Monday, August 25, 2014

A low-carbohydrate diet may prevent end-stage renal failure in type 2 diabetes. A case report

A low-carbohydrate diet may prevent end-stage renal failure in type 2 diabetes. A case report Abstract An obese patient with type 2 diabetes whose diet was changed from the recommended high-carbohydrate, low-fat type to a low-carbohydrate diet showed a significant reduction in bodyweight, improved glycemic control and a reversal of a six year long decline of renal function. The reversal of the renal function was likely caused by both improved glycemic control and elimination of the patient's obesity.

Wednesday, April 02, 2014

Letter: Smoking causes, worsens diabetes.

Letter: Smoking causes, worsens diabetes. EDITOR: Nearly 26 million Americans have diabetes and the number is rising daily. Since 1980, the percentage of people under 45 with diabetes has increased by 167 percent. There are many risk factors for Type 2 diabetes. Many of these, like family history, can’t be changed. But you can avoid or change some risk factors. One of these is smoking. We have known for some time that smoking makes diabetes complications worse. But new findings from the 2014 Surgeon General’s Report now confirm that smoking actually causes Type 2 diabetes. How does smoking cause diabetes, or make diabetes worse? • Smokers have more abdominal or “belly” fat. This kind of fat makes the body more resistant to insulin. • Nicotine in cigarette smoke may make the body more resistant to insulin. This means that smokers with diabetes may need to take more insulin and have worse control of their blood sugar than non-smokers. • Smokers with diabetes are more likely to have diseases that result from damaged blood vessels than are nonsmokers with diabetes. Chemicals in cigarette smoke cause injury to the cells lining the blood vessels. This interferes with the body’s ability to make blood vessels widen and to control blood clotting. The best advice is to cut back or quit smoking. Call 800-Quit-Now or visit Dorothy Kalmon, Central Wisconsin Tobacco-Free Coalition, Wausau

New Study: Is Today’s Wheat Bad for You?

New Study: Is Today’s Wheat Bad for You? Today’s wheat is not the same wheat that your grandmother ate when she was young. Not even close. Today’s wheat is greatly genetically modified to grow faster and provide a higher yield of wheat per acre. More food to the starving poor was a blessing, but could there be disadvantages with the modern super wheat? Could it be bad for our health? Could it, for example, lead to severe digestive issues for many people? Cardiologist William Davis argued this in his best selling book Wheat Belly. Davis got criticized for exaggerating the scientific support for his theories – which he did. But a lack of good evidence doesn’t mean that a theory must be incorrect. A new high quality study, published in British Journal of Nutrition, tests one of Dr. Davis’ speculations, with dramatic results. [...] The difference was clear-cut. When participants with digestive issues consumed modern wheat they felt like they usually did, they suffered from their usual digestive issues. But when for six weeks they ate the ancient wheat their symptoms improved with significantly less abdominal pain, less abdominal bloating and an improved quality of life. The improvements were so great that they could hardly be a coincidence. In addition, reduced levels of inflammatory substances in the blood were recorded in people who avoided modern wheat.

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.


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 -

From Sleep Study, Clues to Happiness -

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


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.