Effects of a carbohydrate-restricted diet with and without supplemental soluble fiber on plasma low-density lipoprotein cholesterol and other clinical markers of cardiovascular risk.  J Clin Endocrinol Metab. 2007 Jan;92(1):284-92. Epub 2006 Oct 24.

Wood RJ,

Fernandez ML,

Sharman MJ,

Silvestre R,

Greene CM,

Zern TL,

Shrestha S,

Judelson DA,

Gomez AL,

Kraemer WJ,

Volek JS.

 

Carbohydrate-restricted diets (CRDs) promote weight loss, reductions in plasma triacylglycerol (TAG) levels, and increases in high-density lipoprotein cholesterol (HDL-C) levels but may cause undesirable low-density lipoprotein cholesterol (LDL-C) responses in some people. The objective of the present study was to determine the effect of adding soluble fiber to a CRD on plasma LDL-C and other traditionally measured markers of cardiovascular disease.

 

Using a parallel-arm, double-blind, placebo-controlled design, 30 overweight and obese men (body mass index, 25-35 kg/m(2)) were randomly assigned to supplement a CRD with soluble fiber (Konjac-mannan, 3g/d) (n = 15) or placebo (n = 15). Plasma lipids, anthropometrics, body composition, blood pressure, and nutrient intake were evaluated at baseline and at 6 and 12 weeks. Compliance was excellent as assessed by 7-day weighed dietary records and ketonuria. Both groups experienced decreases in (P < .01) body weight, percent body fat, systolic blood pressure, waist circumference, and plasma glucose levels.

 

After 12 weeks, HDL-C and TAG improved significantly in the fiber (10% and -34%) and placebo (14%, -43%) groups. LDL-C decreased by 17.6% (P < .01) at week 6 and 14.1% (P < .01) at week 12 in the fiber group. Conversely, LDL-C reductions were significant in the placebo group only after 12 weeks (-6.0%, P < .05).

 

We conclude that although clearly effective at lowering LDL-C, adding soluble fiber to a CRD during active and significant weight loss provides no additional benefits to the diet alone. Furthermore, a CRD led to clinically important positive alterations in cardiovascular disease risk factors.

 

PMID: 17161227 [PubMed - in process]

Recap:

A low-carb diet decreased the risk for heart disease (the #1 cause of premature death) by at least 20% -- in those who were overweight (and 2 thirds of us are "overweight").

High-fat/low-carbohydrate diet reduces insulin-stimulated carbohydrate oxidation but stimulates nonoxidative glucose disposal in humans: an important role for skeletal muscle pyruvate dehydrogenase kinase 4. J Clin Endocrinol Metab. 2007 Jan;92(1):284-92. Epub 2006 Oct 24.

 

Chokkalingam K,

Jewell K,

Norton L,

Littlewood J,

van Loon LJ,

Mansell P,

Macdonald IA,

Tsintzas K.

Aim: The aim of this report was to study the effect of high-fat (HF)/low-carbohydrate (CHO) diet on regulation of substrate metabolism in humans.

 

Methods: Ten healthy men consumed either a HF (75% energy as fat) or control (35%) diet for 6 d in random order. On d 7, blood glucose disappearance rate (R(d)) was determined before and during a hyperinsulinemic euglycemic clamp. Substrate oxidation was determined by indirect calorimetry. Muscle biopsies were obtained prediet, postdiet, and postclamps.

 

Results: R(d) was similar under basal conditions but slightly elevated ( approximately 10%, P < 0.05) during the last 30 min of the clamp after the HF diet. HF diet reduced CHO oxidation under basal (by approximately 40%, P < 0.05) and clamp conditions (by approximately 20%, P < 0.05), increased insulin-mediated whole-body nonoxidative glucose disposal (by 30%, P < 0.05) and muscle glycogen storage (by approximately 25%, P < 0.05). Muscle pyruvate dehydrogenase complex activity was blunted under basal and clamp conditions after HF compared with control (P < 0.05) and was accompanied by an approximately 2-fold increase (P < 0.05) in pyruvate dehydrogenase kinase 4 (PDK4) mRNA and protein expression.

 

Conclusion: Short-term HF/low-CHO dietary intake did not induce whole-body insulin resistance, but caused a shift in im glucose metabolism from oxidation to glycogen storage. Insulin-stimulated CHO oxidation and muscle pyruvate dehydrogenase complex activity were blunted after the HF diet. Up-regulation of muscle PDK4 expression was an early molecular adaptation to these changes, and we showed for the first time in healthy humans, unlike insulin-resistant individuals, that insulin can suppress PDK4 but not PDK2 gene expression in skeletal muscle.

 

PMID: 17062764 [PubMed - in process]

Recap:

A high-fat/low-carb diet increased insulin sensitivity (i.e. whole-body nonoxidative glucose disposal) in healthy men.

