Thursday, December 12, 2013

J Pediatr Endocrinol Metab. 2012;25(7-8):697-704. Metabolic impact of a ketogenic diet compared to a hypocaloric diet in obese children and adolescents. Partsalaki I, Karvela A, Spiliotis BE. BACKGROUND: The effects of carbohydrate-restricted (ketogenic) diets on metabolic parameters in children have been incompletely assessed. OBJECTIVE: To compare the efficacy and metabolic impact of ketogenic and hypocaloric diets in obese children and adolescents. SUBJECTS: Fifty-eight obese subjects were placed on one of the two diets for 6 months. METHODS: Anthropometric measurements, body composition, oral glucose/insulin tolerance test, lipidemic profile, high molecular weight (HMW) adiponectin, whole-body insulin sensitivity index (WBISI), and homeostatic model assessment-insulin resistance (HOMA-IR) were determined before and after each diet. RESULTS: Both groups significantly reduced their weight, fat mass, waist circumference, fasting insulin, and HOMA-IR (p = 0.009 for ketogenic and p = 0.014 for hypocaloric), but the differences were greater in the ketogenic group. Both groups increased WBISI significantly, but only the ketogenic group increased HMW adiponectin significantly (p = 0.025). CONCLUSIONS: The ketogenic diet revealed more pronounced improvements in weight loss and metabolic parameters than the hypocaloric diet and may be a feasible and safe alternative for children's weight loss. Combating insulin resistance is the key, and low carb seems to do this pretty well. I wasn't sure if going low carb only meant you had better responses because your insulin went down, or if your insulin resistance was improved. Seems like the latter.

Ketogenic low-carbohydrate diets have no metabolic advantage over nonketogenic low-carbohydrate diets.

Ketogenic low-carbohydrate diets have no metabolic advantage over nonketogenic low-carbohydrate diets. Am J Clin Nutr. 2006 May;83(5):1055-61. Ketogenic low-carbohydrate diets have no metabolic advantage over nonketogenic low-carbohydrate diets. Johnston CS, Tjonn SL, Swan PD, White A, Hutchins H, Sears B. BACKGROUND: Low-carbohydrate diets may promote greater weight loss than does the conventional low-fat, high-carbohydrate diet. OBJECTIVE: We compared weight loss and biomarker change in adults adhering to a ketogenic low-carbohydrate (KLC) diet or a nonketogenic low-carbohydrate (NLC) diet. DESIGN: Twenty adults [body mass index (in kg/m(2)): 34.4 +/- 1.0] were randomly assigned to the KLC (60% of energy as fat, beginning with approximately 5% of energy as carbohydrate) or NLC (30% of energy as fat; approximately 40% of energy as carbohydrate) diet. During the 6-wk trial, participants were sedentary, and 24-h intakes were strictly controlled. RESULTS: Mean (+/-SE) weight losses (6.3 +/- 0.6 and 7.2 +/- 0.8 kg in KLC and NLC dieters, respectively; P = 0.324) and fat losses (3.4 and 5.5 kg in KLC and NLC dieters, respectively; P = 0.111) did not differ significantly by group after 6 wk. Blood beta-hydroxybutyrate in the KLC dieters was 3.6 times that in the NLC dieters at week 2 (P = 0.018), and LDL cholesterol was directly correlated with blood beta-hydroxybutyrate (r = 0.297, P = 0.025). Overall, insulin sensitivity and resting energy expenditure increased and serum gamma-glutamyltransferase concentrations decreased in both diet groups during the 6-wk trial (P < 0.05). However, inflammatory risk (arachidonic acid:eicosapentaenoic acid ratios in plasma phospholipids) and perceptions of vigor were more adversely affected by the KLC than by the NLC diet. CONCLUSIONS: KLC and NLC diets were equally effective in reducing body weight and insulin resistance, but the KLC diet was associated with several adverse metabolic and emotional effects. The use of ketogenic diets for weight loss is not warranted.

Friday, December 06, 2013

There are still health risks for metabolically healthy obese individuals

There are still health risks for metabolically healthy obese individuals Obese people who are currently metabolically healthy face a higher risk of developing diabetes and cardiovascular disease, according to new research accepted for publication in The Endocrine Society's Journal of Clinical Endocrinology & Metabolism. Research has found conflicting evidence about whether it is possible for some obese people to avoid health complications that increase the risk of metabolic diseases. These complications can include high blood pressure, high blood sugar, insulin resistance and low levels of high-density lipoproteins, the "good" form of cholesterol that reduces heart disease risk. Past studies have found as many as 30 percent of obese people may be metabolically healthy. "Unfortunately, our findings suggest metabolically healthy obesity is not a benign condition," said the study's corresponding author, Carlos Lorenzo, MD, of the University of Texas Health Science Center at San Antonio, Texas. "Regardless of their current metabolic health, people who are obese face an increased risk of developing cardiovascular disease and diabetes in the future." To determine metabolic health, researchers examined whether subjects had elevated blood pressure, elevated triglyceride and blood sugar levels, insulin resistance and decreased HDL cholesterol. People who had none or only one of the characteristics were classified as metabolically healthy. The analysis found that increased body mass index was linked to an elevated risk of developing diabetes. Normal weight people who had multiple metabolic abnormalities also faced an increased risk of developing diabetes. Both groups faced an elevated risk of cardiovascular disease after taking into account demographics and smoking behavior. "Our data demonstrate the importance of continuing to monitor for diabetes and cardiovascular disease in both people with metabolically healthy obesity and those who have metabolically abnormalities despite being a normal weight," Lorenzo said. "If physicians and patients are too complacent about assessing risk, we can miss important opportunities to prevent the development of chronic and even deadly conditions."

Study casts doubt on whether extra vitamin D prevents disease

Study casts doubt on whether extra vitamin D prevents disease By Kate Kelland LONDON (Reuters) - Researchers cast doubt on the prevailing wisdom that vitamin D supplements can prevent conditions like cancer, diabetes and heart disease, saying on Friday low vitamin D may be a consequence, not a cause, of ill health. The findings could have implications for millions of people who take vitamin D pills and other supplements to ward off illness - Americans spend an estimated $600 million a year on them alone. Vitamin D, sometimes known as the "sunshine vitamin" is made in the body when the skin is exposed to sunlight and in found in foods like fish liver oil, eggs and fatty fish such as salmon, herring and mackerel. [...] Researchers led by Philippe Autier of France's International Prevention Research Institute in Lyon analyzed data from several hundred observational studies and clinical trials examining the effects of vitamin D levels on so-called non-bone health - including links to illness such as cancer, diabetes and cardiovascular disease. They found that the benefits of high vitamin D levels seen in observational studies — including reduced risk of cardiovascular events, diabetes and colorectal cancer - were not replicated in randomized trials where participants were given vitamin D to see if it would protect against illness. "What this discrepancy suggests is that decreases in vitamin D levels are a marker of deteriorating health," said Autier. In other words, he explained, serious illness like cancer and diabetes may reduce vitamin D concentrations, but that does not necessarily mean that raising vitamin D levels would prevent the illness from occurring.

