Weight loss surgery is twice as effective as lifestyle changes at preventing type 2 diabetes in people who are obese, a new study found.
The Swedish study followed more than 3,400 obese men and women, roughly half of whom had bariatric surgery, for up to 15 years. It found that bariatric surgery reduced the risk of type 2 diabetes by 78 percent
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The idea that all saturated fat is a health evil permeates the defunct dogma of Western medicine and its Big Pharma toxic pill pushers. It has probably never occurred to them that saturated fat is perhaps the best calorie for energy production, and quite good for long lasting energy if you don’t consume too much. Two studies in the American Journal of Clinical Nutrition continue a long list of studies questioning the assertion that saturated fat causes disease, in and of itself.
The first study comes from researchers at the University of Texas School of Public Health. Researchers followed a multiethnic group of 5,209 adults, aged 45 – 84, for 10 years while tracking their diets, and looking into the diets of those who developed cardiovascular disease (316 cases) during the course of the study. They found that those with the highest intake of saturated fat from dairy had up to a 38 percent risk reduction for developing cardiovascular disease. This is a rather shocking finding for the promoters of skim milk and other no-fat dairy. On the other hand, the study found that those with the highest intake of saturated fat from meat had up to a 48 percent increased risk for cardiovascular disease. Furthermore, replacing two percent of meat calories with dairy fat lowered overall risk by 25 percent.
It is likely that many of the cofactor nutrients in dairy help to metabolize the saturated fat, helping to make it a cardio friendly food. In defense of meat fat, my opinion is that it is really an issue of how the beef was raised, and what it was fed. Many sickly and pathetically unhealthy animals have lived on toxic junk food their entire lives and had no exercise – of course their fat is not worth eating. There is no substitute for quality raised and fed meat, such as range raised and grass fed.
Furthermore, those who eat the most toxic meat are also likely to be eating other junk food and also lacking fiber, fruit, and vegetables. This is not rocket science.
In the second study Danish researchers evaluated 340,234 adults from eight European countries for their intake of dairy and risk of type 2 diabetes. This is a very large study representing four million human years of follow up. Researchers found that dairy intake, regardless of the amount of fat taken in, was not linked to the development of type 2 diabetes. To the contrary, certain types of dairy such as cheese and yogurt were linked to a 12 percent risk reduction.
Americans should keep in mind that the quality of dairy products is much higher in Europe. It is highly advised that Americans consume organic dairy and cheeses of higher quality.
The simple fact of the matter is that there is no need to fear saturated fat. If you consume high quality forms of saturated fat as a reasonable portion of your daily calories, along with omega-3 oils like DHA Docosahexaenoic acid Essential omega 3 fatty acid integral to the health of all cell membranes, nerve and brain function. Must be gotten through the diet via cold water oceanic fish or some very limited plant sources or taken as a supplement., fruit, vegetables, and adequate dietary fiber, then saturated fat is likely to be an energy sustaining friend, which actually helps your metabolism run better, and is not at all associated with risk for disease.
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Researchers examined nearly 350 black and white women in the Pittsburgh area who were between 42 to 52 years old at the start of the study. About 34 percent of the women said they had been victims of some form of childhood abuse.
Compared to other women in the study, which was published online in the journal Health Psychology, those with a history of childhood physical abuse were about twice as likely to have high blood pressure, high blood sugar, a larger waistline and poor cholesterol levels.
Collectively, these health issues are known as metabolic syndrome. Previous research suggests that people with metabolic syndrome are at increased risk for heart disease and type 2 diabetes.
The link between childhood physical abuse and metabolic syndrome was separate from traditional risk factors for the syndrome, such as smoking, lack of physical activity, menopause, alcohol use and depression. This persistent association suggests that abuse plays a unique role in women's cardiovascular health, the researchers said.
"Our research shows us that childhood abuse can have long-lasting consequences -- even decades later -- on women's health, and is related to more health problems down the road," study co-author Aimee Midei, a graduate student in psychology at the University of Pittsburgh, said in a journal news release.
"It's possible that women with histories of physical abuse engage in unhealthy eating behaviors or have poor stress regulation," Midei said. "It appears that psychology plays a role in physical health even when we're talking about traumatic incidents that happened when these women were children."
Although the study found an association between childhood physical abuse and an increased occurrence of metabolic syndrome later in life, it did not prove a cause-and-effect relationship. The study also found no association between childhood sexual and emotional abuse and metabolic syndrome.
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That was the case for Cynthia Zuber when she first went away to college. Although Zuber had type 1 diabetes, also known as insulin-dependent diabetes, she didn't know at the time that mixing an alcohol binge and insulin use might have deadly consequences.
Zuber was just 18 when she went to a fraternity party.
"It was a party of upperclassmen, and my friend and I, both freshmen, felt very young and out of place," she recalled. "To deal with the discomfort, I started drinking beer."
Throughout the evening, she said, she went back for refills on her own, and people also repeatedly brought her refills. "I had no idea how many beers I had," she said, nor did she know her blood sugar levels because she didn't test them during the party.
Alcohol can cause blood sugar levels to drop dangerously low for people on blood sugar-lowering medications for as long as 12 hours after their last drink, according to the American Diabetes Association.
"Things got out of control quickly, and when we went to leave I had to be carried to the car and into my dorm," she explained.
Zuber said she vomited throughout the night, probably from the beer, but she doesn't know for sure because she didn't test her blood sugar levels before going to bed, either. At some point during the night, she passed out, and when she woke in the morning, she was still vomiting.
When she tested her blood sugar, it was low enough that she knew she'd have to eat something or she would quickly be in serious trouble. The problem was, she couldn't keep food down. She even tried drinking water, but threw that up, too. Someone in her dorm drove her to the emergency department.