Caloric intake and Alzheimer's disease. Experimental approaches and therapeutic implications. Interdiscip Top Gerontol. 2007;35:159-75.

Pasinetti GM,

Zhao Z,

Qin W,

Ho L,

Shrishailam Y,

Macgrogan D,

Ressmann W,

Humala N,

Liu X,

Romero C,

Stetka B,

Chen L,

Ksiezak-Reding H,

Wang J.

Alzheimer's disease (AD) is a rapidly growing public health concern with potentially devastating effects. Presently, there are no known cures or effective preventive strategies. While genetic factors are relevant in early-onset cases, they appear to play less of a role in late-onset sporadic AD cases, the most common form of AD. Due to the fact that the disease typically strikes very late in life, delaying symptoms could be as good as a cure for many people. For example, it is now widely accepted that if the onset of the disease could be delayed by even 5 years, the incidence could be cut in half. Both clinical and epidemiological evidence suggests that modification of lifestyle factors such as nutrition may prove crucial to AD management given the mounting experimental evidence suggesting that brain cells are remarkably responsive to "what somebody is doing".

 

 Among other nongenetic factors influencing AD, recent studies strongly support the evidence that caloric intake may play a role in the relative risk for AD clinical dementia. Indeed, the effect of diet in AD has been an area of research that has produced promising results, at least experimentally. Most importantly, as mechanistic pathways are defined and their biochemical functions scrutinized, the evidence supporting a direct link between nutrition and AD neuropathology continues to grow. Our work, as well as that of others, has recently resulted in the development of experimental dietary regimens that might promote, attenuate or even reverse features of AD.

 

Most remarkably, while we found that high caloric intake based on saturated fat promotes AD type Beta-amyloidosis, conversely we found that dietary restriction based on reduced carbohydrate intake is able to prevent it. This evidence is very exciting and is, in part, consistent with current epidemiological studies suggesting that obesity and diabetes are associated with a >4-fold increased risk of developing AD. The clarification of the mechanisms through which dietary restriction may beneficially influence AD neuropathology and the eventual discovery of future "mimetics" capable of anti-Beta-amyloidogenic activity will help in the development of "lifestyle therapeutic strategies" in AD and possibly other neurodegenerative disorders.

 

PMID: 17063038 [PubMed - indexed for MEDLINE]

Recap:

Restricting carbs is your best bet for preventing what I call the "walking-death" (Alzheimer's disease). One researcher once said that, if you live long enough, you will get Alzheimer's disease (or Parkinson's). Brain aging is often thought to be out of human control. My aim is to prove this researcher wrong. Perhaps I ought to introduce, for the first time, a new concept: mind-span (the time-to-consciousness-loss). Step #1: To maximize your mind-span, control your carb intake. 100 grams or less per day of non-fiber carbohydrate -- would be a good start.

;-)

Ed

Restricting carbs is your best bet for preventing what I call the "walking-death" (Alzheimer's disease). One researcher once said that, if you live long enough, you will get Alzheimer's disease (or Parkinson's).

Taking small doses of Jumex or Deprenyl shows a significant chance of seriously delaying or preventing all together the onset of alzheimers.

Toxic Tuna

Mercury in canned tuna: white versus light and temporal variation. Environ Res. 2004 Nov;96(3):239-49.

 

Burger J, Gochfeld M.

 

We analyzed 168 cans individually for total mercury. All values are reported as parts per million (= microg/g) on a wet weight basis. In a subset of samples analyzed for total and inorganic mercury, the inorganic mercury was below detection levels; hence at least 89% of the mercury can be considered methylmercury.

 

… white-style tuna had significantly more total mercury (mean 0.407 ppm) than light-style tuna (mean 0.118 ppm), presumably reflecting that "white" tuna is albacore, a species relatively larger than the skipjack tuna, which is commonly available as "light" or "chunk light." The maximum mercury in a can was 0.997 ppm [Ed’s note: this is ~100mcg mercury/100grams of tuna!], but 25% of white tuna samples exceeded 0.5 ppm.

 

Data suggest a slight increase in levels since 1991, and mercury levels were significantly higher in 2001 than in other years. The mean level of mercury in white tuna (mean 0.407 ppm) was significantly higher than the mean value of 0.17 ppm currently used by the U.S. Food and Drug Administration (FDA) in its risk assessment and public information.

 

There were no significant differences in mercury levels in tuna packed in oil compared to water. Draining contents had no effect on mercury levels, and the fluid, both oil and water, contained little mercury. These data indicate that people who eat canned tuna frequently can choose light tuna and reduce their mercury intake. Canned mackerel had much lower levels of mercury than tuna.

PMID: 15364590 [PubMed - indexed for MEDLINE]