Insulin’s Role in the Aging Body - Scienceline
Insulin, a hormone well known for its role in diabetes, may also lie at the root of another common but serious medical condition: age-related muscle loss, known as sarcopenia.
In fact, sarcopenia is in part due to muscle tissue not responding properly to insulin, according to a new study in the journal Diabetologia.
The researchers found that an increased dose of insulin restored the muscle-building processes that tend to deteriorate with old age. Unfortunately, insulin cannot be used as a treatment for sarcopenia due to its toxic effects in high concentrations. Still, the new results help clarify its role in muscle growth and could serve as a basis for future treatments. Sarcopenia affects 24 percent of adults between 45 and 70 years old, and half of people over 80.
“The new finding serves as a proof of concept,” said Elena Volpi, a researcher at the University of Texas Medical Branch at Galveston. “It confirms our belief that the age-related decline in muscle growth is a true case of insulin resistance, which is an important piece to the larger puzzle of treating sarcopenia.”
[...]
In type 2 diabetes, insulin resistance — a condition in which normal amounts of insulin fail to produce a typical insulin response in the body — prevents the body from storing sugar molecules in cells, eventually leading to high blood sugar. Test subjects in the Texas study, however, had normal blood sugar levels. This suggests the insulin resistance seen in elderly people is not a matter of sugar control.
Instead, the researchers believe insulin resistance seen in old age results from changes in blood flow. In addition to helping store sugar, insulin acts as a signal for the dilation of blood vessels to increase blood flow and deliver nutrients to muscle tissue. When capillaries fail to respond to these signals, blood flow slows down and muscle growth decreases.
Friday, November 06, 2009
Monday, October 19, 2009
Vitamin D May Improve Melanoma Survival HealthDay
HealthDay Vitamin D May Improve Melanoma Survival
Vitamin D May Improve Melanoma Survival
But levels are too low in many Americans, researchers say
By Randy Dotinga
HealthDay Reporter
SATURDAY, Sept. 26 (HealthDay News) -- Higher levels of vitamin D are linked to less severe, less deadly melanoma lesions in people with skin cancer, new research suggests.
The findings provide more support for the idea that vitamin D is crucial to skin health. Many Americans, however, don't get enough of it, perhaps because they limit sun exposure and drink less milk than in the past.
"Although avoiding sunburn is very important in order to prevent melanoma, it is also important to avoid becoming deficient in vitamin D," said Dr. Julia A. Newton-Bishop, a dermatology professor at the University of Leeds in England and a study co-author. "This is especially important for melanoma patients in whom low vitamin D levels appear to be harmful."
Vitamin D May Improve Melanoma Survival
But levels are too low in many Americans, researchers say
By Randy Dotinga
HealthDay Reporter
SATURDAY, Sept. 26 (HealthDay News) -- Higher levels of vitamin D are linked to less severe, less deadly melanoma lesions in people with skin cancer, new research suggests.
The findings provide more support for the idea that vitamin D is crucial to skin health. Many Americans, however, don't get enough of it, perhaps because they limit sun exposure and drink less milk than in the past.
"Although avoiding sunburn is very important in order to prevent melanoma, it is also important to avoid becoming deficient in vitamin D," said Dr. Julia A. Newton-Bishop, a dermatology professor at the University of Leeds in England and a study co-author. "This is especially important for melanoma patients in whom low vitamin D levels appear to be harmful."
Vegetarian diet bad for bone health - Journal Article
SpringerLink - Journal Article
Abstract
Background A long-term vegetarian diet is generally poor in vitamin B group. The lack of vitamin B12 together with vitamin B6 and folate deficiency is closely related to homocysteine metabolism. Hyperhomocysteinemia was found to be associated with increased bone turnover markers and increased fracture risk. Thus, hyperhomocysteinemia, vitamin B12 and folate deficiency may be regarded as novel risk factors for micronutrient deficiency-related osteoporosis.
Aim of the study To assess the possible impact of a vegetarian diet on bone mineral density in cohort of Slovak vegetarian women.
Methods Fasting serum glucose, albumin, calcium, phosphorous and creatinine as well as bone markers, serum vitamin B12, folate and plasma levels of total homocysteine were assessed in two nutritional groups (vegetarians vs. nonvegetarians) of apparently healthy women (age range 20–70 years). Bone mineral density of the femoral neck, trochanter, total femur and lumbar spine was measured in all subjects.
Results Vegetarians had a significantly lower weight (p < 0.05), higher PTH (p < 0.01) and homocysteine (p < 0.001). Vitamin B12 was significantly higher in nonvegetarians (p < 0.001). No differences were observed in folate levels. Univariate analysis showed significant association between homocysteine and B12 (p < 0.01), folate (p < 0.001), creatinine (p < 0.001), total proteins (p < 0.049), age (p < 0.001) and vegetarian food intake (p < 0.001). Vegetarians had a significantly lower TrFBMD (p < 0.05) and ToFBMD (p < 0.05). Age and CTx were significant predictors in all sites of measured BMD and PTH. A strong correlation between homocysteine and FNBMD (r = −0.2009, p < 0.002), TrFBMD (r = −0.1810, p < 0.004) and ToFBMD (r = −0.2225, p < 0.001) was found in all subjects.
Conclusion Homocysteine is one of the predictors of bone mineral density, and hyperhomocysteinemia is associated with lower bone mineral density. In healthy adults, homocysteine levels are dependent on age as well as on nutritional habits. Thus, elderly women on a vegetarian diet seem to be at higher risk of osteoporosis development than nonvegetarian women.
Abstract
Background A long-term vegetarian diet is generally poor in vitamin B group. The lack of vitamin B12 together with vitamin B6 and folate deficiency is closely related to homocysteine metabolism. Hyperhomocysteinemia was found to be associated with increased bone turnover markers and increased fracture risk. Thus, hyperhomocysteinemia, vitamin B12 and folate deficiency may be regarded as novel risk factors for micronutrient deficiency-related osteoporosis.
Aim of the study To assess the possible impact of a vegetarian diet on bone mineral density in cohort of Slovak vegetarian women.
Methods Fasting serum glucose, albumin, calcium, phosphorous and creatinine as well as bone markers, serum vitamin B12, folate and plasma levels of total homocysteine were assessed in two nutritional groups (vegetarians vs. nonvegetarians) of apparently healthy women (age range 20–70 years). Bone mineral density of the femoral neck, trochanter, total femur and lumbar spine was measured in all subjects.
Results Vegetarians had a significantly lower weight (p < 0.05), higher PTH (p < 0.01) and homocysteine (p < 0.001). Vitamin B12 was significantly higher in nonvegetarians (p < 0.001). No differences were observed in folate levels. Univariate analysis showed significant association between homocysteine and B12 (p < 0.01), folate (p < 0.001), creatinine (p < 0.001), total proteins (p < 0.049), age (p < 0.001) and vegetarian food intake (p < 0.001). Vegetarians had a significantly lower TrFBMD (p < 0.05) and ToFBMD (p < 0.05). Age and CTx were significant predictors in all sites of measured BMD and PTH. A strong correlation between homocysteine and FNBMD (r = −0.2009, p < 0.002), TrFBMD (r = −0.1810, p < 0.004) and ToFBMD (r = −0.2225, p < 0.001) was found in all subjects.
Conclusion Homocysteine is one of the predictors of bone mineral density, and hyperhomocysteinemia is associated with lower bone mineral density. In healthy adults, homocysteine levels are dependent on age as well as on nutritional habits. Thus, elderly women on a vegetarian diet seem to be at higher risk of osteoporosis development than nonvegetarian women.
Diets bad for the teeth are also bad for the body
Diets bad for the teeth are also bad for the body
Diets bad for the teeth are also bad for the body
Beyond the immediate distress, dental pain may portend future medical problems
Dental disease may be a wake-up call that your diet is harming your body.
"The five-alarm fire bell of a tooth ache is difficult to ignore," says Dr. Philippe P. Hujoel, professor of dental public health sciences at the University of Washington (UW) School of Dentistry in Seattle. Beyond the immediate distress, dental pain may portend future medical problems. It may be a warning that the high-glycemic diet that led to dental problems in the short term may, in the long term, lead to potentially serious chronic diseases.
Hujoel reviewed the relationships between diet, dental disease, and chronic systemic illness in a report published July 1 in the Journal of Dental Research. He weighed two contradictory viewpoints on the role of dietary carbohydrates in health and disease. The debate surrounds fermentable carbohydates: foods that turn into simple sugars in the mouth. Fermentable carbohydrates are not just sweets like cookies, doughnuts, cake and candy. They also include bananas and several tropical fruits, sticky fruits like raisins and other dried fruits, and starchy foods like potatoes, refined wheat flour, yams, rice, pasta, pretzels, bread, and corn.
One viewpoint is that certain fermentable carbohydrates are beneficial to general health and that the harmful dental consequences of such a diet should be managed by the tools found in the oral hygiene section of drugstores. A contrasting viewpoint suggests that fermentable carbohydrates are bad for both dental and general health, and that both dental and general health need to be maintained by restricting fermentable carbohydrates.
The differing perspectives on the perceived role of dietary carbohydrates have resulted in opposing approaches to dental disease prevention, Hujoel notes, and have prompted debates in interpreting the link between dental diseases and such systemic diseases as obesity, diabetes, and some forms of cancer.
Over the past twenty years or so, Hujoel says, people have been advised to make fermentable dietary carbohydrates the foundation of their diet. Fats were considered the evil food. A high-carbohydrate diet was assumed to prevent a number of systemic chronic diseases. Unfortunately, such a diet - allegedly good for systemic health - was bad for dental health. As a result, cavities or gingival bleeding from fermentable carbohydrates could be avoided only – and not always successfully, as Hujoel points out -- by conscientious brushing, fluorides, and other types of dental preventive measures. When these measures are not successful, people end up with cavities and gum disease.
Hujoel observed that the dental harms of fermentable carbohydrates have been recognized by what looks like every major health organization. Even those fermentable carbohydrates assumed to be good for systemic health break down into simple sugars in the mouth and promote tooth decay. All fermentable carbohydrates have the potential to induce dental decay, Hujoel notes.
But what if fermentable carbohydrates are also bad for systemic health? Hujoel asks. What if dietary guidelines would start incorporating the slew of clinical trial results suggesting that a diet low in fermentable carbohydrates improves cardiovascular markers of disease and decreases body fat? Such a change in perspective on fermentable carbohydrates, and by extension, on people's diets, could have a significant impact on the dental profession, as a diet higher in fat and protein does not cause dental diseases, he notes. Dentists would no longer be pressed to recommend to patients diets that are bad for teeth or remain mum when it comes to dietary advice. Dentists often have been reluctant, Hujoel says, to challenge the prevailing thinking on nutrition. Advising patients to reduce the amount or frequency of fermentable carbohydrate consumption is difficult when official guidelines suggested the opposite.