Sunday, November 24, 2013

The ‘Healthy Obese’ and Their Healthy Fat Cells

The ‘Healthy Obese’ and Their Healthy Fat Cells By ANAHAD O'CONNOR They are a mystery to researchers: people who are significantly overweight and yet show none of the usual metabolic red flags. Despite their obesity, they have normal cholesterol levels, healthy blood pressure levels and no apparent signs of impending diabetes. Researchers call them the metabolically healthy obese, and by some estimates they represent as many as a third of all obese adults. Scientists have known very little about them, but new research may shed some light on the cause of their unusual metabolic profile. A study in the journal Diabetologia has found that compared with their healthier counterparts, people who are obese but metabolically unhealthy have impaired mitochondria, the cellular powerhouses that harvest energy from food, as well as a reduced ability to generate new fat cells. Unlike fat tissue in healthy obese people, which generates new cells to help store fat as it accumulates, the fat cells of the unhealthy obese swell to their breaking point, straining the cellular machinery and ultimately dying off. This is accompanied by inflammation, and it leads to ectopic fat accumulation — the shuttling of fat into organs where it does not belong, like the liver, heart and skeletal muscle. A fatty liver frequently coincides with metabolic abnormalities, and studies suggest that it may be one of the causes of insulin resistance, the fundamental defect in Type 2 diabetes. In the healthy obese, however, the fat tends to remain in the subcutaneous padding just beneath the skin, where it appears to be fairly innocuous. “The group that doesn’t gain fat in the liver as they get obese seems to avoid inflammation and maintain their metabolic health,” said Dr. Jussi Naukkarinen, a research scientist specializing in internal medicine at the University of Helsinki. “There is a complete difference in how they react to obesity.” It is clear that obesity is tightly linked to a host of chronic illnesses, among them heart disease, hypertension and Type 2 diabetes. That there are metabolically normal obese adults suggests that there is a way to safely carry excess fat. But to what extent is not clear. Metabolically healthy obesity is found more frequently among younger adults, as a large study in the journal Diabetes Care demonstrated in August. There is growing evidence that it may be a transition state, and that if followed long enough, some, if not many, people in this category will eventually develop the expected metabolic disturbances. That study followed several thousand Australians for up to a decade, about 12 percent of whom were initially deemed metabolically healthy obese. “We found that about a third of these people progressed down the road to being metabolically unhealthy,” said Sarah Appleton, a research fellow at the University of Adelaide. “Metabolically healthy obesity may essentially be a transient state.” But there is evidence that not everyone will progress down that road, or at least not so quickly. In Dr. Naukkarinen’s new study, for example, the obese subjects had become obese at similar ages and remained so for about a decade — yet some showed no metabolic disturbances. “The metabolically healthy obese individuals are in the minority,” he said. “Most people tend to go along the not so healthy lines. But you do see some who have been obese for a long time and maintain their healthy profile.” Dr. Naukkarinen and his colleagues have studied obesity for years by focusing on identical twins, allowing them to take into account the influence of genetics, environment and other factors. One idea they had was to study pairs of identical twins in which one twin is obese and the other is not. After contacting thousands of families in Finland, they came across 16 such pairs of identical adult twins, six male and 10 female. Once they got them into a lab and began testing, half of the obese twins quickly stood out. “The first thing that popped out was when we looked at the amount of fat stored in their livers,” Dr. Naukkarinen said. “There was a significant difference.” The 16 pairs were split evenly into two groups. In both, the average weight difference between the siblings was about 40 pounds. But in one group, the obese siblings had higher blood pressure, worse cholesterol levels and poorer measures of blood sugar and insulin production, as well as seven times the amount of fat in their livers. In the other group, the obese twins’ blood work and liver fat was similar to that of their lean twins. Extensive tests of each person’s fat tissue revealed some other surprises. The healthy obese had 11 percent more adipocytes, or fat cells, in their subcutaneous fat tissue than their normal weight twins. But the unhealthy obese had 8 percent fewer fat cells than their leaner siblings, despite a higher body fat percentage. The fat cells of the unhealthy obese were larger than those of any other group. They were swollen and riddled with inflammation. The breakdown and mobilization of their fat stores was suppressed, and a closer look showed that their mitochondria were malfunctioning. Their ability to burn fuel and produce adenosine triphosphate, or ATP, the body’s energy currency, was reduced. Properly functioning mitochondria stimulate the creation of new fat cells, which may explain in part why the unhealthy obese had fat cells that were limited in number and bloated to extremes. But it’s not clear what happens first. Is inflammation the initial stressor that impairs the mitochondria? Or do the mitochondria malfunction first, leading to inflammation that arrives to clear away the engorged and dying fat cells? Studies show that the fat tissue of some obese adults can accumulate more immune cells than actual fat cells. Under a microscope, their fat cells are surrounded by white blood cells called macrophages, the dump trucks that engulf and dispose of pathogens and cellular debris. “If your mitochondria are working poorly, the adipose cells don’t divide properly, and that can lead to cell death,” Dr. Naukkarinen said. “But if you have adipose tissue that is inflamed, the inflammation makes the mitochondria function poorly – it’s toxic to them. So we see a vicious cycle.” Metabolically healthy obesity may be one side of a vast spectrum. On the other are people who suffer from lipodystrophy, a severe lack of fat cells. People with this disorder are typically gaunt, carrying little or no subcutaneous fat. But they are also extremely insulin resistant, and they tend to have fatty livers and ectopic fat accumulation. There are many people with Type 2 diabetes who are also physically very lean. It remains to be seen to what extent environment, exercise and genetics determine metabolically healthy obesity. But Dr. Naukkarinen said that anti-inflammatory drugs have been shown to protect mitochondrial function and improve diabetic symptoms and glucose metabolism. And he suspects that heavy alcohol consumption and exposure to high glycemic foods that create spikes in blood glucose and insulin levels, like sugar and white flour, may also play a role. But more study is needed. “People haven’t really paid that much attention to metabolically healthy obesity, but I think it can teach us a lot about usual obesity,” he said. “It’s only recently that people studying depression have done happiness studies showing what goes right, and I’m thinking about the metabolically healthy obese phenomenon in the same way.”

Maps: The Mysterious Link Between Antibiotics and Obesity States where doctors prescribe more antibiotics also have the highest obesity rates. Why?

