The Carb-Sane Asylum

This started out as a comment to my friend Helen from Jimmy Moore's LLVLC discussion board over at my personal blog.  Here's the post:  When to Eat .  That post was mostly thinking out loud about strategies for weight maintenance. I see an Eating Timing/Quantity Spectrum:  ad libitum (eat when hungry, stop when satisfied) - to - strictly structured/controlled.  I postulate that in the middle of this spectrum, which is where many in our modern world "live", is where weight maintenance issues arise due to overeating. I had another discussion about a different middle ground with Peter of Hyperlipid fame in the comments on this thread:   VLC and Insulin Resistance .   I posited that   "Humans seem to do better at the "moderate end of the extremes" if that makes any sense but not so much in the middle. Our appetite signalling and metabolic controls seem ill equipped to handle any significant carb + fat load simultaneously." I blogged some though...

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...

Thanks to Leon for finding this :) Effects of consuming a high carbohydrate diet after eight weeks of exposure to a ketogenic diet Basically they took two groups of rats and fed them (ad libitum) either a ketogenic diet (KD) or regular chow (CH) for 8 weeks.  Then they switched the diet of the KD group to CH (KD:CH) and continued to feed the rats for an additional 8 weeks.  As this was a rat study, the rats gained weight/grew for the entire 16 week duration of the study.   The diets:  KD = 5% carb/15% protein/80% fat             CH = 60% carb/23% protein/17% fat Now I'm not a rat, but I do find these results both interesting and a bit surprising.  Here are the graphics for caloric intake and weight: caloric intake:  Surprise #1:  The KD rats consumed pretty consistently fewer calories (although the difference is not noted with an * for statistical significance) for the first 8 weeks and yet gained consistently more...

In response to my previous post,  The New Low Carb v. Low Fat Study ~ Much Adieu About Not a Helluvalot! , LynMarie Daye commented as follows: Have you seen some of the criticisms of this study? I came across a couple of blog articles suggesting that the researchers are biased against low carb diets and manipulated the data to get results more inline with their beliefs. I would love to hear your thoughts on this. Another Biased Study? Maybe... The Diet Wars: The Saga Continues I decided to comment in a separate post because the comments features here are limited (and no auto-save). First Tom Naughton's analysis raises many of the same questions that I have over the actual dietary interventions in the study.  Absent food diaries of what the participants were ACTUALLY consuming at the various time points, we have no idea what we're really comparing at each timepoint.  While I, too, don't see where the low fat/calorie restriction group increased their intake, I simply ...

Came across this while on another one of my trips around the internet looking for something totally unrelated ... funny how that happens sometimes? Anyway, thought I would "bookmark" it here with a little comment: Daily Melatonin Administration at Middle Age Suppresses Male Rate Visceral Fat, Plasma Leptin, and Plasma Insulin to Youthful Levels Yes, it is a rat study, but as the intro states, endogenous melatonin production decreases with age in both humans and rats.  Basically regular melatonin supplementation reversed the increases in  insulin and visceral fat associated with aging. I don't know about any of you, but this middle aged (well I guess technically not yet, but ...) chick is going to look into this further! In addition, if you scroll down the page, there's a list of articles that cite this study. I plan to check out a few of these.

Note:  This has been in my draft "hopper" for a while.  I thought I might as well dust it off and post it.  ;-) I've been thinking for a while about the whole caloric balance arguments and theories of obesity, etc.  I keep coming back to a simpler model of it all to which there really can be no argument.  That is that matter is neither created nor destroyed.  What goes into a vessel must come out of that vessel or the vessel will weigh more. Intake:  macronutrients, water, oxygen, minerals and other micronutrients -- mostly oral ingestion and inhaling. Outgoing:  excretory products -- mostly expiration and urine, but feces (containing mostly unabsorbed intake) and perspiration as well. Metabolism, bioenergetics, whatever ... it all boils down to the rearranging of atoms and molecules for some purpose.  In the end, forget the purpose and just look at the atoms themselves.  We cannot convert an atom of oxygen to an atom of carbon. ...