The close correlation between the biological mechanisms that cause dental decay and the factors responsible for high average levels of glucose in the blood is intriguing. Hujoel explains that eating sugar or fermentable carbohydrates drops the acidity levels of dental plaque and is considered an initiating cause of dental decay.
"Eating these same foods, he says, is also associated with spikes in blood sugar levels. There is fascinating evidence that suggests that the higher the glycemic level of a food, the more it will drop the acidity of dental plaque, and the higher it will raise blood sugar. So, possibly, dental decay may really be a marker for the chronic high-glycemic diets that lead to both dental decay and chronic systemic diseases. This puts a whole new light on studies that have linked dental diseases to such diverse illnesses as Alzheimer's disease and pancreatic cancer."
The correlations between dental diseases and systemic disease, he adds, provide indirect support for those researchers who have suggested that Alzheimer's disease and pancreatic cancer are due to an abnormal blood glucose metabolism.
The hypotheses on dental diseases as a marker for the diseases of civilization were postulated back in the mid-20th century by two physicians: Thomas Cleave and John Yudkin. Tragically, their work, although supported by epidemiological evidence, became largely forgotten, Hujoel notes. This is unfortunate, he adds, because dental diseases really may be the most noticeable and rapid warning sign to an individual that something is going awry with his or her diet.
"Dental problems from poor dietary habits appear in a few weeks to a few years," Hujoel explains. "Dental improvement can be rapid when habits are corrected. For example, reducing sugar intake can often improve gingivitis scores (a measurement of gum disease) in a couple of weeks. Dental disease reveals very early on that eating habits are putting a person at risk for systemic disease. Because chronic medical disease takes decades to become severe enough to be detected in screening tests, dental diseases may provide plenty of lead-time to change harmful eating habits and thereby decrease the risk of developing the other diseases of civilization."
Diets bad for the teeth are also bad for the body
Beyond the immediate distress, dental pain may portend future medical problems
Dental disease may be a wake-up call that your diet is harming your body.
"The five-alarm fire bell of a tooth ache is difficult to ignore," says Dr. Philippe P. Hujoel, professor of dental public health sciences at the University of Washington (UW) School of Dentistry in Seattle. Beyond the immediate distress, dental pain may portend future medical problems. It may be a warning that the high-glycemic diet that led to dental problems in the short term may, in the long term, lead to potentially serious chronic diseases.
Hujoel reviewed the relationships between diet, dental disease, and chronic systemic illness in a report published July 1 in the Journal of Dental Research. He weighed two contradictory viewpoints on the role of dietary carbohydrates in health and disease. The debate surrounds fermentable carbohydates: foods that turn into simple sugars in the mouth. Fermentable carbohydrates are not just sweets like cookies, doughnuts, cake and candy. They also include bananas and several tropical fruits, sticky fruits like raisins and other dried fruits, and starchy foods like potatoes, refined wheat flour, yams, rice, pasta, pretzels, bread, and corn.
One viewpoint is that certain fermentable carbohydrates are beneficial to general health and that the harmful dental consequences of such a diet should be managed by the tools found in the oral hygiene section of drugstores. A contrasting viewpoint suggests that fermentable carbohydrates are bad for both dental and general health, and that both dental and general health need to be maintained by restricting fermentable carbohydrates.
The differing perspectives on the perceived role of dietary carbohydrates have resulted in opposing approaches to dental disease prevention, Hujoel notes, and have prompted debates in interpreting the link between dental diseases and such systemic diseases as obesity, diabetes, and some forms of cancer.
Over the past twenty years or so, Hujoel says, people have been advised to make fermentable dietary carbohydrates the foundation of their diet. Fats were considered the evil food. A high-carbohydrate diet was assumed to prevent a number of systemic chronic diseases. Unfortunately, such a diet - allegedly good for systemic health - was bad for dental health. As a result, cavities or gingival bleeding from fermentable carbohydrates could be avoided only – and not always successfully, as Hujoel points out -- by conscientious brushing, fluorides, and other types of dental preventive measures. When these measures are not successful, people end up with cavities and gum disease.
Hujoel observed that the dental harms of fermentable carbohydrates have been recognized by what looks like every major health organization. Even those fermentable carbohydrates assumed to be good for systemic health break down into simple sugars in the mouth and promote tooth decay. All fermentable carbohydrates have the potential to induce dental decay, Hujoel notes.
But what if fermentable carbohydrates are also bad for systemic health? Hujoel asks. What if dietary guidelines would start incorporating the slew of clinical trial results suggesting that a diet low in fermentable carbohydrates improves cardiovascular markers of disease and decreases body fat? Such a change in perspective on fermentable carbohydrates, and by extension, on people's diets, could have a significant impact on the dental profession, as a diet higher in fat and protein does not cause dental diseases, he notes. Dentists would no longer be pressed to recommend to patients diets that are bad for teeth or remain mum when it comes to dietary advice. Dentists often have been reluctant, Hujoel says, to challenge the prevailing thinking on nutrition. Advising patients to reduce the amount or frequency of fermentable carbohydrate consumption is difficult when official guidelines suggested the opposite.
The close correlation between the biological mechanisms that cause dental decay and the factors responsible for high average levels of glucose in the blood is intriguing. Hujoel explains that eating sugar or fermentable carbohydrates drops the acidity levels of dental plaque and is considered an initiating cause of dental decay.
"Eating these same foods, he says, is also associated with spikes in blood sugar levels. There is fascinating evidence that suggests that the higher the glycemic level of a food, the more it will drop the acidity of dental plaque, and the higher it will raise blood sugar. So, possibly, dental decay may really be a marker for the chronic high-glycemic diets that lead to both dental decay and chronic systemic diseases. This puts a whole new light on studies that have linked dental diseases to such diverse illnesses as Alzheimer's disease and pancreatic cancer."
The correlations between dental diseases and systemic disease, he adds, provide indirect support for those researchers who have suggested that Alzheimer's disease and pancreatic cancer are due to an abnormal blood glucose metabolism.
The hypotheses on dental diseases as a marker for the diseases of civilization were postulated back in the mid-20th century by two physicians: Thomas Cleave and John Yudkin. Tragically, their work, although supported by epidemiological evidence, became largely forgotten, Hujoel notes. This is unfortunate, he adds, because dental diseases really may be the most noticeable and rapid warning sign to an individual that something is going awry with his or her diet.
"Dental problems from poor dietary habits appear in a few weeks to a few years," Hujoel explains. "Dental improvement can be rapid when habits are corrected. For example, reducing sugar intake can often improve gingivitis scores (a measurement of gum disease) in a couple of weeks. Dental disease reveals very early on that eating habits are putting a person at risk for systemic disease. Because chronic medical disease takes decades to become severe enough to be detected in screening tests, dental diseases may provide plenty of lead-time to change harmful eating habits and thereby decrease the risk of developing the other diseases of civilization."
Wednesday, October 14, 2009
Ketone Bodies, Potential Therapeutic Uses
Ketone Bodies, Potential Therapeutic Uses
Ketone Bodies, Potential Therapeutic Uses
Richard L. Veech, Britton Chance, Yoshihiro Kashiwaya, Henry A. Lardy, George F. Cahill Jr
Keywords
D-BETA-HYDROXYBUTYRATE • Ketone • Bodies • Ketosis • Metabolic • Control • Analysis • Neurologic • Disease
Abstract
Ketosis, meaning elevation of D- -hydroxybutyrate ( R -3-hydroxybutyrate) and acetoacetate, has been central to starving man's survival by providing nonglucose substrate to his evolutionarily hypertrophied brain, sparing muscle from destruction for glucose synthesis. Surprisingly, D- -hydroxybutyrate (abbreviated OHB) may also provide a more efficient source of energy for brain per unit oxygen, supported by the same phenomenon noted in the isolated working perfused rat heart and in sperm. It has also been shown to decrease cell death in two human neuronal cultures, one a model of Alzheimer's and the other of Parkinson's disease. These observations raise the possibility that a number of neurologic disorders, genetic and acquired, might benefit by ketosis. Other beneficial effects from OHB include an increased energy of ATP hydrolysis ( G') and its linked ionic gradients. This may be significant in drug-resistant epilepsy and in injury and anoxic states. The ability of OHB to oxidize co-enzyme Q and reduce NADP + may also be important in decreasing free radical damage. Clinical maneuvers for increasing blood levels of OHB to 2-5 mmol may require synthetic esters or polymers of OHB taken orally, probably 100 to 150 g or more daily. This necessitates advances in food-science technology to provide at least enough orally acceptable synthetic material for animal and possibly subsequent clinical testing. The other major need is to bring the technology for the analysis of multiple metabolic phenotypes up to the level of sophistication of the instrumentation used, for example, in gene science or in structural biology. This technical strategy will be critical to the characterization of polygenic disorders by enhancing the knowledge gained from gene analysis and from the subsequent steps and modifications of the protein products themselves.
Tuesday, September 29, 2009
Sept. 29, 1898: Stalin’s Scientist Sees First Light | This Day In Tech | Wired.com
Sept. 29, 1898: Stalin’s Scientist Sees First Light | This Day In Tech | Wired.com
Early Soviet propagandists often relied on “miracles of science” to boost the status of their fledgling state. The young plant breeder Trofim Lysenko seemingly provided them with a whopper in 1927, reporting that he had developed a method of fertilizing fields without actually relying on fertilizers or minerals. The spinmeisters at Pravda had a field day, proclaiming that Lysenko had delivered on the Stalinist dream of using science to conquer nature.
Through a process he called “vernalization,” Lysenko reported growing peas in winter on the frozen steppe of Azerbaijan, causing Pravda to report breathlessly that Lysenko had turned …
the barren fields of the Trans-Caucasus green in winter, so that cattle will not perish from poor feeding, and the peasant Turk will live through the winter without trembling for tomorrow.
In fact, Lysenko’s methods were practically devoid of any science at all, and the “peasant Turk” continued to go hungry. But in a country where Joseph Stalin determined the truth and famine was ever present, the efficacy of vernalization was not to be denied. Top agricultural officials warmly embraced the process, and the tightly controlled state press dutifully pronounced it another miracle of Soviet science.
Except for the fact that crop vernalization didn’t work, it was, indeed, a miracle.
Lysenko’s star was definitely on the rise, thanks to officialdom’s alarming ability to ignore the facts in order to obtain the desired results. He also came to Moscow’s attention because of his talent for rallying the country’s peasantry, a surly segment of the population openly hostile to Stalinism. The hostility was thanks to Uncle Joe’s forced collectivization of small farms, which caused widespread starvation and the deaths of millions.
Lysenko, the semi-educated son of peasants, was able to put a human face on the regime back in the Kremlin. He spoke the peasants’ language and reassured them that science would fix everything.