Maps: States where doctors prescribe more antibiotics also have the highest obesity rates. Why? Indeed, a growing body of evidence suggests that antibiotics might be linked to weight gain. A 2012 New York University study found that antibiotic use in the first six months of life was linked with obesity later on. Another 2012 NYU study found that mice given antibiotics gained more weight than their drug-free counterparts. As my colleague Tom Philpott has noted repeatedly, livestock operations routinely dose animals with low levels of antibiotics to promote growth. No one knows exactly how antibiotics help animals (and possibly humans) pack on the pounds, but there are some theories. One is that antibiotics change the composition of the microbiome, the community of microorganisms in your body that scientists are just beginning to understand. (For a more in-depth look at the connection between bacteria and weight loss, read Moises Velasquez-Manoff's piece on the topic.) Hicks says that more research is needed on the potential connection between antibiotics and obesity

Friday, September 20, 2013

Harvard Study: Eating White Rice Increases Risk Of Type 2 Diabetes A recent Harvard study has discovered a link between higher white rice intake and a significantly elevated risk of type 2 diabetes, especially among Asian populations. White rice is the predominant type of rice eaten worldwide and has high glycemic index (GI) values. High GI diets have been shown to be associated with an increased risk of developing type 2 diabetes. Compared to brown rice, it has a lower content of nutrients including fiber, magnesium, and vitamins, which may contribute to the increased risk, the authors report. The authors caution that an increased intake of other sources of refined carbohydrates such as pastries, white bread, and sugar sweetened beverages may also contribute to type 2 diabetes, not simply just white rice. They recommend eating whole grains instead of refined carbohydrates, which they hope will help slow down the global diabetes epidemic. Both Asian and Western cultures are susceptible to this diabetes risk, the authors say, although it is thought that Asian countries are at a higher risk due to a generally higher rice consumption.

Tuesday, May 07, 2013

Excess Glucose May Harden Heart and Lungs

Excess Glucose May Harden Heart and Lungs

Excess Glucose May Harden Heart and Lungs

Research found that glucose suppressed ferroelectricity up to 50%....

New research conducted at the University of Washington and Boston University has shown that excess glucose in the body could damage the elastic proteins found in important organs such as the heart and lungs, which aid in breathing and pumping blood.

In this study, aortic tissue was separated into two types of proteins, elastin and collagen. Ferroelectric switching is what allows the elastin to be flexible and convey repeated pulses, in organs such as the arteries. It is a response to an electric field in which a molecule switches from having a positive charge to a negative charge. Recent discoveries in animal tissue have traced this property to elastin in animal tissues.

When researchers treated the elastin with sugar, they noticed a 50% suppression of the ferroelectric switching. The sugar-protein interaction mimics glycation, a process where sugar molecules attach to proteins and degrade their structure and function. Consequently, hardening of the tissues, and degradation of ligaments and arteries has been observed, leading to an overall loss of function.

Co-author, Jiangyu Li, says, "This could be associated with aging and diabetes."

Yuanming Liu, Yunjie Wang, Ming-Jay Chow, Nataly Q. Chen, Feiyue Ma, Yanhang Zhang, and Jiangyu Li. Glucose suppresses biological ferroelectricity in aortic elastin. Physical Review Letters, 2013

The Inter-Relationships between Vegetarianism and Eating Disorders among Females

The Inter-Relationships between Vegetarianism and Eating Disorders among Females

The Inter-Relationships between Vegetarianism and Eating Disorders among Females
Accepted 24 April 2012.

Abstract

When individuals with a suspected or diagnosed eating disorder adopt a vegetarian diet, health care professionals might worry that this choice could function as a socially acceptable way to legitimize food avoidance. Yet only limited research has examined vegetarianism in relation to eating disorders. Our study objectives were to compare individuals with and without an eating disorder history and individuals at different stages of eating disorder recovery on past and current vegetarianism and motivations for and age at becoming vegetarian.
[...]
The three recovery status groups (fully recovered, partially recovered, and active eating disorder) did not differ significantly in percentiles endorsing a history of vegetarianism or weight-related reasons as primary, but they differed significantly in current vegetarianism (33% of active cases, 13% of partially recovered, 5% of fully recovered; P<0.05). Most perceived that their vegetarianism was related to their eating disorder (68%) and emerged after its onset. Results shed light on the vegetarianism-eating disorders relation and suggest intervention considerations for clinicians (eg, investigating motives for vegetarianism).

Monday, April 01, 2013

From Sleep Study, Clues to Happiness - NYTimes.com

From Sleep Study, Clues to Happiness - NYTimes.com

A little over a decade ago, scientists discovered that narcolepsy, the neurological disorder that leads to episodes of irresistible sleepiness, is caused by the loss of brain cells that produce hypocretin, a neurotransmitter that promotes wakefulness.

But the discovery did not shed light on two other mysterious problems associated with the disorder. Narcoleptics have profoundly high rates of depression — up to six times the rate in the general population — and they have a tendency to collapse when swept by some emotions, a phenomenon known as cataplexy.

Now research shows that in addition to regulating sleep, hypocretin also appears to govern emotion, particularly experiences of joy and happiness.

The study has implications that extend beyond narcolepsy. It suggests that the brain has several different arousal systems, and that one of them, driven by hypocretin, has the specific function of keeping people awake for pleasure.

Friday, March 29, 2013

Ketogenic Diet Reverses Kidney Disease (Nephropathy) - YouTube

Lol, this is rich. "Ketogenic Diet Reverses Kidney Disease (Nephropathy)"

OMG! This is incredible! Kidney failure is irreversible! But eating this strange high fat diet COMPLETELY CURED IT within 2 months for mice! Let's start testing the diet on people whose total lack of kidney function is a death sentence, right?

Wrong- quote "a high fat diet could have other problems. We don't want to actually put people on the diet, we want to figure out how the diet works and make a drug that does the same thing", Lol. Yeah,  not like kids with epilepsy have been on ketogenic diets for years since the 1950's with no ill effects. Maybe someday someone will find evidence dietary fat causes heart disease, ha ha


Ketogenic Diet Reverses Kidney Disease (Nephropathy) - YouTube: Ketogenic Diet Reverses Kidney Disease (Nephropathy)

Charles Mobbs, a scientist at Mount Sinai School of Medicine in New York, discovers how a low carb, ketogenic diet reverses kidney failure in diabetic mice.

Wednesday, March 27, 2013

After weight-loss surgery, new gut bacteria keep obesity away | Reuters

After weight-loss surgery, new gut bacteria keep obesity away | Reuters

The logic behind weight-loss surgery seems simple: rearrange the digestive tract so the stomach can hold less food and the food bypasses part of the small intestine, allowing fewer of a meal's calories to be absorbed. Bye-bye, obesity.

A study of lab mice, published on Wednesday, begs to differ. It concludes that one of the most common and effective forms of bariatric surgery, called Roux-en-Y gastric bypass, melts away pounds not - or not only - by re-routing the digestive tract, as long thought, but by changing the bacteria in the gut.

