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
Tuesday, May 07, 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).
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.
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.
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.
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.
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.
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.
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.
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.
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.
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
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.
ABSTRACT
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.
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.
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!
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.
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
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.
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"
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.
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.
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.”
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.”
Saturday, December 15, 2012
'Plethora' of diseases caused by low vitamin D - Telegraph
'Plethora' of diseases caused by low vitamin D - Telegraph:
A lack of awareness about vitamin D deficiency and the 'plethora' of disease it is linked to is fuelling a rise in preventable illnesses among children, experts at the Royal College of Paediatrics and Child Health have said.
Despite low cost supplements being widely available health care professionals and parents do not know the importance of taking them, they said.
Doctors have said the poor summer weather will contribute to an epidemic of vitamin D deficiency as the lack of sunshine will have meant depleted stores of the vitamin which the body can make from sunlight.
The College has launched a campaign to ensure all pregnant women, those breastfeeding, children aged between six months and five years and the elderly aged over 65 take vitamin D supplements in accordance with guidelines.
It comes as figures show that cases of rickets, poor bone growth causing pain and bowed legs, have risen fourfold in the last 15 years.
[...]
Vitamin D can be found naturally in some margarines, eggs and in oily fish but it can be added to milk and cereals.
Vitamin D deficiency is known to increase the risk of diabetes, tuberculosis, multiple sclerosis and rickets and a quarter of children and around half of the white adults have a serious lack of the vitamin.
Professor Mitch Blair, Officer for Health Promotion at the RCPCH, said: “We know vitamin D deficiency is a growing problem – and localised research reveals startling high levels of vitamin deficiency amongst certain groups including children.
“People can only get a fraction of their recommended daily amount of vitamin D through food and very little from sunlight. So getting out in the sun more or eating more oily fish isn’t going to solve the problem.
This is a total BS statement. After years of telling us to avoid the sun because of cancer risks, now we're told that sunlight, which can produce tens of thousands of IU of vitamin D on bare skin, doesn't produce much at all. We need supplements? How in the world did we get Vitamin D before the great epidemic of low vitamin D levels started on 15 years ago then!
"Lack of vitamin D is related to a plethora of serious illnesses in children and adults that could be prevented through relatively simple steps such as taking supplements.”
The RCPCH is launching a campaign calling for: vitamin D supplements to be readily available at low-cost and high quality; an investigation into the pros and cons of further fortification of food with vitamin D; professional guidance for health care professionals on how to diagnose and treat diseases linked to vitamin D deficiency; and a public awareness campaign.
[...]
“And equally as important is making sure that all health care professionals can spot the signs of vitamin D deficiency in children; aches and pains, poor growth, muscle weakness and seizures – and make sure they get appropriately treated.”
A lack of awareness about vitamin D deficiency and the 'plethora' of disease it is linked to is fuelling a rise in preventable illnesses among children, experts at the Royal College of Paediatrics and Child Health have said.
Despite low cost supplements being widely available health care professionals and parents do not know the importance of taking them, they said.
Doctors have said the poor summer weather will contribute to an epidemic of vitamin D deficiency as the lack of sunshine will have meant depleted stores of the vitamin which the body can make from sunlight.
The College has launched a campaign to ensure all pregnant women, those breastfeeding, children aged between six months and five years and the elderly aged over 65 take vitamin D supplements in accordance with guidelines.
It comes as figures show that cases of rickets, poor bone growth causing pain and bowed legs, have risen fourfold in the last 15 years.
[...]
Vitamin D can be found naturally in some margarines, eggs and in oily fish but it can be added to milk and cereals.
Vitamin D deficiency is known to increase the risk of diabetes, tuberculosis, multiple sclerosis and rickets and a quarter of children and around half of the white adults have a serious lack of the vitamin.
Professor Mitch Blair, Officer for Health Promotion at the RCPCH, said: “We know vitamin D deficiency is a growing problem – and localised research reveals startling high levels of vitamin deficiency amongst certain groups including children.
“People can only get a fraction of their recommended daily amount of vitamin D through food and very little from sunlight. So getting out in the sun more or eating more oily fish isn’t going to solve the problem.
This is a total BS statement. After years of telling us to avoid the sun because of cancer risks, now we're told that sunlight, which can produce tens of thousands of IU of vitamin D on bare skin, doesn't produce much at all. We need supplements? How in the world did we get Vitamin D before the great epidemic of low vitamin D levels started on 15 years ago then!
"Lack of vitamin D is related to a plethora of serious illnesses in children and adults that could be prevented through relatively simple steps such as taking supplements.”
The RCPCH is launching a campaign calling for: vitamin D supplements to be readily available at low-cost and high quality; an investigation into the pros and cons of further fortification of food with vitamin D; professional guidance for health care professionals on how to diagnose and treat diseases linked to vitamin D deficiency; and a public awareness campaign.