He became a darling of Stalin’s, and after the dictator delivered a speech placing ideological needs above scientific research, Lysenko’s ascent was swift. In the early 1930s he was appointed head of the Academy of Agricultural Sciences and became the de facto arbiter of all the sciences, a mini-commissar, if you will. It was a catastrophe for Soviet science.
The little scientific theory absorbed by Lysenko came by way of Jean-Baptiste Lamarck, the early–19th-century French biologist who promulgated the theory, later refuted by Darwinism, that acquired characteristics could be passed from one generation to the next. This fit neatly with the Stalinist idea that nature could be manipulated to suit the needs of man.
Lysenko was hot-tempered, and he brooked no criticism of himself or his work. Legitimate Soviet geneticists and other scientists who dared oppose him often learned this hard truth with a one-way ticket to the gulag. Lysenko, in fact, despised his more-learned colleagues in a way that only a complete fraud with near-absolute power can.
He mercilessly rooted out perceived enemies of the state in what amounted to a crusade against science. With Stalin’s blessing, thousands of lab coats were shipped to Siberia, and hundreds died — or were killed — in the camps. In his own way, Lysenko proved to be as destructive to the Soviet Union as Stalin was with his purge of the Red Army officer corps.
For as long as Stalin lived, Lysenko was untouchable. After the dictator’s death in 1953, and his subsequent denunciation by Nikita Khrushchev at the 20th Communist Party Congress, Lysenko gradually lost influence. Although he held on to his offices for a time, scientists could now criticize him openly without fear of retribution. They did, with esteemed physicist Andrei Sakharov delivering the most withering blow in a 1964 address.
That same year, Lysenko saw his theories officially discredited and discarded by the Soviet Union. He was stripped of all his privileges, no small price to pay in Soviet society. In spite of everything, he kept showing up for work until his death in 1976.
Science thrown under the wagon in the name of politics. I think we're seeing similar things today, in terms of the "fat is bad for you" and "humans are warming the earth" theories. The government has already decided the answer to those two questions. Now do you want to help us save the world, or "confuse" people with contrary evidence?
Early Soviet propagandists often relied on “miracles of science” to boost the status of their fledgling state. The young plant breeder Trofim Lysenko seemingly provided them with a whopper in 1927, reporting that he had developed a method of fertilizing fields without actually relying on fertilizers or minerals. The spinmeisters at Pravda had a field day, proclaiming that Lysenko had delivered on the Stalinist dream of using science to conquer nature.
Through a process he called “vernalization,” Lysenko reported growing peas in winter on the frozen steppe of Azerbaijan, causing Pravda to report breathlessly that Lysenko had turned …
the barren fields of the Trans-Caucasus green in winter, so that cattle will not perish from poor feeding, and the peasant Turk will live through the winter without trembling for tomorrow.
In fact, Lysenko’s methods were practically devoid of any science at all, and the “peasant Turk” continued to go hungry. But in a country where Joseph Stalin determined the truth and famine was ever present, the efficacy of vernalization was not to be denied. Top agricultural officials warmly embraced the process, and the tightly controlled state press dutifully pronounced it another miracle of Soviet science.
Except for the fact that crop vernalization didn’t work, it was, indeed, a miracle.
Lysenko’s star was definitely on the rise, thanks to officialdom’s alarming ability to ignore the facts in order to obtain the desired results. He also came to Moscow’s attention because of his talent for rallying the country’s peasantry, a surly segment of the population openly hostile to Stalinism. The hostility was thanks to Uncle Joe’s forced collectivization of small farms, which caused widespread starvation and the deaths of millions.
Lysenko, the semi-educated son of peasants, was able to put a human face on the regime back in the Kremlin. He spoke the peasants’ language and reassured them that science would fix everything.
He became a darling of Stalin’s, and after the dictator delivered a speech placing ideological needs above scientific research, Lysenko’s ascent was swift. In the early 1930s he was appointed head of the Academy of Agricultural Sciences and became the de facto arbiter of all the sciences, a mini-commissar, if you will. It was a catastrophe for Soviet science.
The little scientific theory absorbed by Lysenko came by way of Jean-Baptiste Lamarck, the early–19th-century French biologist who promulgated the theory, later refuted by Darwinism, that acquired characteristics could be passed from one generation to the next. This fit neatly with the Stalinist idea that nature could be manipulated to suit the needs of man.
Lysenko was hot-tempered, and he brooked no criticism of himself or his work. Legitimate Soviet geneticists and other scientists who dared oppose him often learned this hard truth with a one-way ticket to the gulag. Lysenko, in fact, despised his more-learned colleagues in a way that only a complete fraud with near-absolute power can.
He mercilessly rooted out perceived enemies of the state in what amounted to a crusade against science. With Stalin’s blessing, thousands of lab coats were shipped to Siberia, and hundreds died — or were killed — in the camps. In his own way, Lysenko proved to be as destructive to the Soviet Union as Stalin was with his purge of the Red Army officer corps.
For as long as Stalin lived, Lysenko was untouchable. After the dictator’s death in 1953, and his subsequent denunciation by Nikita Khrushchev at the 20th Communist Party Congress, Lysenko gradually lost influence. Although he held on to his offices for a time, scientists could now criticize him openly without fear of retribution. They did, with esteemed physicist Andrei Sakharov delivering the most withering blow in a 1964 address.
That same year, Lysenko saw his theories officially discredited and discarded by the Soviet Union. He was stripped of all his privileges, no small price to pay in Soviet society. In spite of everything, he kept showing up for work until his death in 1976.
Science thrown under the wagon in the name of politics. I think we're seeing similar things today, in terms of the "fat is bad for you" and "humans are warming the earth" theories. The government has already decided the answer to those two questions. Now do you want to help us save the world, or "confuse" people with contrary evidence?
Quest for a Long Life Gains Scientific Respect - NYTimes.com
Quest for a Long Life Gains Scientific Respect - NYTimes.com
Some attendees were so convinced of the virtues of less food that they have begun severe diets of various kinds. Cynthia Kenyon, of the University of California, San Francisco, said she had gone on a low-carb diet in 2002 after finding that food with even 2 percent sugar reduced the lifespan of the laboratory roundworms she studies. “Basically I try to steer clear of desserts and starches, though I do eat chocolate,” she said.
Her willowy figure makes her look at least a decade younger than her age.
from wikipedia...
Personal diet
Kenyon's research prompted her to make personal dietary changes. She stopped eating high glycemic index carbohydrates when she discovered that putting sugar on the worms' food shortened their lifespans.[1]
Kenyon follows a low glycemic index diet similar to the Atkins diet[1] and the South Beach Diet[2].
No desserts. No sweets. No potatoes. No rice. No bread. No pasta. When I say ‘no,’ I mean ‘no, or not much,’ she notes. Instead, eat green vegetables. Eat the fruits that aren't the sweet fruits, like melon. Bananas? Bananas are a little sweet. Meat? Meat, yes, of course. Avocados. All vegetables. Nuts. Fish. Chicken. That's what I eat. Cheese. Eggs. And one glass of red wine a day.[3]
I have a fabulous blood profile. My triglyceride level is only 30, and anything below 200 is good.[3]
You have to eat something, and you just have to make your best judgement. And that's my best judgement. Plus, I feel better. Plus, I'm thin—I weigh what I weighed when I was in college. I feel great —you feel like you're a kid again. It's amazing.[3]
In the past, Kenyon had also briefly experimented with a calorie restriction diet for two days, but couldn't stand the constant hunger.[1]
Interesting. Over time, it seems as if the antioxidant theory of aging is losing ground to the insulin theory of aging. This scientist is applying her research to her own health.
Some attendees were so convinced of the virtues of less food that they have begun severe diets of various kinds. Cynthia Kenyon, of the University of California, San Francisco, said she had gone on a low-carb diet in 2002 after finding that food with even 2 percent sugar reduced the lifespan of the laboratory roundworms she studies. “Basically I try to steer clear of desserts and starches, though I do eat chocolate,” she said.
Her willowy figure makes her look at least a decade younger than her age.
from wikipedia...
Personal diet
Kenyon's research prompted her to make personal dietary changes. She stopped eating high glycemic index carbohydrates when she discovered that putting sugar on the worms' food shortened their lifespans.[1]
Kenyon follows a low glycemic index diet similar to the Atkins diet[1] and the South Beach Diet[2].
No desserts. No sweets. No potatoes. No rice. No bread. No pasta. When I say ‘no,’ I mean ‘no, or not much,’ she notes. Instead, eat green vegetables. Eat the fruits that aren't the sweet fruits, like melon. Bananas? Bananas are a little sweet. Meat? Meat, yes, of course. Avocados. All vegetables. Nuts. Fish. Chicken. That's what I eat. Cheese. Eggs. And one glass of red wine a day.[3]
I have a fabulous blood profile. My triglyceride level is only 30, and anything below 200 is good.[3]
You have to eat something, and you just have to make your best judgement. And that's my best judgement. Plus, I feel better. Plus, I'm thin—I weigh what I weighed when I was in college. I feel great —you feel like you're a kid again. It's amazing.[3]
In the past, Kenyon had also briefly experimented with a calorie restriction diet for two days, but couldn't stand the constant hunger.[1]
Interesting. Over time, it seems as if the antioxidant theory of aging is losing ground to the insulin theory of aging. This scientist is applying her research to her own health.
Friday, September 25, 2009
Cardiovascular Diabetology | Full text | Beneficial effects of a Paleolithic diet on cardiovascular risk factors in type 2 diabetes: a randomized cross-over pilot study
Cardiovascular Diabetology | Full text | Beneficial effects of a Paleolithic diet on cardiovascular risk factors in type 2 diabetes: a randomized cross-over pilot study
Results
Study participants had on average a diabetes duration of 9 years, a mean HbA1c of 6,6% units by Mono-S standard and were usually treated with metformin alone (3 subjects) or metformin in combination with a sulfonylurea (3 subjects) or a thiazolidinedione (3 subjects). Mean average dose of metformin was 1031 mg per day.
Compared to the diabetes diet, the Paleolithic diet resulted in lower mean values of
HbA1c (-0.4% units, p = 0.01),
triacylglycerol (-0.4 mmol/L, p = 0.003),
diastolic blood pressure (-4 mmHg, p = 0.03),
weight (-3 kg, p = 0.01), BMI (-1 kg/m2, p = 0.04) and waist circumference (-4 cm, p = 0.02), and
higher mean values of high density lipoprotein cholesterol (+0.08 mmol/L, p = 0.03).
The Paleolithic diet was mainly lower in cereals and dairy products, and higher in fruits, vegetables, meat and eggs, as compared with the Diabetes diet. Further, the Paleolithic diet was lower in total energy, energy density, carbohydrate, dietary glycemic load, saturated fatty acids and calcium, and higher in unsaturated fatty acids, dietary cholesterol and several vitamins. Dietary GI was slightly lower in the Paleolithic diet (GI = 50) than in the Diabetic diet (GI = 55).