Or, in non-scientific terms, the surgery somehow replaces fattening microbes with slimming ones.

If that occurs in people, too, then the same bacteria-changing legerdemain achieved by gastric bypass might be accomplished without putting obese patients under the knife in an expensive and risky operation.

[...]

For many obese patients, particularly those with type 2 diabetes, gastric bypass has succeeded where nothing else has. Severely obese patients routinely lose 65 to 75 percent of their excess weight and fat after the operation, studies show, and leave their diabetes behind.

Oddly, however, the diabetes remission often occurs before significant weight loss. That has made bypass surgeons and weight-loss experts suspect that Roux-en-Y changes not only anatomy but also metabolism or the endocrine system. In other words, the surgery does something besides re-plumb the gut.

That "something," according to previous studies, includes altering the mix of trillions of microbes in the digestive tract. Not only are the "gut microbiota" different in lean people and obese people, but the mix of microbes changes after an obese patient undergoes gastric bypass and becomes more like the microbiota in lean people.
[...]

Another new study found that figuring out whether you have slimming microbiota or fattening ones might be as easy as breathing.

In a study published on Tuesday in the online edition of the Journal of Clinical Endocrinology & Metabolism, researchers at Cedars-Sinai Medical Center in Los Angeles report that people whose breath has high concentrations of both hydrogen and methane gases are more likely to have a higher body mass index and higher percentage of body fat.

Methane is associated with bacteria called Methanobrevibacter smithii, which in overabundance may cause weight gain by extracting calories from food super-efficiently, Cedars' Ruchi Mathur, who led the study, said: "It could allow a person to harvest more calories from their food."

The breath test could provide a warning that someone is at risk of obesity because he harbors fattening microbiota.

It could also validate what many overweight people have long suspected: if their slim friends eat two slices of bacon-cheeseburger pizza the 600 calories go through them like celery, but if the overweight person indulges then every calorie seems to turn into more fat. People absorb different quantities of calories from the exact same food, thanks to their gut microbiota.

Thursday, March 21, 2013

Whole Milk Linked to Slimmer Kids - Neatorama

Whole Milk Linked to Slimmer Kids - Neatorama

The American Academy of Pediatrics recommends that children switch from whole milk to a lower fat milk at age two. The conventional wisdom is that getting children used to reduced fat milk will help keep them at a healthy weight. Skim, 1%, or 2% milk has fewer calories per cup. It just makes sense, doesn't it?

So here's where things gets confusing. A new study of preschool-aged children published in the Archives of Disease in Childhood, a sister publication of the British Medical Journal, finds that low-fat milk was associated with higher weight.

That's right, kids drinking low-fat milk tended to be heavier.

Thursday, March 07, 2013

Changes in the basal metabolic ... [J Nutr Sci Vitaminol (Tokyo). 1989] - PubMed - NCBI

Changes in the basal metabolic rate of a normal woman induced by short-term and long-term alterations of energy intake. [J Nutr Sci Vitaminol (Tokyo). 1989] - PubMed - NCBI

Abstract

A long-term experiment was carried out to study the effects of alterations in energy intake and meal contents on basal metabolic rate (BMR) of a normal woman. Alterations of energy intake induced changes in BMR and pulse rate in addition to body weight changes. Whether BMR was expressed per whole body, per unit body weight, or per unit body surface area, it increased progressively during long-term overeating periods, and decreased markedly during long-term undereating periods. These results suggest that there exists 'Luxuskonsumption', or adaptive diet-induced thermogenesis, during an overeating period and hypometabolism during an undereating period. BMR was affected significantly by the menstrual cycle but not by nutrient composition when daily energy intake was fixed at 2000 kcal for a long time.

Sunday, March 03, 2013

Discovery Lecture explores brain’s sensitivity to insulin | VUMC Reporter | Vanderbilt University

Discovery Lecture explores brain’s sensitivity to insulin | VUMC Reporter | Vanderbilt University

Diabetes has a big impact on the brain.

Patients with diabetes have more cognitive dysfunction, are at increased risk for developing Alzheimer’s disease, and have higher rates of depression and eating disorders.

What’s going on is the brain is actually a metabolic organ, exquisitely sensitive to insulin, internationally known diabetes researcher C. Ronald Kahn, M.D., said during last week’s Flexner Discovery Lecture/Irwin Eskind Lecture in Biomedical Science at Vanderbilt University Medical Center.

“Changing insulin signaling in the brain changes brain function in terms of things the brain normally does, which is mood and behavior activity,” said Kahn, the Mary K. Iaccoca Professor of Medicine at Harvard Medical School.

Through studies of genetically manipulated “knock-out” mice lacking brain receptors for insulin, Kahn and his colleagues have shown that insulin signaling affects the function of neurotransmitters including dopamine and serotonin, which in turn regulate mood and behavior.

These mice “show increased anxiety and signs of depression, which improve through treatment by antidepressant drugs,” he said.

Thursday, February 28, 2013

Desk workers - stand up for your health: Millions may be making themselves ill by spending their working lives sitting down - Health News - Health & Families - The Independent

Desk workers - stand up for your health: Millions may be making themselves ill by spending their working lives sitting down - Health News - Health & Families - The Independent

The research, published in the journal Diabetologica, found a range of behaviours: some of the people in the study spent as little as three hours a day sitting, but most spent more than 10 hours in a chair, and a few regularly sat down for 16 hours a day. The conclusion was that people at risk of diabetes could be well advised to spend less time sitting and more time standing up, said Joseph Henson, a diabetes researcher at Leicester University.

"The longer the time you spend sitting, the higher the amount of sugars and fats that accumulate in your bloodstream regardless of the time you spend exercising," Dr Henson said.

"There's a significant difference between people who sit a lot and those who don't. Those who spend the least time sitting have the lowest values of glucose and fats in their blood."

Scientists have found that a person's metabolic rate crashes to a minimum when sitting and that standing up for an extra three hours a day, even without exercising, would on average burn off about 3.6kg of fat a year.

Wednesday, February 06, 2013

Normal cardiac rhythm during hypocaloric die... [Arch Intern Med. 1983] - PubMed - NCBI

Normal cardiac rhythm during hypocaloric die... [Arch Intern Med. 1983] - PubMed - NCBI

Normal cardiac rhythm during hypocaloric diets of varying carbohydrate content.
Phinney SD, Bistrian BR, Kosinski E, Chan DP, Hoffer LJ, Rolla A, Schachtel B, Blackburn GL.
Abstract

Cardiac arrhythmias have been implicated in the deaths of 17 morbidly obese individuals subsisting on a collagen hydrolysate preparation ("liquid protein") during a modified fasting regimen for weight loss. Serious cardiac arrhythmias have been noted in three of six subjects studied prospectively within 28 days of starting a similar regimen, which used an inadequate protein source and was nearly devoid of all essential minerals. A comparative study of three 28-day weight loss diets of varying carbohydrate, protein, and energy content (450 to 820 kcal/day) but employing protein of good quality and adequate in micronutrients did not disclose substantial diet-related arrhythmias in five subjects on each of the three diets. The incidence of arrhythmia seen with liquid protein diets is not likely to be related to the absolute energy or carbohydrate content of the modified fasting regimen itself.