[...]
“And equally as important is making sure that all health care professionals can spot the signs of vitamin D deficiency in children; aches and pains, poor growth, muscle weakness and seizures – and make sure they get appropriately treated.”
Diabetes and heart health link | Diabetes Federation of Ireland
Diabetes and heart health link | Diabetes Federation of Ireland:
It is known that people with poorly controlled diabetes are at higher risk for heart failure but new data from the UK shows that they may have additional causes of heart disease, may develop heart disease younger and have more severe heart disease. But poor recording practices in Ireland means that the HSE cannot provide detailed information about the links between hearth health and diabetes.
“Medical data about the health of the Irish population is especially ill suited to planning of health services. If we in Diabetes Ireland or Department of Health wanted to examine the link between diabetes and heart disease we can’t depend on extracting robust figures from the HSE’s Hospital In-Patient Enquiry (HIPE) system nor is there a diabetes register” says Dr. Anna Clarke, Health Promotion and Research Manager with Diabetes Ireland.
[...]
Diabetes Ireland’s advice to people with diabetes has always been that they are 2 to 4 times more likely to develop heart disease than people in the general populations, but this is hardly the type of precise information which the HSE needs to plan health services and prevention programmes.
Over the years, high blood sugar damages blood vessels and puts people at risk for coronary artery disease and congestive heart failure. Patients with diabetes are at a significantly higher risk for having heart disease,” according to Dr. Clarke.
Having heart failure means your heart is not pumping blood around the body as well as it used to. The most common reason is that your heart muscle has been damaged, for example, after a heart attack.
It is known that people with poorly controlled diabetes are at higher risk for heart failure but new data from the UK shows that they may have additional causes of heart disease, may develop heart disease younger and have more severe heart disease. But poor recording practices in Ireland means that the HSE cannot provide detailed information about the links between hearth health and diabetes.
“Medical data about the health of the Irish population is especially ill suited to planning of health services. If we in Diabetes Ireland or Department of Health wanted to examine the link between diabetes and heart disease we can’t depend on extracting robust figures from the HSE’s Hospital In-Patient Enquiry (HIPE) system nor is there a diabetes register” says Dr. Anna Clarke, Health Promotion and Research Manager with Diabetes Ireland.
[...]
Diabetes Ireland’s advice to people with diabetes has always been that they are 2 to 4 times more likely to develop heart disease than people in the general populations, but this is hardly the type of precise information which the HSE needs to plan health services and prevention programmes.
Over the years, high blood sugar damages blood vessels and puts people at risk for coronary artery disease and congestive heart failure. Patients with diabetes are at a significantly higher risk for having heart disease,” according to Dr. Clarke.
Having heart failure means your heart is not pumping blood around the body as well as it used to. The most common reason is that your heart muscle has been damaged, for example, after a heart attack.
Race, daytime sleepiness, and vitamin D related in new study - Birmingham science news | Examiner.com
Race, daytime sleepiness, and vitamin D related in new study - Birmingham science news | Examiner.com
Race, the occurrence of daytime sleepiness, and vitamin D have been definitively connected by a new study conducted David McCarty, MD at the American Academy of Sleep Medicine, and published in the Journal of Clinical Sleep Medicine on December 14, 2012.
This is the first study to demonstrate a significant relationship between sleepiness and vitamin D. Race is a factor because previous research has shown that increased skin pigmentation is an established risk factor for low vitamin D.
“Results show that in patients with normal vitamin D levels, progressively higher levels of daytime sleepiness were correlated inversely with progressively lower levels of vitamin D. Among patients with vitamin D deficiency, sleepiness and vitamin D levels were associated only among black patients. Surprisingly, this correlation was observed in a direct relationship, with higher vitamin D levels associated with a higher level of sleepiness among black patients.”
The majority of Birmingham’s population is Afro-American.
Daytime sleepiness due to the lack of vitamin D could be affecting your children's performance in school.
Race, the occurrence of daytime sleepiness, and vitamin D have been definitively connected by a new study conducted David McCarty, MD at the American Academy of Sleep Medicine, and published in the Journal of Clinical Sleep Medicine on December 14, 2012.
This is the first study to demonstrate a significant relationship between sleepiness and vitamin D. Race is a factor because previous research has shown that increased skin pigmentation is an established risk factor for low vitamin D.
“Results show that in patients with normal vitamin D levels, progressively higher levels of daytime sleepiness were correlated inversely with progressively lower levels of vitamin D. Among patients with vitamin D deficiency, sleepiness and vitamin D levels were associated only among black patients. Surprisingly, this correlation was observed in a direct relationship, with higher vitamin D levels associated with a higher level of sleepiness among black patients.”
The majority of Birmingham’s population is Afro-American.
Daytime sleepiness due to the lack of vitamin D could be affecting your children's performance in school.
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