Conclusion
Over a 3-month study period, a Paleolithic diet improved glycemic control and several cardiovascular risk factors compared to a Diabetes diet in patients with type 2 diabetes.
Results
Study participants had on average a diabetes duration of 9 years, a mean HbA1c of 6,6% units by Mono-S standard and were usually treated with metformin alone (3 subjects) or metformin in combination with a sulfonylurea (3 subjects) or a thiazolidinedione (3 subjects). Mean average dose of metformin was 1031 mg per day.
Compared to the diabetes diet, the Paleolithic diet resulted in lower mean values of
HbA1c (-0.4% units, p = 0.01),
triacylglycerol (-0.4 mmol/L, p = 0.003),
diastolic blood pressure (-4 mmHg, p = 0.03),
weight (-3 kg, p = 0.01), BMI (-1 kg/m2, p = 0.04) and waist circumference (-4 cm, p = 0.02), and
higher mean values of high density lipoprotein cholesterol (+0.08 mmol/L, p = 0.03).
The Paleolithic diet was mainly lower in cereals and dairy products, and higher in fruits, vegetables, meat and eggs, as compared with the Diabetes diet. Further, the Paleolithic diet was lower in total energy, energy density, carbohydrate, dietary glycemic load, saturated fatty acids and calcium, and higher in unsaturated fatty acids, dietary cholesterol and several vitamins. Dietary GI was slightly lower in the Paleolithic diet (GI = 50) than in the Diabetic diet (GI = 55).
Conclusion
Over a 3-month study period, a Paleolithic diet improved glycemic control and several cardiovascular risk factors compared to a Diabetes diet in patients with type 2 diabetes.
Men's Blood Pressure Increased By High-Sugar Diet
Men's Blood Pressure Increased By High-Sugar Diet
Study 1 highlights:
* Just two weeks on a high-fructose diet raises blood pressure in men.
* A drug used to treat gout seems to protect against that blood pressure increase and some aspects of metabolic syndrome.
Study 1 highlights:
* Just two weeks on a high-fructose diet raises blood pressure in men.
* A drug used to treat gout seems to protect against that blood pressure increase and some aspects of metabolic syndrome.
Tuesday, September 22, 2009
Consumption of 2 and 4 egg yolks/d for 5 wk increases macular pigment concentrations in older adults with low macular pigment taking cholesterol-lower
Consumption of 2 and 4 egg yolks/d for 5 wk increases macular pigment concentrations in older adults with low macular pigment taking cholesterol-lowering statins -- Vishwanathan et al., 10.3945/ajcn.2009.28013 -- American Journal of Clinical Nutrition
ABSTRACT
Background: Lutein and zeaxanthin may reduce the risk of dry, age-related macular degeneration because of their photo-oxidative role as macular pigment.
Objective: The present study evaluated serum lutein, zeaxanthin, and macular pigment optical density (MPOD) responses at 0.25°, 0.5°, and 1° retinal eccentricities to the consumption of 2 and 4 egg yolks/d by older adults taking cholesterol-lowering medications.
Design: Subjects consumed foods containing 2 followed by 4 egg yolks/d for 5 wk each with a 4-wk egg-free period at baseline and between the 2 interventions.
Results: Changes in MPOD (n = 37) with egg yolk consumption were inversely associated (P < 0.05) with baseline MPOD. Subjects with low-baseline MPOD (defined as MPOD ≤0.5 at 0.25°, ≤0.4 at 0.5°, and ≤0.35 at 1°) showed increases of ≤50% (P < 0.05) with 4 egg yolks at the 3 retinal eccentricities. MPOD increased by 31% (P = 0.059) at 0.5° with 2 egg yolks. Serum lutein increased by only 16% and 24% (P < 0.05) compared with increases of 36% and 82% (P < 0.001) in serum zeaxanthin (n = 52) after consumption of 2 and 4 egg yolks, respectively. Serum HDL cholesterol increased by 5% (P < 0.05) after consumption of 2 and 4 egg yolks. Serum LDL cholesterol did not change with either egg yolk treatment.
Conclusions: Consumption of 4 egg yolks/d, and possibly of 2 egg yolks/d, for 5 wk benefited macular health in older adults with low MPOD. Serum HDL cholesterol increased without an increase in LDL cholesterol in this study population, most of whom were taking cholesterol-lowering statins.
ABSTRACT
Background: Lutein and zeaxanthin may reduce the risk of dry, age-related macular degeneration because of their photo-oxidative role as macular pigment.
Objective: The present study evaluated serum lutein, zeaxanthin, and macular pigment optical density (MPOD) responses at 0.25°, 0.5°, and 1° retinal eccentricities to the consumption of 2 and 4 egg yolks/d by older adults taking cholesterol-lowering medications.
Design: Subjects consumed foods containing 2 followed by 4 egg yolks/d for 5 wk each with a 4-wk egg-free period at baseline and between the 2 interventions.
Results: Changes in MPOD (n = 37) with egg yolk consumption were inversely associated (P < 0.05) with baseline MPOD. Subjects with low-baseline MPOD (defined as MPOD ≤0.5 at 0.25°, ≤0.4 at 0.5°, and ≤0.35 at 1°) showed increases of ≤50% (P < 0.05) with 4 egg yolks at the 3 retinal eccentricities. MPOD increased by 31% (P = 0.059) at 0.5° with 2 egg yolks. Serum lutein increased by only 16% and 24% (P < 0.05) compared with increases of 36% and 82% (P < 0.001) in serum zeaxanthin (n = 52) after consumption of 2 and 4 egg yolks, respectively. Serum HDL cholesterol increased by 5% (P < 0.05) after consumption of 2 and 4 egg yolks. Serum LDL cholesterol did not change with either egg yolk treatment.
Conclusions: Consumption of 4 egg yolks/d, and possibly of 2 egg yolks/d, for 5 wk benefited macular health in older adults with low MPOD. Serum HDL cholesterol increased without an increase in LDL cholesterol in this study population, most of whom were taking cholesterol-lowering statins.
Monday, September 14, 2009
low carb diet beats low fat for improving metabolic syndrome, again
SpringerLink - Journal Article
Abstract We recently proposed that the biological markers improved by carbohydrate restriction were precisely those that define the metabolic syndrome (MetS), and that the common thread was regulation of insulin as a control element. We specifically tested the idea with a 12-week study comparing two hypocaloric diets (~1,500 kcal): a carbohydrate-restricted diet (CRD) (%carbohydrate:fat:protein = 12:59:28) and a low-fat diet (LFD) (56:24:20) in 40 subjects with atherogenic dyslipidemia. Both interventions led to improvements in several metabolic markers, but subjects following the CRD had consistently reduced glucose (−12%) and insulin (−50%) concentrations, insulin sensitivity (−55%), weight loss (−10%), decreased adiposity (−14%), and more favorable triacylglycerol (TAG) (−51%), HDL-C (13%) and total cholesterol/HDL-C ratio (−14%) responses. In addition to these markers for MetS, the CRD subjects showed more favorable responses to alternative indicators of cardiovascular risk: postprandial lipemia (−47%), the Apo B/Apo A-1 ratio (−16%), and LDL particle distribution. Despite a threefold higher intake of dietary saturated fat during the CRD, saturated fatty acids in TAG and cholesteryl ester were significantly decreased, as was palmitoleic acid (16:1n-7), an endogenous marker of lipogenesis, compared to subjects consuming the LFD. Serum retinol binding protein 4 has been linked to insulin-resistant states, and only the CRD decreased this marker (−20%). The findings provide support for unifying the disparate markers of MetS and for the proposed intimate connection with dietary carbohydrate. The results support the use of dietary carbohydrate restriction as an effective approach to improve features of MetS and cardiovascular risk.
Abstract We recently proposed that the biological markers improved by carbohydrate restriction were precisely those that define the metabolic syndrome (MetS), and that the common thread was regulation of insulin as a control element. We specifically tested the idea with a 12-week study comparing two hypocaloric diets (~1,500 kcal): a carbohydrate-restricted diet (CRD) (%carbohydrate:fat:protein = 12:59:28) and a low-fat diet (LFD) (56:24:20) in 40 subjects with atherogenic dyslipidemia. Both interventions led to improvements in several metabolic markers, but subjects following the CRD had consistently reduced glucose (−12%) and insulin (−50%) concentrations, insulin sensitivity (−55%), weight loss (−10%), decreased adiposity (−14%), and more favorable triacylglycerol (TAG) (−51%), HDL-C (13%) and total cholesterol/HDL-C ratio (−14%) responses. In addition to these markers for MetS, the CRD subjects showed more favorable responses to alternative indicators of cardiovascular risk: postprandial lipemia (−47%), the Apo B/Apo A-1 ratio (−16%), and LDL particle distribution. Despite a threefold higher intake of dietary saturated fat during the CRD, saturated fatty acids in TAG and cholesteryl ester were significantly decreased, as was palmitoleic acid (16:1n-7), an endogenous marker of lipogenesis, compared to subjects consuming the LFD. Serum retinol binding protein 4 has been linked to insulin-resistant states, and only the CRD decreased this marker (−20%). The findings provide support for unifying the disparate markers of MetS and for the proposed intimate connection with dietary carbohydrate. The results support the use of dietary carbohydrate restriction as an effective approach to improve features of MetS and cardiovascular risk.
Diabetes of the Liver: The Link Between Nonalcoholic Fatty Liver Disease and High fructose corn syrup
Obesity - Abstract of article: Diabetes of the Liver: The Link Between Nonalcoholic Fatty Liver Disease and HFCS-55
Nonalcoholic fatty liver disease (NAFLD) is associated with obesity and insulin resistance. It is also a predisposing factor for type 2 diabetes. Dietary factors are believed to contribute to all three diseases. NAFLD is characterized by increased intrahepatic fat and mitochondrial dysfunction, and its etiology may be attributed to excessive fructose intake. Consumption of high fructose corn syrup-55 (HFCS-55) stands at up to 15% of the average total daily energy intake in the United States, and is linked to weight gain and obesity. The aim of this study was to establish whether HFCS-55 could contribute to the pathogenesis of NAFLD, by examining the effects of HFCS-55 on hepatocyte lipogenesis, insulin signaling, and cellular function, in vitro and in vivo. Exposure of hepatocytes to HFCS-55 caused a significant increase in hepatocellular triglyceride (TG) and lipogenic proteins. Basal production of reactive oxygen metabolite (ROM) was increased, together with a decreased capacity to respond to an oxidative challenge. HFCS-55 induced a downregulation of the insulin signaling pathway, as indicated by attenuated ser473phosphorylation of AKT1. The c-Jun amino-terminal kinase (JNK), which is intimately linked to insulin resistance, was also activated; and this was accompanied by an increase in endoplasmic reticulum (ER) stress and intracellular free calcium perturbation. Hepatocytes exposed to HFCS-55 exhibited mitochondrial dysfunction and released cytochrome C (CytC) into the cytosol. Hepatic steatosis and mitochondrial disruption was induced in vivo by a diet enriched with 20% HFCS 55; accompanied by hypoadiponectinemia and elevated fasting serum insulin and retinol-binding protein-4 (RBP4) levels.