Good to know. Phinney's recent book on low carb diets and his book on low carb performance are excellent. Having finished a recent fast (lost 77lbs in 19 days- lots of water weight, which is good). I've been reading quite a bit about PSMF protein sparing modified fasts. The idea is to cut carbs and fat (except your own body fat which you burn), and consume enough lean protein to fight muscle tissue loss. I've seen different estimates of how much lean tissue is lost during fasting.

Metabolic consequences of very-low-calorie diet the... [Diabetes. 1986] - PubMed - NCBI

Metabolic consequences of very-low-calorie diet the... [Diabetes. 1986] - PubMed - NCBI: Abstract

To determine the effects of very-low-calorie diets on the metabolic abnormalities of diabetes and obesity, we have studied 10 obese, non-insulin-dependent diabetic (NIDDM) and 5 obese, nondiabetic subjects for 36 days on a metabolic ward during consumption of a liquid diet of 300 kcal/day with 30 g of protein.

[...]

The composition of the weight lost at completion was similar in both groups and ranged from 21.6% to 31.3% water, 3.9% to 7.8% protein, and 60.9% to 74.5% fat.

[...]

This study demonstrates that short-term treatment with a very-low-calorie diet in both obese diabetic and nondiabetic subjects results in: safe and effective weight loss associated with the normalization of elevated glucose and lipid levels, a large individual variability in total nitrogen loss determined principally by the initial lean body mass, and progressive increments in the contribution of fat to weight loss with stable caloric requirements and no evidence of a hypometabolic response.


Saturday, January 26, 2013

Ebony - Man fasts 4 months, loses 180 lbs.

Ebony - Google Books

http://books.google.com/books?id=-1rJTL1zGTwC&pg=PA42&lpg=PA42&dq=Ernst+J.+Drenick+fasting&source=bl&ots=HM8xJVbpW0&sig=-p7prWjJ7oFjLo_CJUhu8Co0hjI&hl=en&sa=X&ei=Af8DUaXmKa3h0wHh4YCIDg&ved=0CGoQ6AEwBzgK#v=onepage&q=Ernst%20J.%20Drenick%20fasting&f=false

JAMA Network | JAMA | Comparison of the Atkins, Zone, Ornish, and LEARN Diets for Change in Weight and Related Risk Factors Among Overweight Premenopausal WomenThe A TO Z Weight Loss Study: A Randomized Trial

JAMA Network | JAMA | Comparison of the Atkins, Zone, Ornish, and LEARN Diets for Change in Weight and Related Risk Factors Among Overweight Premenopausal WomenThe A TO Z Weight Loss Study: A Randomized Trial

Context  Popular diets, particularly those low in carbohydrates, have challenged current recommendations advising a low-fat, high-carbohydrate diet for weight loss. Potential benefits and risks have not been tested adequately.
Objective  To compare 4 weight-loss diets representing a spectrum of low to high carbohydrate intake for effects on weight loss and related metabolic variables.
Design, Setting, and Participants  Twelve-month randomized trial conducted in the United States from February 2003 to October 2005 among 311 free-living, overweight/obese (body mass index, 27-40) nondiabetic, premenopausal women.
Intervention  Participants were randomly assigned to follow the Atkins (n = 77), Zone (n = 79), LEARN (n = 79), or Ornish (n = 76) diets and received weekly instruction for 2 months, then an additional 10-month follow-up.
Main Outcome Measures  Weight loss at 12 months was the primary outcome. Secondary outcomes included lipid profile (low-density lipoprotein, high-density lipoprotein, and non–high-density lipoprotein cholesterol, and triglyceride levels), percentage of body fat, waist-hip ratio, fasting insulin and glucose levels, and blood pressure. Outcomes were assessed at months 0, 2, 6, and 12. The Tukey studentized range test was used to adjust for multiple testing.
Results  Weight loss was greater for women in the Atkins diet group compared with the other diet groups at 12 months, and mean 12-month weight loss was significantly different between the Atkins and Zone diets (P<.05). Mean 12-month weight loss was as follows: Atkins, −4.7 kg (95% confidence interval [CI], −6.3 to −3.1 kg), Zone, −1.6 kg (95% CI, −2.8 to −0.4 kg), LEARN, −2.6 kg (−3.8 to −1.3 kg), and Ornish, −2.2 kg (−3.6 to −0.8 kg). Weight loss was not statistically different among the Zone, LEARN, and Ornish groups. At 12 months, secondary outcomes for the Atkins group were comparable with or more favorable than the other diet groups.
Conclusions  In this study, premenopausal overweight and obese women assigned to follow the Atkins diet, which had the lowest carbohydrate intake, lost more weight and experienced more favorable overall metabolic effects at 12 months than women assigned to follow the Zone, Ornish, or LEARN diets. While questions remain about long-term effects and mechanisms, a low-carbohydrate, high-protein, high-fat diet may be considered a feasible alternative recommendation for weight loss.

Paleolithic diets: Should we eat like our ancestors? | PCC Natural Markets

Paleolithic diets: Should we eat like our ancestors? | PCC Natural Markets

By the time modern humans emerged roughly 50,000 years ago, our ancestors had adopted an omnivorous diet of cooked starches, meats (including organs), nuts, fruit and other plant foods. Although very few hunter-gatherer groups survive today, we know they eat a wide range of diets, from the nut-based diet of the African !Kung, and the palm starch diet of New Guinean hunter-gatherers, to the meat- and fat-rich diet of the Arctic Inuit.

As Michael Pollan writes in "Food Rules," "There is no single, ideal human diet."

Modern hunter-gatherer diets, however, tend to have certain things in common. They don't rely heavily on foods that became dominant after the development of agriculture, including dairy, grains and legumes. Starch comes from root vegetables similar to sweet potatoes, potatoes and taro. But most important, they do not eat industrial, processed foods. Other aspects of lifestyle, such as physical activity, also differ from industrialized populations.
Modern research

A small group of researchers is beginning to test the idea that pre-agricultural "Paleolithic" diets might hold the key to improving modern human health. Dr. Lindeberg and his colleagues have conducted two remarkable clinical trials.

In the first, they recruited diabetic and pre-diabetic volunteers with heart disease and placed them on one of two diets: 1) a "Paleolithic" diet, focused on lean meat, fish, fruit, vegetables, starchy root vegetables, eggs and nuts, or 2) a "Mediterranean" diet focused on whole grains, low-fat dairy, vegetables, fruit, fish, oils and margarine. Over the 12-week study period, the Mediterranean group lost body fat and enjoyed an improvement in markers of diabetes. Of nine participants with diabetic blood sugar levels at the beginning of the study, four had normal levels by the end.

