The Carb-Sane Asylum

Postprandial de novo lipogenesis and metabolic changes induced by a high-carbohydrate, low-fat meal in lean and overweight men Background: Adjustments of carbohydrate intake and oxidation occur in both normal-weight and overweight individuals. Nevertheless, the contribution of carbohydrates to the accumulation of fat through either reduction of fat oxidation or stimulation of fat synthesis in obesity remains poorly investigated. Objective: The objective of this study was to assess the postprandial metabolic changes and the fractional hepatic de novo lipogenesis (DNL) induced by a high-carbohydrate, low-fat meal in lean and overweight young men. Design: A high-carbohydrate, low-fat meal was administered to 6 lean and 7 overweight men after a 17.5-h fast. During the fasting and postprandial periods, energy expenditure (EE), macronutrient oxidation, diet-induced thermogenesis, and serum insulin, glucose, triacylglycerol, and fatty acids were measured. To determine

Came across this so just putting it out there.  It's a meta study of 7 clinical trials in which fiber was studied or reported.  In 6 of 7 CRP was reduced.  One study involving just psyllium showed no effect. The effects of dietary fibre on C-reactive protein, an inflammation marker predicting cardiovascular disease Conclusions: In the presence of weight loss and modified saturated, monounsaturated and polyunsaturated fat intakes, significantly lower CRP concentrations (25–54%) are seen with increased fibre consumption 3.3 g/MJ). Mechanisms are inconclusive but may involve the effect of DF on weight loss, and/or changes in the secretion, turnover or metabolism of insulin, glucose, adiponectin, interleukin-6, free fatty acids and triglycerides. Clinical studies of high- and low-fibre diets are needed to explore the potential favourable effects as observed epidemiologically, and to understand individual susceptibility to its anti-inflammatory effect and long-term cardiovascular red

Gary Taubes pointed fingers at just the excess carbohydrates in diets as the cause of the obesity epidemic. Lustig narrows the finger pointing even more to just one little sugar molecule:  fructose. Where he gets off saying that fructose is poison is beyond me.  When not consumed in excess/acute doses, there's no evidence that fructose if bad for humans.  Given that we have a separate metabolic pathway to handle it AND convert it to another form for energy storage fructose being a poison doesn't make sense.  Furthermore, evidence abounds that paleo man consumed most carbs from fruits and honey (honey having the fructose:glucose ratio similar to HFCS). AFAIC, it is a no-brainer, or should be, that consuming Mega Gulps of sugary sodas or several glasses of fruit juices and/or drinks is just plain stupid.  Why do Americans do this?  Lustig implies some addictive new ingredients in the secret formulas.  Sheesh!  It is not the American government, or the low-fat advocates who hav

One of the issues Dr. Lustig points to in his crusade against fructose is that of the obesity epidemic amongst 6 month olds.  Surely they can't be "eating more and moving less" like the rest of us, so there must be some bogey man here.  He points to sucrose in one brand of formula.  This got me to looking into whether or not there was a link between breastfeeding and obesity.   The results of numerous studies are inconclusive except for controlled studies limiting protein content.  So this got me to thinking of the usual tactic of correlating trends to identify the culprit.  One would expect a negative relationship between breastfeeding rates and obesity rates, when in fact the opposite seems to be the case. Formula feeding was even more popular in the 50's, and I've seen the resurging breastfeeding rates continue through at least 2003.  It hardly seems plausible, given the varied contents of formulas, that fructose in formula is singly responsible for the obes

Carbohydrate restriction regulates the adaptive response to fasting The importance of either carbohydrate or energy restriction in initiating the metabolic response to fasting was studied in five normal volunteers. The subjects participated in two study protocols in a randomized crossover fashion. In one study the subjects fasted for 84 h (control study), and in the other a lipid emulsion was infused daily to meet resting energy requirements during the 84-h oral fast (lipid study). Glycerol and palmitic acid rates of appearance in plasma were determined by infusing [2H5]glycerol and [1-13C]palmitic acid, respectively, after 12 and 84 h of oral fasting. Changes in plasma glucose, free fatty acids, ketone bodies, insulin, and epinephrine concentrations during fasting were the same in both the control and lipid studies. Glycerol and palmitic acid rates of appearance increased by 1.63 +/- 0.42 and 1.41 +/- 0.46 mumol.kg-1.min-1, respectively, during fasting in the control study and by 1.

I did a lot of research on this a while back and believe it may be the answer for some folks.