Taken together our findings indicate a potential mechanism by which HFCS-55 may contribute to the pathogenesis of NAFLD.
Nonalcoholic fatty liver disease (NAFLD) is associated with obesity and insulin resistance. It is also a predisposing factor for type 2 diabetes. Dietary factors are believed to contribute to all three diseases. NAFLD is characterized by increased intrahepatic fat and mitochondrial dysfunction, and its etiology may be attributed to excessive fructose intake. Consumption of high fructose corn syrup-55 (HFCS-55) stands at up to 15% of the average total daily energy intake in the United States, and is linked to weight gain and obesity. The aim of this study was to establish whether HFCS-55 could contribute to the pathogenesis of NAFLD, by examining the effects of HFCS-55 on hepatocyte lipogenesis, insulin signaling, and cellular function, in vitro and in vivo. Exposure of hepatocytes to HFCS-55 caused a significant increase in hepatocellular triglyceride (TG) and lipogenic proteins. Basal production of reactive oxygen metabolite (ROM) was increased, together with a decreased capacity to respond to an oxidative challenge. HFCS-55 induced a downregulation of the insulin signaling pathway, as indicated by attenuated ser473phosphorylation of AKT1. The c-Jun amino-terminal kinase (JNK), which is intimately linked to insulin resistance, was also activated; and this was accompanied by an increase in endoplasmic reticulum (ER) stress and intracellular free calcium perturbation. Hepatocytes exposed to HFCS-55 exhibited mitochondrial dysfunction and released cytochrome C (CytC) into the cytosol. Hepatic steatosis and mitochondrial disruption was induced in vivo by a diet enriched with 20% HFCS 55; accompanied by hypoadiponectinemia and elevated fasting serum insulin and retinol-binding protein-4 (RBP4) levels.
Taken together our findings indicate a potential mechanism by which HFCS-55 may contribute to the pathogenesis of NAFLD.
ScienceDirect - Nutrition, Metabolism and Cardiovascular Diseases : Carbohydrate restriction favorably alters lipoprotein metabolism in Emirati subjects classified with the metabolic syndrome
ScienceDirect - Nutrition, Metabolism and Cardiovascular Diseases : Carbohydrate restriction favorably alters lipoprotein metabolism in Emirati subjects classified with the metabolic syndrome
Background and aims
Carbohydrate restriction (CR) has been shown to improve dyslipidemias associated with metabolic syndrome (MetS). We evaluated the effects of CR on lipoprotein subfractions and apolipoproteins in Emirati adults classified with the MetS.
Methods and results
39 subjects (15 men/24 women) were randomly allocated to a CR diet [20–25% energy from carbohydrate (CHO)] for 12 wk (CRD group) or a combination treatment consisting of CRD for 6 wk followed by the American Heart Association diet (50–55% CHO, AHA group) for an additional 6 wk. All subjects reduced body weight, LDL cholesterol and triglycerides (P < 0.01). At baseline all subjects had low concentrations of medium VLDL and total HDL particles associated with the very low plasma triglycerides and HDL cholesterol in this population. After 12 wk, the large VLDL subfraction was decreased over time for subjects in the CRD group (P < 0.01) while these changes were not observed in those subjects who changed to the AHA diet. The number of medium and small LDL particles decreased for all subjects rendering a less atherogenic lipoprotein profile. In agreement with these results, a significant decrease in apolipoprotein (apo) B was observed (P < 0.01). The medium HDL subfraction and apo A-II, which can be considered pro-atherogenic, were also decreased over time in the CRD group only.
Conclusions
These results suggest that weight loss favorably affects lipoprotein metabolism and that the CRD had a better effect on atherogenic VLDL and HDL than the low fat diet recommended by AHA.
Background and aims
Carbohydrate restriction (CR) has been shown to improve dyslipidemias associated with metabolic syndrome (MetS). We evaluated the effects of CR on lipoprotein subfractions and apolipoproteins in Emirati adults classified with the MetS.
Methods and results
39 subjects (15 men/24 women) were randomly allocated to a CR diet [20–25% energy from carbohydrate (CHO)] for 12 wk (CRD group) or a combination treatment consisting of CRD for 6 wk followed by the American Heart Association diet (50–55% CHO, AHA group) for an additional 6 wk. All subjects reduced body weight, LDL cholesterol and triglycerides (P < 0.01). At baseline all subjects had low concentrations of medium VLDL and total HDL particles associated with the very low plasma triglycerides and HDL cholesterol in this population. After 12 wk, the large VLDL subfraction was decreased over time for subjects in the CRD group (P < 0.01) while these changes were not observed in those subjects who changed to the AHA diet. The number of medium and small LDL particles decreased for all subjects rendering a less atherogenic lipoprotein profile. In agreement with these results, a significant decrease in apolipoprotein (apo) B was observed (P < 0.01). The medium HDL subfraction and apo A-II, which can be considered pro-atherogenic, were also decreased over time in the CRD group only.
Conclusions
These results suggest that weight loss favorably affects lipoprotein metabolism and that the CRD had a better effect on atherogenic VLDL and HDL than the low fat diet recommended by AHA.
Monday, September 07, 2009
High protein intake reduces intrahepatocellular lipid deposition in humans -- Bortolotti et al., 10.3945/ajcn.2008.27296 -- American Journal of Clinical Nutrition
High protein intake reduces intrahepatocellular lipid deposition in humans -- Bortolotti et al., 10.3945/ajcn.2008.27296 -- American Journal of Clinical Nutrition
Background: High sugar and fat intakes are known to increase intrahepatocellular lipids (IHCLs) and to cause insulin resistance. High protein intake may facilitate weight loss and improve glucose homeostasis in insulin-resistant patients, but its effects on IHCLs remain unknown.
Objective: The aim was to assess the effect of high protein intake on high-fat diet–induced IHCL accumulation and insulin sensitivity in healthy young men.
Increasing protein in the diet reduces the dangerous buildup of fat in the liver. This fatty liver problem is fond in alcoholics and people consuming large amounts of fructose, i.e. metabolic syndrome.
Background: High sugar and fat intakes are known to increase intrahepatocellular lipids (IHCLs) and to cause insulin resistance. High protein intake may facilitate weight loss and improve glucose homeostasis in insulin-resistant patients, but its effects on IHCLs remain unknown.
Objective: The aim was to assess the effect of high protein intake on high-fat diet–induced IHCL accumulation and insulin sensitivity in healthy young men.
Increasing protein in the diet reduces the dangerous buildup of fat in the liver. This fatty liver problem is fond in alcoholics and people consuming large amounts of fructose, i.e. metabolic syndrome.
Access : Connecting obesity, aging and diabetes : Nature
Access : Connecting obesity, aging and diabetes : Nature:
"Obesity accelerates the aging of adipose tissue, a process only now beginning to come to light at the molecular level. Experiments in mice suggest that obesity increases the formation of reactive oxygen species in fat cells, shortens telomeres—and ultimately results in activation of the p53 tumor suppressor, inflammation and the promotion of insulin resistance (pages 1082–1087).
Obesity accelerates the aging of adipose tissue, leading to inflammation and insulin resistance.
As technology has improved hygiene, the food supply and living standards overall, there has been a rise in such age-related illnesses as cardiovascular disease, cancer, degenerative diseases of the brain and other organs, and metabolic disorders such as diabetes. Age-related disorders have become widespread throughout the world, replacing infectious diseases as the leading cause of death in developed countries."
"Obesity accelerates the aging of adipose tissue, a process only now beginning to come to light at the molecular level. Experiments in mice suggest that obesity increases the formation of reactive oxygen species in fat cells, shortens telomeres—and ultimately results in activation of the p53 tumor suppressor, inflammation and the promotion of insulin resistance (pages 1082–1087).
Obesity accelerates the aging of adipose tissue, leading to inflammation and insulin resistance.
As technology has improved hygiene, the food supply and living standards overall, there has been a rise in such age-related illnesses as cardiovascular disease, cancer, degenerative diseases of the brain and other organs, and metabolic disorders such as diabetes. Age-related disorders have become widespread throughout the world, replacing infectious diseases as the leading cause of death in developed countries."
Over 70% of American children deficient in vitamin D! - Kumar et al. 124 (3): e362 -- Pediatrics
Prevalence and Associations of 25-Hydroxyvitamin D Deficiency in US Children: NHANES 2001-2004 -- Kumar et al. 124 (3): e362 -- Pediatrics:
OBJECTIVES: To determine the prevalence of 25-hydroxyvitamin D (25[OH]D) deficiency and associations between 25(OH)D deficiency and cardiovascular risk factors in children and adolescents.
"CONCLUSIONS: 25(OH)D deficiency is common in the general US pediatric population and is associated with adverse cardiovascular risks."
Over 70% of American children deficient in vitamin D!
OBJECTIVES: To determine the prevalence of 25-hydroxyvitamin D (25[OH]D) deficiency and associations between 25(OH)D deficiency and cardiovascular risk factors in children and adolescents.
"CONCLUSIONS: 25(OH)D deficiency is common in the general US pediatric population and is associated with adverse cardiovascular risks."
Over 70% of American children deficient in vitamin D!
7 Reasons to Eat More Saturated Fat
7 Reasons to Eat More Saturated Fat
7 Reasons to Eat More Saturated Fat 108 Comments
Written by Tim Ferriss Topics: Physical Performance
7 Reasons to Eat More Saturated Fat
In the not-so-distant past, the medical establishment considered all fats equally loathsome: all fats were created equal and they’re all bad for you. Things have changed in that quarter, if only slightly. You have no doubt heard the drumbeat of current medical thinking on fats: some fats are now good for you—olive oil and canola oil*—but others are bad for you—trans fats and all saturated fats. That’s an improvement from the old cry, but far from the truth.
It seems that no matter how the story spins from the denizens of the anti-fat camp, one piece of their advice remains staunchly constant: “You should sharply limit your intake of saturated fats.” The next admonition will invariably be, “which have been proven to raise cholesterol and cause heart disease.” Their over-arching belief is that saturated fat is bad, bad, bad.
You see with just a glance at [our suggested meal plans] that we’ve included fatty cuts of meat, chicken with the skin, bacon, eggs, butter, coconut oil, organic lard, and heavy cream in the plan. Aren’t we worried that these foods will increase your risk of heart disease and raise your cholesterol? In a word, nope. In fact, we encourage you to make these important fats a regular part of your healthy diet. Why? Because humans need them and here are just a few reasons why.