Those in the Paleo group fared significantly better. They lost 70 percent more body fat than the Mediterranean group and experienced a remarkable normalization of blood sugar. All 10 participants with diabetic blood sugar levels at baseline reached non-diabetic levels by the end of the study. It's important to note that the volunteers in Dr. Lindeberg's study were mild, early cases of diabetes. A second study of long-term diabetics showed that a Paleo diet did not cure them but it did improve their condition significantly.

Should we all eat a hunter-gatherer diet? Not necessarily. Human evolution did not end with the Paleolithic era. Each person carries a particular set of genetic adaptations that result from the unique dietary environment of his own ancestors, so it's important to emphasize that traditionally prepared grains, legumes and dairy can be healthy foods for many people.

Stephan Guyenet is an obesity researcher at the University of Washington. Visit his blog, wholehealthsource.org, to read more of his writing on nutrition and health.

Stephan is also a big proponent of the palatability school of low carb, and had a big debate with Taubes about that. Taubes focuses mostly on the role of insulin in hunger and fat deposition. Richard at free the animal is eating the potatoes because of (in part) what he learned from Stephan- that we overeat certain foods because they are nutritionally dense and taste good. So when we low carb, we also avoid most of the worst foods like cake and sweets, which we are prone to overeat anyways, because they taste awesome. The low carb diet is blander and less likely to make us binge. But we could achieve a similar effect with a bland yet nutritious food like potatoes. Now whether a starchy vegetable has the same health impact as meat is another question. But I think the ideas of Stephen and Richard are a pushback against the super extreme ketogenic zero carb wing of the low carb movement. So living in fear of healthy carbs is wrong, just as the low fat people, during their age, told us that as long as we cut out fat (the more extremely the better- Ornish), we would have great health and lose weight.

Fat Head - Why We Get Fat: Interview With Gary Taubes

Fat Head Why We Get Fat: Interview With Gary Taubes

Fat Head: Dr. Robert Lustig insists it’s fructose that makes us insulin resistant, not starchy foods. If he’s right, then it was the Coca-Cola and Captain Crunch that turned me into a fat kid, not the mashed potatoes. But as an adult, I’ve avoided sugar yet found that starches most definitely make me gain weight. So assuming for the sake of argument that Lustig is correct, would you say that once fructose has done the damage, we lose our tolerance for carbohydrates in general? If so, why?

Gary Taubes: That’s exactly the possibility I’m discussing. Once you become insulin resistant, your body responds to carbs by secreting more insulin. So it is quite possible — and laboratory work backs this up — that sugar causes the initial insulin resistance because of the effect of the fructose on the liver. So if we never had sugar, we’d be able to eat the other carbs with relative impunity. But being possible doesn’t mean it’s true. I suspect it is, but I’m not sure exactly how this can be tested.

And I agree with you: the world is full of obese and diabetic people who know enough not to eat sugar, but remain obese and diabetic. I could avoid sugar and go back to eating starches and put on 20 pounds of fat effortlessly. I’ve done it in the past — distant past. So I don’t buy the idea that avoiding sugar is enough to make an obese person lean again. And the people I know who believe that all tend to be somewhat plump despite their beliefs. In fact, I recently heard Dr. Lustig give a talk in San Francisco, and he acknowledged that he still has a weight problem, but doesn’t know what to do about it. Hmmm….

Fat Head: Have you come across any evidence that starches can turn people into fat diabetics without fructose being part of the diet?

Gary Taubes: It’s tricky. Typically consumption of sugar, white flour and starchy vegetables all tend to go hand-in-hand. So it’s hard to tease out this one. I suspect beer could, but I don’t know if even beer drinkers who don’t eat sugar tend to become diabetic or not. What we’d need is a population of white-flour eaters who didn’t eat any sugar at all. If we could find such a thing, naturally, then we’d have some idea.

[...]

Fat Head: In Why We Get Fat, you wrote that some people might have to give up dairy products and nuts to lose weight. Dr. Mike Eades has also mentioned that nuts and cheese seem to inhibit weight loss in some low-carb dieters. What is it about those foods that can stall weight loss? Is it just that they’re so calorically dense, or do they produce a higher insulin response than their low carbohydrate content would suggest?

Gary Taubes: I think the caloric density thing is nonsense. Remember, I’m trying to get every last one of us away from thinking in terms of calories as the variable of interest. What we want to know is whether these foods stimulate insulin secretion, or cause insulin resistance, or have some other effect on the storage of fat in the fat tissue or the oxidation of fatty acids by other tissues in the body. So nuts still have carbs in them, and for some people they might contain too many carbs. Same is true for nut butters.

Dairy products can stimulate insulin secretion beyond what you would expect from the carbohydrate content. I don’t know if this is true of cheese because I’ve never seen data on this, but it is possible. And some cheeses could be better than others — hard cheeses, for instance, may be better than soft cheeses.

[...]

Fat Head: You wrote something in Why We Get Fat that I think every frustrated dieter needs to hear: the proper diet will help us become as lean as we can be, but not necessarily as lean as we’d like to be. Once we become fat, is there a limit to how much fat we can lose without starving away our lean tissue? If so, what’s the barrier to mobilizing and burning those last 10 or 20 pounds of excess fat?

Gary Taubes: Simple answer, I don’t know. But it’s obvious that not every woman can have the body of an Angelina Jolie, regardless of how few carbs they eat. And not every man can have the body or the body-fat percentage of, I don’t know, a Matthew McConaughey, one of these actors who’s always taking his shirt off in movies.

That’s for starters. Some of us are wired to have more body fat than others from the get-go. Then I think when we grow up in a carb-rich environment, some degree of chronic damage is done to the way we partition fuel. Maybe our muscle tissue never quite loses its insulin resistance, or our fat tissue remains more insulin sensitive than it would be had we never seen carbs. Maybe our pancreas secretes a little too much insulin.

It’s hard to tell, but the way I describe it is this: if I grew up in a hunter-gatherer environment — and my mother did as well, because there are effects that are passed from mother to child through the uterus — I’d probably weigh around 175 pounds, even as an adult. Had I stopped eating carbs in my late teens, I might naturally weigh about 190 or 200, which was my football weight in high school. The fact that I not only kept eating carbohydrates into my forties but gorged on them during the low-fat, you-can’t-get-fat-if-a-food-doesn’t-have-fat-in-it years of the late 1980s and early 1990s means the best I can do now, even eating virtually no carbs at all, is about 220. And there’s nothing I can do to go lower, short of starving myself. Semi-starving myself doesn’t work. I tried that long ago.