I just came across the following article, and haven't quite digested the whole thing just yet.  Still, it is interesting so I thought I would share it here.  This post will be about the most curious topic in this paper, but I hope to revisit this in a series of future blog posts (hence the "I" in the title).   Adiposopathy Is a More Rational Treatment Target for Metabolic Disease than Obesity Alone Near as I can tell, the lead author, Harold Bays, is the doctor who coined the term "adiposopathy" or "sick fat".   Adiposopathy is pathologic adipose tissue dysfunction that may be initiated and/or exacerbated by fat accumulation (adiposity) in genetically susceptible patients [1••].  Adipocytes are metabolically active and adipose tissue is an important endocrine organ (Table 1) [2••]. Abnormalities of adipocyte factors contribute to dysmetabolism (Fig. 1), and adiposopathy [1••,3•] promotes some of the most...

Came across this (yes rodent) mouse study recently: Acylation-stimulating Protein (ASP) Deficiency Induces Obesity Resistance and Increased Energy Expenditure in ob/obMice* Here is where dietary fat leading to obesity seems to come into play.  I consider it indisputable fact at this point that accumulation of fat in adipose tissue has far less to do with insulin "trapping" fatty acids in than it has to do with ASP-mediated sequestering of triglycerides into adipose tissue.   I encourage any new readers to start here .   Basically, dietary fat is transported from the intestines to fat tissue as chylomicrons.  Chylo stimulate ASP (and are the major stimulator of ASP action, insulin does have an effect but many fold lower).  ASP stimulates both glucose transporters and the esterification of free fatty acids.  ASP's role is to clear dietary fat from the bloodstream.  The "energy" form of fats is free fatty acids (NEFA/FFA) and levels of this are contro...

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...

Just a "bookmarking" post to share an interesting article. Minireview: Weapons of Lean Body Mass Destruction: The Role of Ectopic Lipids in the Metabolic Syndrome

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 ...

This is mostly a post of a personal nature, but I thought I would put it here on the science side of things because I'll try to tie observations and anecdotes in with some scientific backing/references. Personal background for my interest in this:   As a child I had a rather boyish body until around age 12 or so.  At that age my shape (butt and thighs) started coming out (not fat though), but I was a rather late bloomer.  I didn't gain my "puberty weight" until I was 16 or so -- perhaps 20 lbs -- again mostly in my butt/thighs.  Anyone remember Tracey Gold from Growing Pains?  That would be pretty close (pre-anorexia) to my shape.  I lost the weight then yo-yo'd most of my 20's on various diet plans (none of which were low carb).  Although cycling as high as the 200-210 range and as low as 145 during that time, my general body type did not change.  I would always gain or lose weight mostly in my butt/thighs only getting the back and belly bulge...

I found this article almost a year ago, posted it on an LC discussion board, and was mostly greeted with silence so I had sort of forgotten about it.  In any case, I was reminded of the article while recently reading LynMarie's latest post on her blog:   Fat Fails First?   (Incidentally, that post corresponds well with my own recent offering on the topic:   The Progression of Insulin Resistance  ).   On to the subject of this post:   Role of a critical visceral adipose tissue threshold (CVATT) in metabolic syndrome: implications for controlling dietary carbohydrates: a review

So the LC Hills are alive with the sound of music to the ears of low carbers once again.  A 2-year NIH funded study pitted a classic lowfat CRD against a DANDR stye low carb diet.  DANDR fared equally with low fat on most measures and even posted a modest sustained improvement in HDL. Here's the summary : Background: Previous studies comparing low-carbohydrate and low-fat diets have not included a comprehensive behavioral treatment, resulting in suboptimal weight loss. Objective: To evaluate the effects of 2-year treatment with a low-carbohydrate or low-fat diet, each of which was combined with a comprehensive lifestyle modification program. Design: Randomized parallel-group trial. (ClinicalTrials.gov registration number: NCT00143936) Setting: 3 academic medical centers. Patients: 307 participants with a mean age of 45.5 years (SD, 9.7years) and mean body mass index of 36.1 kg/m2 (SD, 3.5 kg/m2). Intervention: A low-carbohydrate diet, which consisted of limited carbohydrate...