1) Improved cardiovascular risk factors
Though you may not have heard of it on the front pages of your local newspaper, online news source, or local television or radio news program, saturated fat plays a couple of key roles in cardiovascular health. The addition of saturated fat to the diet reduces the levels of a substance called lipoprotein (a)—pronounced “lipoprotein little a” and abbreviated Lp(a)—that correlates strongly with risk for heart disease. Currently there are no medications to lower this substance and the only dietary means of lowering Lp(a) is eating saturated fat. Bet you didn’t hear that on the nightly news. Moreover, eating saturated (and other) fats also raises the level of HDL, the so-called good cholesterol. Lastly, research has shown that when women diet, those eating the greatest percentage of the total fat in their diets as saturated fat lose the most weight.
2) Stronger bones
In middle age, as bone mass begins to decline, an important goal (particularly for women) is to build strong bones. You can’t turn on the television without being told you need calcium for your bones, but do you recall ever hearing that saturated fat is required for calcium to be effectively incorporated into bone? According to one of the foremost research experts in dietary fats and human health, Mary Enig, Ph.D., there’s a case to be made for having as much as 50 percent of the fats in your diet as saturated fats for this reason. That’s a far cry from the 7 to 10 percent suggested by mainstream institutions. If her reasoning is sound—and we believe it is— is it any wonder that the vast majority of women told to avoid saturated fat and to selectively use vegetable oils instead would begin to lose bone mass, develop osteoporosis, and get put on expensive prescription medications plus calcium to try to recover the loss in middle age?
3) Improved liver health
Adding saturated fat to the diet has been shown in medical research to encourage the liver cells to dump their fat content. Clearing fat from the liver is the critical first step to calling a halt to middle-body fat storage. Additionally, saturated fat has been shown to protect the liver from the toxic insults of alcohol and medications, including acetaminophen and other drugs commonly used for pain and arthritis, such as nonsteroidal anti-inflammatory drugs or NSAIDs, and even to reverse the damage once it has occurred. Since the liver is the lynchpin of a healthy metabolism, anything that is good for the liver is good for getting rid of fat in the middle. Polyunsaturated vegetable fats do not offer this protection.
4) Healthy lungs
For proper function, the airspaces of the lungs have to be coated with a thin layer of what’s called lung surfactant. The fat content of lung surfactant is 100 percent saturated fatty acids. Replacement of these critical fats by other types of fat makes faulty surfactant and potentially causes breathing difficulties. Absence of the correct amount and composition of this material leads to collapse of the airspaces and respiratory distress. It’s what’s missing in the lungs of premature infants who develop the breathing disorder called infant respiratory distress syndrome. Some researchers feel that the wholesale substitution of partially hydrogenated (trans) fats for naturally saturated fats in commercially prepared foods may be playing a role in the rise of asthma among children. Fortunately, the heyday of trans fats is ending and their use is on the decline. Unfortunately, however, the unreasoning fear of saturated fat leads many people to replace trans fats with an overabundance of polyunsaturated vegetable oils, which may prove just as unhealthful.
5) Healthy brain
You will likely be astounded to learn that your brain is mainly made of fat and cholesterol. Though many people are now familiar with the importance of the highly unsaturated essential fatty acids found in cold-water fish (EPA and DHA) for normal brain and nerve function, the lion’s share of the fatty acids in the brain are actually saturated. A diet that skimps on healthy saturated fats robs your brain of the raw materials it needs to function optimally.
6) Proper nerve signaling
Certain saturated fats, particularly those found in butter, lard, coconut oil, and palm oil, function directly as signaling messengers that influence the metabolism, including such critical jobs as the appropriate release of insulin. And just any old fat won’t do. Without the correct signals to tell the organs and glands what to do, the job doesn’t get done or gets done improperly.
7) Strong immune system
Saturated fats found in butter and coconut oil (myristic acid and lauric acid) play key roles in immune health. Loss of sufficient saturated fatty acids in the white blood cells hampers their ability to recognize and destroy foreign invaders, such as viruses, bacteria, and fungi. Human breast milk is quite rich in myristic and lauric acid, which have potent germ-killing ability. But the importance of the fats lives on beyond infancy; we need dietary replenishment of them throughout adulthood, middle age, and into seniority to keep the immune system vigilant against the development of cancerous cells as well as infectious invaders.
7 Reasons to Eat More Saturated Fat 108 Comments
Written by Tim Ferriss Topics: Physical Performance
7 Reasons to Eat More Saturated Fat
In the not-so-distant past, the medical establishment considered all fats equally loathsome: all fats were created equal and they’re all bad for you. Things have changed in that quarter, if only slightly. You have no doubt heard the drumbeat of current medical thinking on fats: some fats are now good for you—olive oil and canola oil*—but others are bad for you—trans fats and all saturated fats. That’s an improvement from the old cry, but far from the truth.
It seems that no matter how the story spins from the denizens of the anti-fat camp, one piece of their advice remains staunchly constant: “You should sharply limit your intake of saturated fats.” The next admonition will invariably be, “which have been proven to raise cholesterol and cause heart disease.” Their over-arching belief is that saturated fat is bad, bad, bad.
You see with just a glance at [our suggested meal plans] that we’ve included fatty cuts of meat, chicken with the skin, bacon, eggs, butter, coconut oil, organic lard, and heavy cream in the plan. Aren’t we worried that these foods will increase your risk of heart disease and raise your cholesterol? In a word, nope. In fact, we encourage you to make these important fats a regular part of your healthy diet. Why? Because humans need them and here are just a few reasons why.
1) Improved cardiovascular risk factors
Though you may not have heard of it on the front pages of your local newspaper, online news source, or local television or radio news program, saturated fat plays a couple of key roles in cardiovascular health. The addition of saturated fat to the diet reduces the levels of a substance called lipoprotein (a)—pronounced “lipoprotein little a” and abbreviated Lp(a)—that correlates strongly with risk for heart disease. Currently there are no medications to lower this substance and the only dietary means of lowering Lp(a) is eating saturated fat. Bet you didn’t hear that on the nightly news. Moreover, eating saturated (and other) fats also raises the level of HDL, the so-called good cholesterol. Lastly, research has shown that when women diet, those eating the greatest percentage of the total fat in their diets as saturated fat lose the most weight.
2) Stronger bones
In middle age, as bone mass begins to decline, an important goal (particularly for women) is to build strong bones. You can’t turn on the television without being told you need calcium for your bones, but do you recall ever hearing that saturated fat is required for calcium to be effectively incorporated into bone? According to one of the foremost research experts in dietary fats and human health, Mary Enig, Ph.D., there’s a case to be made for having as much as 50 percent of the fats in your diet as saturated fats for this reason. That’s a far cry from the 7 to 10 percent suggested by mainstream institutions. If her reasoning is sound—and we believe it is— is it any wonder that the vast majority of women told to avoid saturated fat and to selectively use vegetable oils instead would begin to lose bone mass, develop osteoporosis, and get put on expensive prescription medications plus calcium to try to recover the loss in middle age?
3) Improved liver health
Adding saturated fat to the diet has been shown in medical research to encourage the liver cells to dump their fat content. Clearing fat from the liver is the critical first step to calling a halt to middle-body fat storage. Additionally, saturated fat has been shown to protect the liver from the toxic insults of alcohol and medications, including acetaminophen and other drugs commonly used for pain and arthritis, such as nonsteroidal anti-inflammatory drugs or NSAIDs, and even to reverse the damage once it has occurred. Since the liver is the lynchpin of a healthy metabolism, anything that is good for the liver is good for getting rid of fat in the middle. Polyunsaturated vegetable fats do not offer this protection.
4) Healthy lungs
For proper function, the airspaces of the lungs have to be coated with a thin layer of what’s called lung surfactant. The fat content of lung surfactant is 100 percent saturated fatty acids. Replacement of these critical fats by other types of fat makes faulty surfactant and potentially causes breathing difficulties. Absence of the correct amount and composition of this material leads to collapse of the airspaces and respiratory distress. It’s what’s missing in the lungs of premature infants who develop the breathing disorder called infant respiratory distress syndrome. Some researchers feel that the wholesale substitution of partially hydrogenated (trans) fats for naturally saturated fats in commercially prepared foods may be playing a role in the rise of asthma among children. Fortunately, the heyday of trans fats is ending and their use is on the decline. Unfortunately, however, the unreasoning fear of saturated fat leads many people to replace trans fats with an overabundance of polyunsaturated vegetable oils, which may prove just as unhealthful.
5) Healthy brain
You will likely be astounded to learn that your brain is mainly made of fat and cholesterol. Though many people are now familiar with the importance of the highly unsaturated essential fatty acids found in cold-water fish (EPA and DHA) for normal brain and nerve function, the lion’s share of the fatty acids in the brain are actually saturated. A diet that skimps on healthy saturated fats robs your brain of the raw materials it needs to function optimally.
6) Proper nerve signaling
Certain saturated fats, particularly those found in butter, lard, coconut oil, and palm oil, function directly as signaling messengers that influence the metabolism, including such critical jobs as the appropriate release of insulin. And just any old fat won’t do. Without the correct signals to tell the organs and glands what to do, the job doesn’t get done or gets done improperly.
7) Strong immune system
Saturated fats found in butter and coconut oil (myristic acid and lauric acid) play key roles in immune health. Loss of sufficient saturated fatty acids in the white blood cells hampers their ability to recognize and destroy foreign invaders, such as viruses, bacteria, and fungi. Human breast milk is quite rich in myristic and lauric acid, which have potent germ-killing ability. But the importance of the fats lives on beyond infancy; we need dietary replenishment of them throughout adulthood, middle age, and into seniority to keep the immune system vigilant against the development of cancerous cells as well as infectious invaders.
Monday, August 31, 2009
The Heart Scan Blog: Weight loss and vitamin D
The Heart Scan Blog: Weight loss and vitamin D
Weight loss and vitamin D
At the start of her program, Penny's 25-hydroxy vitamin D blood level showed the usual deficiency at 22 ng/ml.
She supplemented with 8000 units of vitamin D. Another 25-hydroxy vitamin D blood level several months later showed a level of 67.8 ng/ml, right on target.
But Penny also began our diet, including the elimination of wheat, cornstarch, and sugars, and, over 6 months, lost 34 lbs.
Now a much trimmer 146 lbs (still more to go!), another vitamin D blood level: 111 ng/ml.
Penny's weight loss means that the vitamin D is distributed in a smaller total volume, particularly a lower volume of fat.
This is a common phenomenon with substantial weight loss: lose weight and the need for vitamin D is reduced. The reduction in dose is roughly proportion to the weight lost. Vitamin D should therefore be reassessed with any substantial change in weight of, say, 10 lbs or more, either up or down, because of the influence of fat on vitamin D blood levels.
Some references on this effect:
Men and women over age 65:
Adiposity in relation to vitamin D status and parathyroid hormone levels: a population-based study in older men and women.
