes v. Frayn ) This work, however wasn't referenced in GCBC, so this post addresses what Frayn had to say about the topic in the 1995 text that was:   Metabolic Regulation . Let's review some GCBC excerpts: The muscle cells become insulin-resistant in response to the "repeated high levels of insulinemia that result from excessive ingestion of highly refined carbohydratesand/or over-alimentation," but the fat cells fail to compensate.  They remain stubbornly sensitive to insulin.  So, as Neel explained, the fat tissue accumulates more and more fat, but "mobilization of stored fat would be inhibited." Now the accumulation of fat in the adipose tissue drives the vicious cycle. "Over the years, prominent diabetologists and endocrinologists -- from Yalow an

Mass MUST be conserved ... v. 2.0

Do you ever have those "I wish I said that" moments?  I've been having a few after my recent Jimmy Moore interview.  We discussed the whole insulin thing a bit and I mentioned that you can't gain more than a pound of fat eating a pound of any food.  As time would be used discussing other things, we never really got to Jimmy's initial reaction that he didn't believe that.  I wish I had a chance to suggest this simple experiment to Jimmy to prove this point beyond all doubt. Here is my experiment for you.  Right now, go get on a scale and weigh yourself.  Then, go get a pound bag of something "evil" ... be it cookies, chips, bread, etc.  Lift it up while still on the scale (for best results, hold close to your body) -- hopefully your scale is accurate enough to register the difference.  You should weigh the initial weight + 1 lb.   If you will need to drink anything to down the food, have that in the other hand -- IOW weigh yourself + 1 lb food + liqu

LC Cookbook author acknowledges LC reality!

(Not really a science post, but not really specifically personal either, so posted here). I have been a somewhat regular follower of Dana Carpender's Hold the Toast blog lately.  Some might consider my occasional mentions of Dana as being critical, but really that is not my intent.  I look to her, as a long-term, seemingly consistent low carber, who is not all that much older than myself, as an example of possible LC outcomes.   Where else should I be looking to move forward from here?  Those who follow other approaches have their Denise Austin's out there.  For better or worse, we don't really have too many such role models. When I first discovered her, I was looking at pictures of a woman who, frankly, more closely resembled a "before" picture than an "after".  Sorry if that sounds blunt or cruel, but at the time I was coming from the viewpoint of a long stall and/or slightly regaining (or feeling like I was), and Dana had clearly regained some of h

The research strategy of Gary Taubes -- In his own words

How Taubes himself describes his research strategy, in his own words, from GCBC: "My background is as a journalist with scientific training in college and graduate school.  Since 1984, my journalistic endeavors have focused on controversial science and the excruciating difficulties of getting the right answer in any scientific pursuit.  More often than not, I have chronicled the misfortunes of researchers who have come upon the wrong answer and found reason, sooner or later, to regret it.  I began reporting on public-health and medical issues in the early 1990s, when I realized that the research in these critically important disciplines often failed to live up to the strict standards necessary to establish reliable knowledge.  In a series of lengthy articles written for the journal Science, I then developed the approach to the convention wisdom of public-health recommendations that I applied in this book. It begins with the obvious question:  what is the evidence to support the cu

Fat Futile Cycling from Carb Excess - A more lay-person friendly version

I think I misunderstood the confusion many seemed to have over this recent post: Fat Futile Cycling ~ From Carb Excess? One of my readers posted a link to that post over at Mark Sisson's forum ... the responses were ... erm ... interesting.  Perhaps I'm not worthy of "writting" (<- commenter spelling, not mine) on this subject, but I can tell y'all that I'm definitely not some "poser" with an agenda to oppose low carb.  I'm not sure my diet these days qualifies as low carb in the VLC circles, but it certainly fits in with Sisson's 80/20% primal plan.  And I did lose most of my weight eating VLC most of the time.   In any case, apparently I presumed a bit more background on this topic than I should have.  So, here goes the laymen's terms explanation. In LC circles, there are many proponents of a so-called "Metabolic Advantage" of low carb dieting.  According to this theory, people lose more weight eating more L

That Twinkie Diet Story

By now, most of the LC community has read about this professor who lost 27 lbs eating mostly twinkies and other junk food. This DOES prove that a caloric deficit, consistently maintained, WILL result in weight (and fat) loss.  What else did it prove?   There can be no doubt, really, that when a caloric deficit is achieved and maintained, weight/fat will be lost.  This doesn't "diss" low carb in any way.  For most people, low carb diets make doing so easier (less hunger) with larger spontaneous caloric deficits.  Don't knock that!! What I think surprised many is the improvements in his bloodwork given the likelihood of a poor O6/O3 ratio, transfats, refined carbs, etc.  Which just goes to show a few things.  Firstly, I know I've read somewhere that a person's LDL level is largely correlated with their weight status.  For me, this has been the case in my life.  He lost >10% of his in

Just finished my interview with Jimmy Moore :-)

I think I got a little animated at times ;-) ... we'll see how it went.  For anyone interested in hearing this, he estimated the air date to be around the Jan 20th time frame (sooner than I thought), but obviously I'll get bumped if some big wig guru agrees to an interview!   Jimmy was a very gracious host and put me at ease.  Hmmm... maybe too much at times?  LOL ... again, we'll see. When it airs I'll definitely post the link here, and I'll probably put up a post linking to various relevant blog posts and/or studies too -- sorta my own "show notes" since it is obviously difficult to get everything in within an hour phone exchange. OK ... now I can stop shaking LOL.  Really, it wasn't so bad once we got going, but this was the first time in a long time I had such butterflies! Thanks to all of you for reading my blog!!  Without you I would have never had such a unique opportunity!

GCBC Reference Check ~ Part I of ? ~ Metabolic Adaptability & Energy Balance

Ever since I discovered that Taubes had actually cited the 2003 Reshef paper in GCBC, I've been intrigued by what many of his other references ACTUALLY said.    In that regard, I've picked up a few of these older text books by various authors and experts cited by Taubes in the book. One such expert is Keith Frayn, who I've dubbed "the English guy" as Taubes previously described him.  I've been sharing some of his more scholarly contributions (e.g. peer review journal articles), and have more to come on that front.  None of these made it into GCBC, however.  I'll leave it to you, my readers, to decide for yourselves what this says about the quality of Taubes' research on the topic. But this post is looking at the words of Keith Frayn that Taubes DID include in GCBC.   Chapter 17 of GCBC opens as follows: Before World War II, the proposition that obesity was caused by overeating - the positive-caloric-balance hypothesis - was one of sever com