Fat Head: So what’s the message for those people? Lose what you can and focus on being healthy, as opposed to obsessing with squeezing into a size-8 dress?

Gary Taubes: Precisely.

Fat Head: One of the anti-Taubes articles going around the internet claims that we don’t need insulin to store fat, and that insulin is an appetite suppressant. Can we store any significant amount of fat without insulin? If so, why do untreated type 1 diabetics waste away?

Gary Taubes: Short answer, probably not. We don’t need insulin to burn glucose for fuel, but if we don’t have insulin, we don’t store fat.

Fat Head: In Why We Get Fat, you also stated that elevated insulin in the brain suppresses appetite. Since so many obese people have high levels of circulating insulin, why aren’t their appetites suppressed? Is there a difference between the effects of insulin in the brain and insulin in the bloodstream?

Gary Taubes: That’s the key point. A few years ago I was interviewing the director of the Joslin Diabetes Center, and I asked him what the role of insulin was in obesity, and he said its role was to suppress appetite in the brain. And it does. Three researchers at the University of Washington spent 10 to 15 years trying to convince people that insulin had this role. They had injected insulin into the cerebral spinal fluid of primates and it did indeed suppress appetite.

The problem is these people succeeded so well in their crusade that the rest of the community — this guy at the Joslin among them — simply forgot about what insulin does in the body, which is to promote fat accumulation and energy storage. And it makes perfect sense that a hormone that responds to eating will work to store fuel in the body while it also works, secondarily, to tell the brain that fuel is coming in and eating can cease in a bit. That’s the kind of feedback loop you find all over homeostatic systems. But the fundamental issue is that in the body, insulin promotes fat accumulation and that’s where the problem is.

Ketogenic low-carbohydrate diets have no metabolic advantage over nonketogenic low-carbohydrate diets

Ketogenic low-carbohydrate diets have no metabolic advantage over nonketogenic low-carbohydrate diets

Ketogenic low-carbohydrate diets have no metabolic advantage over nonketogenic low-carbohydrate diets1,2,3

Carol S Johnston,
Sherrie L Tjonn,
Pamela D Swan,
Andrea White,
Heather Hutchins, and
Barry Sears

+ Author Affiliations

1From the Department of Nutrition, Arizona State University, Mesa, AZ (CSJ, PDS, and AW); Conscious Cuisine, Scottsdale, AZ (SLT); and Inflammation Research Foundation, Marblehead, MA (HH and BS)

Abstract

Background:Low-carbohydrate diets may promote greater weight loss than does the conventional low-fat, high-carbohydrate diet.

Objective:We compared weight loss and biomarker change in adults adhering to a ketogenic low-carbohydrate (KLC) diet or a nonketogenic low-carbohydrate (NLC) diet.

Design:Twenty adults [body mass index (in kg/m2): 34.4 ± 1.0] were randomly assigned to the KLC (60% of energy as fat, beginning with ≈5% of energy as carbohydrate) or NLC (30% of energy as fat; ≈40% of energy as carbohydrate) diet. During the 6-wk trial, participants were sedentary, and 24-h intakes were strictly controlled.

Results:Mean (±SE) weight losses (6.3 ± 0.6 and 7.2 ± 0.8 kg in KLC and NLC dieters, respectively; P = 0.324) and fat losses (3.4 and 5.5 kg in KLC and NLC dieters, respectively; P = 0.111) did not differ significantly by group after 6 wk. Blood β-hydroxybutyrate in the KLC dieters was 3.6 times that in the NLC dieters at week 2 (P = 0.018), and LDL cholesterol was directly correlated with blood β-hydroxybutyrate (r = 0.297, P = 0.025). Overall, insulin sensitivity and resting energy expenditure increased and serum γ-glutamyltransferase concentrations decreased in both diet groups during the 6-wk trial (P < 0.05). However, inflammatory risk (arachidonic acid:eicosapentaenoic acid ratios in plasma phospholipids) and perceptions of vigor were more adversely affected by the KLC than by the NLC diet. Conclusions:KLC and NLC diets were equally effective in reducing body weight and insulin resistance, but the KLC diet was associated with several adverse metabolic and emotional effects. The use of ketogenic diets for weight loss is not warranted. I've been reading Phinney's books on ketogenic diets for weight loss and athletic performance. Also reviewing the A to Z study in which Atkins beat out Barry Sears The Zone diet, which allows more carbs. This study seems to exonerate the Zone approach, allowing more carbs. I suspect each of us, for genetic reasons, or because of our current state of health, has different requirements or tolerances for, carbohydrate. I have also been thinking about the Lustig/Taubes combo, that perhaps glucose ain't so bad, until the fructose damages our liver and makes us insulin resistant. If so, some of us with bad IR, diabetes or heart failure may be unable to tolerate carbs well at all. The original Atkins diet had the right idea, perhaps. Drastically cut carbs to 20g a day until you lose the weight you want (or can reasonably expect) to lose, then slowly add carbs to find the level at which you start to add weight.

I also find myself finding more truth in the "calories DO count" school of thought. Insulin probably does encourage fat deposition. It definitely increases hunger. But study after study also shows that free feeding of protein and fat causes people to voluntarily eat less. If that's the beginning and end of what low carb can do, that's pretty damn good, especially if you add in the other positive health benefits. We've gone to far if we suggest unlimited amounts of fat and protein can be consumed with no weight gain. Still putting all the pieces together and learning new things about low carb, even after first doing it 15 years ago!

Synthesis: Low-Carb and Food Reward/Palatability, and Why Calories Count | Free The Animal

Synthesis: Low-Carb and Food Reward/Palatability, and Why Calories Count | Free The Animal

What's the distinction? Food Reward & Palatability is the short answer. Again, I'll get to that in more depth later. First, let me ask you a few questions, aimed at LC/Paleo, or Plain Vanilla LC.

Do you find it pretty easy to draw a distinction between say, a free range, organically fed whole turkey you bake in the oven, and supermarket turkey franks with a side helping of "animal by-products," hormones, fillers, texture enhancers, preservatives, nitrites, added sodium, coloring, and cruelty...that you nuke?
Additionally, do you find it easy to draw a distinction between say, leaf lard from a pastured pig that gets lots of time in the sunshine, and industrially processed, extracted, heated, churned, & turned, deodorized and left out to dry soy oil...in a plastic container?
Yes and yes? OK, then how come you find it so difficult to draw a distinction between a loaf of Wonder Bread in a wrapper, and 5 pounds of potatoes straight & dirty from your organic farmer's field....to your door?

So have I abandoned low-carb? Not exactly. Do I think it's effective? Yes, in a limited capacity for some...even most who are substantially overweight or obese, or where otherwise, it just fits with any individual's lifestyle of work & play and they feel great and have good results naturally (I'm leaving diabetics out of this post as outliers). Do I think it's the best approach for fat loss? It depends on the individual. Why does it depend? Food Reward/Palatability shakes out individually, likely on a Bell Curve distribution, that's why.