Obese women:
Low 25-hydroxyvitamin D concentrations in obese women: their clinical significance and relationship with anthropometric and body composition variables
Obese children:
Hypovitaminosis D in obese children and adolescents: relationship with adiposity, insulin sensitivity, ethnicity, and season.
African-Americans:
Relationship of vitamin D and parathyroid hormone to obesity and body composition in African Americans.
Although the bulk of the effect is most likely due to sequestration by fatty tissue, perhaps less sun exposure in obese people also contributes:
Body mass index determines sunbathing habits: implications on vitamin D levels.
Weight loss and vitamin D
At the start of her program, Penny's 25-hydroxy vitamin D blood level showed the usual deficiency at 22 ng/ml.
She supplemented with 8000 units of vitamin D. Another 25-hydroxy vitamin D blood level several months later showed a level of 67.8 ng/ml, right on target.
But Penny also began our diet, including the elimination of wheat, cornstarch, and sugars, and, over 6 months, lost 34 lbs.
Now a much trimmer 146 lbs (still more to go!), another vitamin D blood level: 111 ng/ml.
Penny's weight loss means that the vitamin D is distributed in a smaller total volume, particularly a lower volume of fat.
This is a common phenomenon with substantial weight loss: lose weight and the need for vitamin D is reduced. The reduction in dose is roughly proportion to the weight lost. Vitamin D should therefore be reassessed with any substantial change in weight of, say, 10 lbs or more, either up or down, because of the influence of fat on vitamin D blood levels.
Some references on this effect:
Men and women over age 65:
Adiposity in relation to vitamin D status and parathyroid hormone levels: a population-based study in older men and women.
Obese women:
Low 25-hydroxyvitamin D concentrations in obese women: their clinical significance and relationship with anthropometric and body composition variables
Obese children:
Hypovitaminosis D in obese children and adolescents: relationship with adiposity, insulin sensitivity, ethnicity, and season.
African-Americans:
Relationship of vitamin D and parathyroid hormone to obesity and body composition in African Americans.
Although the bulk of the effect is most likely due to sequestration by fatty tissue, perhaps less sun exposure in obese people also contributes:
Body mass index determines sunbathing habits: implications on vitamin D levels.
Vitamin B12 deficiency is associated with coronary...[Clin Chem Lab Med. 2009] - PubMed Result
Vitamin B12 deficiency is associated with coronary...[Clin Chem Lab Med. 2009] - PubMed Result
BACKGROUND: The incidence of coronary artery disease (CAD) is increasing at an alarming rate, especially in developing countries, such as India. It is often advocated that a vegetarian lifestyle could reduce the burden of CAD. However, in spite of a majority of Indians being vegetarians, the incidence of CAD is highest in this population. This may be due to deficiency of vitamin B12, a micronutrient, sourced only from animal products.
RESULTS: We found that vitamin B12 levels were significantly lower in coronary artery disease patients than in controls (p<0.0001). Also, vegetarians were found to have significantly lower vitamin B12 concentrations (p=0.0001) and higher incidence of coronary artery disease (p=0.01). Interestingly, elevated homocysteine levels, a hallmark of vitamin B12 deficiency, was not associated with CAD. In contrast, cysteine levels were significantly higher in CAD patients than in controls (p=0.004). CONCLUSIONS: We believe that, when vitamin B12 is deficient, homocysteine is rapidly metabolized via the transsulfuration pathway leading to increased cysteine levels.
BACKGROUND: The incidence of coronary artery disease (CAD) is increasing at an alarming rate, especially in developing countries, such as India. It is often advocated that a vegetarian lifestyle could reduce the burden of CAD. However, in spite of a majority of Indians being vegetarians, the incidence of CAD is highest in this population. This may be due to deficiency of vitamin B12, a micronutrient, sourced only from animal products.
RESULTS: We found that vitamin B12 levels were significantly lower in coronary artery disease patients than in controls (p<0.0001). Also, vegetarians were found to have significantly lower vitamin B12 concentrations (p=0.0001) and higher incidence of coronary artery disease (p=0.01). Interestingly, elevated homocysteine levels, a hallmark of vitamin B12 deficiency, was not associated with CAD. In contrast, cysteine levels were significantly higher in CAD patients than in controls (p=0.004). CONCLUSIONS: We believe that, when vitamin B12 is deficient, homocysteine is rapidly metabolized via the transsulfuration pathway leading to increased cysteine levels.
Low plasma vitamin B12 in pregnancy is associated with gestational ‘diabesity’ and later diabetes
SpringerLink - Journal Article
Conclusions/interpretation Maternal vitamin B12 deficiency is associated with increased adiposity and, in turn, with insulin resistance and GDM. Vitamin B12 deficiency may be an important factor underlying the high risk of ‘diabesity’ in south Asian Indians.
Conclusions/interpretation Maternal vitamin B12 deficiency is associated with increased adiposity and, in turn, with insulin resistance and GDM. Vitamin B12 deficiency may be an important factor underlying the high risk of ‘diabesity’ in south Asian Indians.
Thursday, August 27, 2009
Slashdot Science Story | Depression May Provide Cognitive Advantages
Slashdot Science Story | Depression May Provide Cognitive Advantages
"Paul W. Andrews and J. Anderson Thomson, Jr. argue in Scientific American that although depression is considered a mental disorder, depression may in fact be a mental adaptation which provides real benefits. This is not to say that depression is not a problem. Depressed people often have trouble performing everyday activities, they can't concentrate on their work, they tend to socially isolate themselves, they are lethargic, and they often lose the ability to take pleasure from such activities such as eating and sex. So what could be so useful about depression? "Depressed people often think intensely about their problems," write the authors. "These thoughts are called ruminations; they are persistent and depressed people have difficulty thinking about anything else. Numerous studies have also shown that this thinking style is often highly analytical. They dwell on a complex problem, breaking it down into smaller components, which are considered one at a time." Various studies have found that people in depressed mood states are better at solving social dilemmas and there is evidence that people who get more depressed while they are working on complex problems in an intelligence test tend to score higher on the test (PDF). "When one considers all the evidence, depression seems less like a disorder where the brain is operating in a haphazard way, or malfunctioning. Instead, depression seems more like the vertebrate eye--an intricate, highly organized piece of machinery that performs a specific function.""
"Paul W. Andrews and J. Anderson Thomson, Jr. argue in Scientific American that although depression is considered a mental disorder, depression may in fact be a mental adaptation which provides real benefits. This is not to say that depression is not a problem. Depressed people often have trouble performing everyday activities, they can't concentrate on their work, they tend to socially isolate themselves, they are lethargic, and they often lose the ability to take pleasure from such activities such as eating and sex. So what could be so useful about depression? "Depressed people often think intensely about their problems," write the authors. "These thoughts are called ruminations; they are persistent and depressed people have difficulty thinking about anything else. Numerous studies have also shown that this thinking style is often highly analytical. They dwell on a complex problem, breaking it down into smaller components, which are considered one at a time." Various studies have found that people in depressed mood states are better at solving social dilemmas and there is evidence that people who get more depressed while they are working on complex problems in an intelligence test tend to score higher on the test (PDF). "When one considers all the evidence, depression seems less like a disorder where the brain is operating in a haphazard way, or malfunctioning. Instead, depression seems more like the vertebrate eye--an intricate, highly organized piece of machinery that performs a specific function.""
Wednesday, August 26, 2009
Half of healthcare workers say no to swine flu jab - Healthcare Republic News
Half of healthcare workers say no to swine flu jab - Healthcare Republic News
Most DR.s may reject swine flu vaccine
(HEALTHCARE REPUBLIC) Up to 60% of GPs may choose not to be vaccinated against swine flu, with many concerned about the safety of the vaccine, a GP newspaper survey suggests.
Of 216 GPs who responded to the survey, 29% said they would not opt to receive the swine flu vaccine and a further 29% said they were not sure whether they would or not.
Of those who would refuse vaccination, 71% said they were concerned that the vaccine had not been through sufficient trials to guarantee its safety.
Professor David Salisbury, DoH director of immunisation, toldHealthcare Republic, the website for GP newspaper, that frontline health workers have a duty to themselves regarding vaccination.
‘They have a duty to their patients not to infect their patients and they have a duty to their families,’ he said.
Most DR.s may reject swine flu vaccine
(HEALTHCARE REPUBLIC) Up to 60% of GPs may choose not to be vaccinated against swine flu, with many concerned about the safety of the vaccine, a GP newspaper survey suggests.
Of 216 GPs who responded to the survey, 29% said they would not opt to receive the swine flu vaccine and a further 29% said they were not sure whether they would or not.
Of those who would refuse vaccination, 71% said they were concerned that the vaccine had not been through sufficient trials to guarantee its safety.
Professor David Salisbury, DoH director of immunisation, toldHealthcare Republic, the website for GP newspaper, that frontline health workers have a duty to themselves regarding vaccination.
‘They have a duty to their patients not to infect their patients and they have a duty to their families,’ he said.
Tuesday, August 18, 2009
Fructose But Not Glucose-Sweetened Beverages Increased Insulin Resistance And Belly Fat In Overweight And Obese People, Study
Fructose But Not Glucose-Sweetened Beverages Increased Insulin Resistance And Belly Fat In Overweight And Obese People, Study
We all know that too much sugar is not good for us, but researchers from the US have discovered that drinks sweetened with fructose as opposed to glucose were significantly more likely to increase insulin resistance and belly fat in obese and overweight people, leading to medical conditions that increased their risk of heart attack and stroke.
The study was the work of Dr Peter Havel, a researcher in the Department of Nutrition at the University of California at Davis, and colleagues, and was published in the April 20 issue of the Journal of Clinical Investigation.
Over the twelve months of 2005, the average American consumed about 64 kg of extra sugar from drinking sweetened soft drinks: this is approximately the weight of an average height, slim American woman.
But although studies in animals have shown that compared with glucose, dietary fructose leads to increased insulin resistance plus higher levels of blood cholesterol and fats, there has been little equivalent research on humans.
Over the 10 weeks of the study, Havel and colleagues showed that human consumption of beverages sweetened with fructose but not glucose can worsen the body's sensitivity to insulin and how it handles fat.
For the study, which involved 32 overweight and obese men and women aged around 50, the participants spent 2 weeks in a closely observed inpatient setting and then 8 weeks in an outpatient setting. Over the two phases they drank beverages sweetened with glucose (15 subjects) or fructose (17 subjects) comprising 25 per cent of their daily calorie intake.
During the 10 weeks in total of the study, participants in both groups put on about the same amount of weight, but only those in the fructose group showed an increase in belly fat.
Also, only the participants in the fructose group became less sensitive to insulin (the hormone that controls how much glucose is in the bloodstream), and developed higher levels of total and LDL or "bad" cholesterol.
The fructose group also showed higher levels of hepatic DNL (de novo lipogenesis, fat that is produced from excess digested carbohydrate) and other signs that their bodies were producing fat differently to the glucose group.