Is a calorie a calorie? Andrea C Buchholz and Dale A Schoeller   Wanted to post this here for my own organization.  This review looks at the results of various studies comparing high protein (OK, OK, yeah Atkins is high fat not high protein ...) low carb diets to low fat.  Their ultimate conclusion is, basically, yes.   Given the Eades/Colpo dust-up over at their respective blog/sites, this whole thing has come up again.  I think it's important to remember that food calories are a measure of metabolizable energy .  The 4/4/9 P/C/F numbers are averages that were determined for mixed meals.  But this should be accountable for in excretory products, because not only do we have thermodynamic laws, there's ultimately a conservation of mass issue.  Changing the proportions of macronutrients doesn't change the way(s) they are metabolized, though in the case of protein its use is changed.  A fatty acid that goes into the fatty acid spiral will produce the same amount of ATP whet

The ancestral human diet: what was it and should it be a paradigm for contemporary nutrition? Awareness of the ancestral human diet might advance traditional nutrition science. The human genome has hardly changed since the emergence of behaviourally-modern humans in East Africa 100–50 · 103 years ago; genetically, man remains adapted for the foods consumed then. The best available estimates suggest that those ancestors obtained about 35% of their dietary energy from fats, 35% from carbohydrates and 30% from protein. Saturated fats contributed approximately 7.5% total energy and harmful trans-fatty acids contributed negligible amounts. Polyunsaturated fat intake was high, with n-6:n-3 approaching 2:1 (v. 10:1 today). Cholesterol consumption was substantial, perhaps 480 mg/d. Carbohydrate came from uncultivated fruits and vegetables, approximately 50% energy intake as compared with the present level of 16% energy intake for Americans. High fruit and vegetable intake and minimal grain an

A few studies and such on protein and satiety: Weight, Protein, Fat, and Timing of Preloads Affect Food Intake Two foods, one rich in protein (HP) and one rich in fat (HF), were employed to evaluate the effect of macronutrients on food intake and to underline the differences that occurred when the foods were served as uniform meal, as first course of a varied meal, and as a snack 2 h before a varied meal. Our results showed that HP food always exerted a higher effect on both intrameal satiation and postingestive satiety than HF food. When a uniform meal was consumed, satiation for the specific food was reached before fullness; in this condition, sensory characteristics of foods played an important role in controlling food intake and made the uniform meal more satiating than the varied one. The consumption of a snack far from a meal did not contribute to satiety; consequently, gastric filling seems to be an important factor determining the amount consumed in a varied meal. Add this t

Lipotoxicity: When tissues overeat Recent findings Excess lipid accumulation in non-adipose tissues may arise in the setting of high plasma free fatty acids or triglycerides.  Alternatively, lipid overload results from mismatch between free fatty acid import and utilization. Evidence from human studies and animal models suggests that lipid accumulation in the heart, skeletal muscle, pancreas, liver, and kidney play an important role in the pathogenesis of heart failure, obesity and diabetes.  Excess free fatty acids may impair normal cell signaling, causing cellular dysfunction. In some circumstances, excess free fatty acids induce apoptotic cell death. Having stumbled across some disturbing information on elevated free fatty acids, I went back and dug up this review paper I had found a while back.  IF the low carb gurus are correct -- and LC essentially makes MORE NEFA/FFA's available in circulation -- then I do worry about the long term benefits of LC. Fats in circulation ca

One of my big issues with TNA is the concept of subtracting sugar alcohols from Net Carbs. IMO, the most fraudulent practice in the LC field is the total subtraction of SA's in the calculation of net carbs.  There are 1.5-2.5 cal/g for most of them (except erythritol which is 0.2 cal/g) and these calories are from carbs! Here's what TNA says on the subject: "When it comes to low-carb foods, you subtract grams of sugar alcohols (including glycerin), as well as of fiber, from total grams of carbs to get the Net Carb count." "Many low-carb products are sweetened with such ingredients as glycerin, mannitol, sorbitol, xylitol, erythritol, isomalt, lactitos and maltitol. ... Because sugar alcohols are not fully absorbed by the gut, they provide roughly half the calories that sugar does, although each one varies slightly. The incomplete and slower absorption results in a minimal impact on blood sugar and insulin response. This means that sugar alcohols don't sig

This post is a general review of: The New Atkins for a New You by Drs. Westman, Phinney, and Volek. I probably haven't posted enough here to expose my sometimes cynical side of low carb eating, but if there are any visitors from the LC-www who recognize me, you've probably have seen this side of me.  I didn't expect to learn anything groundbreakingly new in this book but was curious to see what was updated and how it was presented by these respected researchers.  Overall, I was pleasantly surprised. Overall Rating:    ☼ ☼ ☼  ☼ ☼ The Good:   Reads well Well organized Success stories are separated (so folks like me can skip over them ), and appear to avoid the sensational (based on my skimming of a few). Referenced throughout Encouraging Lays out the plan clearly Focuses on long term way of life over a "diet" Acknowledges that for Maintenance there are two paths -- one of which being maintaining a significantly restricted carb intake for life.  Less ob

Just putting this one out there: C-Reactive Protein and CVD Risk    (full text article available at link, abstract below) The role of C-reactive protein (CRP) in cardiovascular disease risk remains controversial, and several interrelated questions are unresolved. Although it is clear that higher circulating CRP levels are associated with coronary heart disease (CHD) incidence and mortality rates in prospective studies, the magnitude of this association has been downgraded in recent years (1). It is also clear that CRP levels are strongly related to many potential confounding factors that influence CHD incidence and mortality rates. In predictive models that appropriately account for these confounders, the magnitude of the association between CRP levels and CHD outcomes is considerably attenuated toward the null (2). Whether CRP is a marker of cardiovascular disease risk or is causally related to cardiovascular disease is uncertain. Nonetheless, some authors have recently claimed tha