Here's how I think it works in general.

You're fat. You go low carb per se. You lose water weight because liver and muscle glycogen is being depleted. This is very motivational; or, rewarding, even "palatable." So you continue on. By virtue of blanket LC, you're excluding highly rewarding and palatable fast food, pizza, pasta, ice cream, sugar drinks, Hot Pockets, and all the other crap in favor of meat, veggies, nuts, cheese, and maybe some LC junk food if that's your thang. Yea, it's great to eat red meat again, and while some can pack away 16oz ribeye steaks one after the other, most can't. They're satisfied, and satisfied sooner, with less caloric intake, more often. It subtracts down. They lose weight. Was LC effective? Yes. Why? Food reward/palatability. And because calories count.
The problem is that while a few get all the way to ripped leanness this way, huge numbers don't (including me), and that's why LC and LC/Paleo have not only to recruit the new and uniformed (do keep it going, Jimmy & Co.), but have growing numbers amongst adherents who range from slightly disillusioned to royally pissed off...because they can't get rid of that last 10-20 pounds...or more, in some cases.
In various degrees of frustration and despair, you console yourself with the various cheats—from foods you love and have missed—that got you fat before. But you're smarter this time around, see? You don't toss the baby out with the bathwater. Rather, you "cover" or redeem your indiscretions at the drive through and freezer section with bouts of zero to very low carb over days, and manage to eek out some sort of a homeostasis—maintaining your moderately overweight composition. Or, in many cases, LC as you practice it ceases to be effective in shedding any more fat—even without drive through, freezer section, or Jamba Juice excursions.
This is not necessarily an altogether bad thing. Better than really fat or obese.

So how do we take the next step, beyond the huge value LC had been to get off that initial 40, 50, 60, 80, 160, 320 pounds (60 in my case)? We recognize that it wasn't really any magic about LC that got us there. LC simply, effectively, lowered our food reward/palatability and as a consequence, we spontaneously lowered our average daily intake of calories.

Calories count.

Richard is eating 400 calories of potatoes a day as part of his latest challenge. Bland yet nutritious. Always new ideas in the paleo world, hard to keep up sometimes.

JAMA Network | JAMA Internal Medicine | Therapeutic Fasting in Morbid ObesityLong-term Follow-up

JAMA Network | JAMA Internal Medicine | Therapeutic Fasting in Morbid ObesityLong-term Follow-up

ABSTRACT

The weights of 207 morbidly obese patients were reduced via prolonged fasting. Half the patients fasted for close to two months, losing a mean of 28.2 kg; one fourth fasted for less than one month; and the other fourth fasted for more than two months, with a mean 41.4-kg loss. This latter group was heavier initially, and more than 50% attained near-normal weight. Patients with onset of obesity in childhood had the lowest tolerance for fasting and the lowest success rate in attaining normal weight. Over a 7.3-year follow-up period in 121 patients, the reduced weight was maintained for the first 12 to 18 months. Subsequently, regain proceeded equally in all groups irrespective of length of fast, extent of weight loss, or age at onset of obesity. Regain to original weight occurred in 50% within two to three years and only seven patients remained at their reduced weights. Regain to greater than original weight was more common in childhoodonset obesity.

(Arch Intern Med 137:1381-1382, 1977)
Daisie Johnson; Ernst J. Drenick, MD

Influence of fasting and refeeding on Body Composition

http://ajph.aphapublications.org/doi/pdf/10.2105/AJPH.58.3.477

Article by Dr. Drenick on the patients he fasted. Take away, muscle was lost in small amounts, but obese people have more muscle to begin with to support their large frames, so protein loss is not a burning issue.

LIFE - Google Books The zero calorie diet- a 315lb patient eats nothing for 117 days

LIFE - Google Books

Page 105, the zero calorie diet. Article about Dr. Drenick fasting patients in 1968. "The zero calorie diet- a 315lb patient eats nothing for 117 days"

Friday, January 11, 2013

DNA pioneer James Watson takes aim at cancer establishments and antioxidants

DNA pioneer James Watson takes aim at cancer establishments | Reuters

One such commonality is oxygen radicals. Those forms of oxygen rip apart other components of cells, such as DNA. That is why antioxidants, which have become near-ubiquitous additives in grocery foods from snack bars to soda, are thought to be healthful: they mop up damaging oxygen radicals.

That simple picture becomes more complicated, however, once cancer is present. Radiation therapy and many chemotherapies kill cancer cells by generating oxygen radicals, which trigger cell suicide. If a cancer patient is binging on berries and other antioxidants, it can actually keep therapies from working, Watson proposed.

"Everyone thought antioxidants were great," he said. "But I'm saying they can prevent us from killing cancer cells."

'ANTI-ANTIOXIDANTS'

Research backs him up. A number of studies have shown that taking antioxidants such as vitamin E do not reduce the risk of cancer but can actually increase it, and can even shorten life. But drugs that block antioxidants - "anti-antioxidants" - might make even existing cancer drugs more effective.

Anything that keeps cancer cells full of oxygen radicals "is likely an important component of any effective treatment," said cancer biologist Robert Benezra of Sloan-Kettering.

Sunday, January 06, 2013

Profits over your dead body | Ars Technica

Profits over your dead body | Ars Technica:

Profits over your dead body
Health regulatory and advocacy groups are deliberately corrupted.

Now, the conspiracy minded among you might be thinking of cartoon villains covering up dastardly poison pills, but this is not actually the case. Ben Goldacre, a physician who writes the Bad Science blog, has now made a comprehensive catalog of these practices published in a book called Bad Pharma. In examining the healthcare industry, he paints a complicated picture in which almost all the actors are both bad guys and good guys. It can be read as a stinging rebuke, but more than anything it's criticism from someone who appreciates everything modern medicine has done—but wants to see it do even better.

Thursday, January 03, 2013

Appetite Heightened By Ingestion Of Fructose - Health News - redOrbit

Appetite Heightened By Ingestion Of Fructose - Health News - redOrbit

A new study from Yale University School of Medicine examines possible factors regarding the association between fructose consumption and weight gain.

The researchers used brain magnetic resonance imaging, which indicated that ingestion of glucose but not fructose reduces cerebral blood flow. Activity in brain regions that regulate appetite was also reduced. The participants reported an increase in feeling sated and full from the ingestion of glucose but not fructose.

“Increases in fructose consumption have paralleled the increasing prevalence of obesity, and high-fructose diets are thought to promote weight gain and insulin resistance. Fructose ingestion produces smaller increases in circulating satiety hormones compared with glucose ingestion, and central administration of fructose provokes feeding in rodents, whereas centrally administered glucose promotes satiety,” according to the authors. “Thus, fructose possibly increases food-seeking behavior and increases food intake.”