The researchers concluded that:
"These data suggest that dietary fructose specifically increases DNL, promotes dyslipidemia, decreases insulin sensitivity, and increases visceral adiposity in overweight/obese adults."
We all know that too much sugar is not good for us, but researchers from the US have discovered that drinks sweetened with fructose as opposed to glucose were significantly more likely to increase insulin resistance and belly fat in obese and overweight people, leading to medical conditions that increased their risk of heart attack and stroke.
The study was the work of Dr Peter Havel, a researcher in the Department of Nutrition at the University of California at Davis, and colleagues, and was published in the April 20 issue of the Journal of Clinical Investigation.
Over the twelve months of 2005, the average American consumed about 64 kg of extra sugar from drinking sweetened soft drinks: this is approximately the weight of an average height, slim American woman.
But although studies in animals have shown that compared with glucose, dietary fructose leads to increased insulin resistance plus higher levels of blood cholesterol and fats, there has been little equivalent research on humans.
Over the 10 weeks of the study, Havel and colleagues showed that human consumption of beverages sweetened with fructose but not glucose can worsen the body's sensitivity to insulin and how it handles fat.
For the study, which involved 32 overweight and obese men and women aged around 50, the participants spent 2 weeks in a closely observed inpatient setting and then 8 weeks in an outpatient setting. Over the two phases they drank beverages sweetened with glucose (15 subjects) or fructose (17 subjects) comprising 25 per cent of their daily calorie intake.
During the 10 weeks in total of the study, participants in both groups put on about the same amount of weight, but only those in the fructose group showed an increase in belly fat.
Also, only the participants in the fructose group became less sensitive to insulin (the hormone that controls how much glucose is in the bloodstream), and developed higher levels of total and LDL or "bad" cholesterol.
The fructose group also showed higher levels of hepatic DNL (de novo lipogenesis, fat that is produced from excess digested carbohydrate) and other signs that their bodies were producing fat differently to the glucose group.
The researchers concluded that:
"These data suggest that dietary fructose specifically increases DNL, promotes dyslipidemia, decreases insulin sensitivity, and increases visceral adiposity in overweight/obese adults."
Monday, August 17, 2009
Omega-3 Polyunsaturated Fatty Acids and Cardiovascular Diseases -- Lavie et al. 54 (7): 585 -- Journal of the American College of Cardiology
Omega-3 Polyunsaturated Fatty Acids and Cardiovascular Diseases -- Lavie et al. 54 (7): 585 -- Journal of the American College of Cardiology:
"Omega-3 polyunsaturated fatty acid ({omega}-3 PUFA) therapy continues to show great promise in primary and, particularly in secondary prevention of cardiovascular (CV) diseases. The most compelling evidence for CV benefits of {omega}-3 PUFA comes from 4 controlled trials of nearly 40,000 participants randomized to receive eicosapentaenoic acid (EPA) with or without docosahexaenoic acid (DHA) in studies of patients in primary prevention, after myocardial infarction, and most recently, with heart failure (HF). We discuss the evidence from retrospective epidemiologic studies and from large randomized controlled trials showing the benefits of {omega}-3 PUFA, specifically EPA and DHA, in primary and secondary CV prevention and provide insight into potential mechanisms of these observed benefits. The target EPA DHA consumption should be at least 500 mg/day for individuals without underlying overt CV disease and at least 800 to 1,000 mg/day for individuals with known coronary heart disease and HF. Further studies are needed to determine optimal dosing and the relative ratio of DHA and EPA {omega}-3 PUFA that provides maximal cardioprotection in those at risk of CV disease as well in the treatment of atherosclerotic, arrhythmic, and primary myocardial disorders."
"Omega-3 polyunsaturated fatty acid ({omega}-3 PUFA) therapy continues to show great promise in primary and, particularly in secondary prevention of cardiovascular (CV) diseases. The most compelling evidence for CV benefits of {omega}-3 PUFA comes from 4 controlled trials of nearly 40,000 participants randomized to receive eicosapentaenoic acid (EPA) with or without docosahexaenoic acid (DHA) in studies of patients in primary prevention, after myocardial infarction, and most recently, with heart failure (HF). We discuss the evidence from retrospective epidemiologic studies and from large randomized controlled trials showing the benefits of {omega}-3 PUFA, specifically EPA and DHA, in primary and secondary CV prevention and provide insight into potential mechanisms of these observed benefits. The target EPA DHA consumption should be at least 500 mg/day for individuals without underlying overt CV disease and at least 800 to 1,000 mg/day for individuals with known coronary heart disease and HF. Further studies are needed to determine optimal dosing and the relative ratio of DHA and EPA {omega}-3 PUFA that provides maximal cardioprotection in those at risk of CV disease as well in the treatment of atherosclerotic, arrhythmic, and primary myocardial disorders."
Sunday, August 16, 2009
Low vitamin D levels linked to metabolic syndrome
Low vitamin D levels linked to metabolic syndrome
Increasing blood levels of vitamin D are linked to a lower prevalence of the metabolic syndrome, as well as improved ‘good’ cholesterol levels, says a new study.
According to findings published in the Journal of Clinical Lipidology, the lowest levels of the sunshine vitamin were associated with a 31 per cent prevalence of metabolic syndrome, compared to only 10 per cent for people wit the highest average levels.
The researchers noted that the results do not prove that low vitamin D levels contributes or causes metabolic syndrome, and called for more studies to “assess whether increasing vitamin D intake will improve the metabolic cardiovascular risk factor profile”.
“Although previous surveys have also reported associations between low 25(OH)D concentration and metabolic syndrome components, to our knowledge, the present investigation is the first to report this finding in a sample with a high prevalence of vitamin D dietary supplement users in which frequencies of vitamin D insufficiency and deficiency were low,” wrote the researchers, led by Kevin Maki from Illinois-based Provident Clinical Research
Metabolic syndrome (MetS) is a condition characterised by central obesity, hypertension, and disturbed glucose and insulin metabolism. The syndrome has been linked to increased risks of both type-2 diabetes and cardiovascular disease (CVD).
Increasing blood levels of vitamin D are linked to a lower prevalence of the metabolic syndrome, as well as improved ‘good’ cholesterol levels, says a new study.
According to findings published in the Journal of Clinical Lipidology, the lowest levels of the sunshine vitamin were associated with a 31 per cent prevalence of metabolic syndrome, compared to only 10 per cent for people wit the highest average levels.
The researchers noted that the results do not prove that low vitamin D levels contributes or causes metabolic syndrome, and called for more studies to “assess whether increasing vitamin D intake will improve the metabolic cardiovascular risk factor profile”.
“Although previous surveys have also reported associations between low 25(OH)D concentration and metabolic syndrome components, to our knowledge, the present investigation is the first to report this finding in a sample with a high prevalence of vitamin D dietary supplement users in which frequencies of vitamin D insufficiency and deficiency were low,” wrote the researchers, led by Kevin Maki from Illinois-based Provident Clinical Research
Metabolic syndrome (MetS) is a condition characterised by central obesity, hypertension, and disturbed glucose and insulin metabolism. The syndrome has been linked to increased risks of both type-2 diabetes and cardiovascular disease (CVD).
Canada examines vitamin D for swine flu protection
Canada examines vitamin D for swine flu protection:
The Public Health Agency of Canada (PHAC) has confirmed that it will be investigating the role of vitamin D in protection against swine flu, NutraIngredients-USA.com has learned.
The agency started a study last year on the role of vitamin D in severe seasonal influenza, which it said it will now adapt to the H1N1 swine flu virus.
Part of the researchers’ goal is to understand if vitamin D levels are in any way responsible for the fact that most people with seasonal influenza develop a mild illness but a small minority go on to develop severe symptoms.
According to PHAC, results from its study will indicate the extent and nature of the role of vitamin D in sever seasonal influenza. The agency said it would most likely take at least three influenza seasons to be able to recruit a sufficient sample size of individuals with severe disease and controls before the results can be “meaningfully” analyzed.
In addition, PHAC said that epidemiological evidence suggests a role for vitamin D in seasonal influenza in general.
“Influenza infection is correlated geographically and seasonally with levels of solar ultraviolet radiation (Cannell, 2006). Given that vitamin D is synthesisized in our skin on exposure to sunlight, low serum levels of 25(OH) vitamin D in winter months appear to correlate with the occurrence of seasonal influenza in the winter. However a direct causal relationship between low vitamin D levels and the risk of influenza remains to be proven.”
“How vitamin D might protect against influenza infection is not fully understood. However new research suggests that vitamin D induces the production of antimicrobial substances in the body that possess neutralizing activity against a variety of infectious agents including influenza virus (Doss, 2009).”
So, Vitamin D's attributes as the main substance to activate the body's immune system should make it protective against swine flu. Notice also that overweight people have had the highest death rates from swine flu, and also have lower Vit D levels. Low Vitamin D has been related to metabolic syndrome. This puts the lie to the whole "tanning beds are more dangerous than arsenic" garbage the WHO has been pushing lately. When fall comes, and I'm surrounded by sick teenagers, I'll be tanning without fear.
The Public Health Agency of Canada (PHAC) has confirmed that it will be investigating the role of vitamin D in protection against swine flu, NutraIngredients-USA.com has learned.
The agency started a study last year on the role of vitamin D in severe seasonal influenza, which it said it will now adapt to the H1N1 swine flu virus.
Part of the researchers’ goal is to understand if vitamin D levels are in any way responsible for the fact that most people with seasonal influenza develop a mild illness but a small minority go on to develop severe symptoms.
According to PHAC, results from its study will indicate the extent and nature of the role of vitamin D in sever seasonal influenza. The agency said it would most likely take at least three influenza seasons to be able to recruit a sufficient sample size of individuals with severe disease and controls before the results can be “meaningfully” analyzed.
In addition, PHAC said that epidemiological evidence suggests a role for vitamin D in seasonal influenza in general.
“Influenza infection is correlated geographically and seasonally with levels of solar ultraviolet radiation (Cannell, 2006). Given that vitamin D is synthesisized in our skin on exposure to sunlight, low serum levels of 25(OH) vitamin D in winter months appear to correlate with the occurrence of seasonal influenza in the winter. However a direct causal relationship between low vitamin D levels and the risk of influenza remains to be proven.”
“How vitamin D might protect against influenza infection is not fully understood. However new research suggests that vitamin D induces the production of antimicrobial substances in the body that possess neutralizing activity against a variety of infectious agents including influenza virus (Doss, 2009).”
So, Vitamin D's attributes as the main substance to activate the body's immune system should make it protective against swine flu. Notice also that overweight people have had the highest death rates from swine flu, and also have lower Vit D levels. Low Vitamin D has been related to metabolic syndrome. This puts the lie to the whole "tanning beds are more dangerous than arsenic" garbage the WHO has been pushing lately. When fall comes, and I'm surrounded by sick teenagers, I'll be tanning without fear.
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