"I was so oblivious to the danger I'd put myself in," Zuber recalled. "The doctor, who was wearing Birkenstock sandals and an earring, actually slapped me across the face -- not hard, but to get my attention." The doctor then explained to her a number of ways that alcohol could cause serious problems, or even death, for someone with type 1 diabetes.
Zuber said she didn't give up drinking entirely after that incident, but did cut way back and never again drank enough to have to go to the hospital. Now 36, Zuber recently gave up alcohol entirely because, she said, she just feels better if she doesn't drink.
For anyone with diabetes, the American Diabetes Association recommends having a snack at the same time you're consuming an alcoholic beverage, and to not have more than one drink a day for women and two a day for men. But most important, the association says, is to check your blood sugar before going to sleep after drinking alcohol -- striving for a level between 100 and 140 milligrams per deciliter.
The latest research, published online July 2 by the American Heart Association's journal Circulation, found that people who consume fast food even once a week increase their risk of dying from coronary heart disease by 20 percent in comparison to people who avoid fast food. For people eating fast food two-three times each week, the risk increases by 50 percent, and the risk climbs to nearly 80 percent for people who consume fast food items four or more times each week.
Eating fast food two or more times a week was also found to increase the risk of developing Type 2 diabetes by 27 percent.
According to University of Minnesota researchers, the few existing studies on the association of fast food and metabolic risk have looked almost exclusively at Western-Caucasian populations from the United States.
"We wanted to examine the association of Western-style fast food with cardio-metabolic risk in a Chinese population in Southeast Asia that has become a hotbed for diabetes and heart disease," said the study's lead researcher, University of Minnesota post-doctoral researcher Andrew Odegaard, Ph.D., M.P.H. "What we found was a dramatic public health impact by fast food, a product that is primarily a Western import into a completely new market."
To arrive at their results, School of Public Health researchers worked alongside researchers from the National University of Singapore. Together, they examined results of a study conducted over a period of 16 years beginning in 1993, which looked at the eating habits of 52,000 Chinese residents of Singapore who have experienced a recent and sudden transition from traditional foods to Western-style fast food.
"What's interesting about the results is that study participants who reported eating fast food most frequently were younger, better educated, smoked less and were more likely to be physically active," said Odegaard. "This profile is normally associated with lower cardio-metabolic risk."
According to the study's senior researcher, Mark Pereira, Ph.D., M.P.H., of the School of Public Health's Division of Epidemiology and Community Health, the new research provides an important perspective on global health and the nutrition transfer when cultures developing in different parts of the world start moving away from their traditional diet and mode of exercise.
"The big picture is that this
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This is contrary to concerns that long-term use of insulin may cause heart disease, says Dr. Hertzel Gerstein, principal investigator of the study, professor of medicine at McMaster's Michael G. DeGroote School of Medicine and deputy director of the Population Health Research Institute at McMaster University and Hamilton Health Sciences.
"People have been debating the question of whether there are adverse consequences to long-term insulin use for years," he said. "This study provides the clearest answer yet to that question: No, there are not."
Gerstein recently presented the findings of the ORIGIN study (Outcome Reduction with an Initial Glargine Intervention study), at the scientific sessions of the American Diabetes Association in Philadelphia. The results were also recently published in two papers in the medical journal New England Journal of Medicine (NEJM).
A second important finding of the study is that people with pre-diabetes who received daily basal insulin injections with insulin glargine had a 28 per cent lower chance of developing type 2 diabetes, even after the injections stopped.
Gerstein jointly led the study with Dr. Salim Yusuf, professor of medicine and director of the Population Health Research Institute.
Today, more than nine million Canadians are living with diabetes or pre-diabetes. Diabetes is a chronic condition, often debilitating and sometimes fatal disease, in which the body either cannot produce insulin or cannot properly use the insulin it produces. This leads to high levels of glucose in the blood which can damage organs, blood vessels and nerves. The body needs insulin to use glucose as a source of energy.
In the ORIGIN study, more than 12,500 people at 537 sites in 40 countries with an average age of 64, who are at high risk for, or in the early stages of type 2 diabetes, were randomized to either one daily injection of insulin (glargine) or no insulin (standard care) for an average of six years.
Researchers found no difference among the two groups in cardiovascular outcomes or in the development of any type of cancer. This suggests daily insulin injections (with insulin glargine) to normalize glucose levels are not harmful when taken over long periods of time. Throughout the study, most of the participants given insulin maintained normal fasting glucose levels (below 6 mmol/l).
The study confirmed the presence of two previously known side effects of insulin -- hypoglycemia (low blood sugar) and modest weight gain. Both were considered minor from a medical point of view, with participants gaining an average of 3.5 pounds during the study and experiencing a low, 0.7 per cent higher risk of severe hypoglycemia per year than the people not on insulin.
"We now know what the risks are of taking insulin on a long-term basis, and they are low," Gerstein said.
The study also discovered that daily doses of one-gram omega-3 fatty acid capsules did not prevent cardiac-related deaths in people with type 2 diabetes or prediabetes.
"There was neither benefit nor harm in the participants who were studied," said Jackie Bosch, associate professor of McMaster's School of Rehabilitation Science and project manager for the trial. "However, the effect of these supplements in other groups, and the effect of a diet rich in omega 3 fatty acids was not studied."
The study was funded by the drug company Sanofi Inc. and the omega-3 supplement was provided by Pronova Biocare AS, the Norwegian manufacturer of omega-3, and independently conducted by the Population Health Research Institute at McMaster University and Hamilton Health Sciences.
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The key to the oil's potential lies in its ability to affect certain microorganisms living in our bellies.
In a study presented June 18 at the American Society for Microbiology's general meeting in San Francisco, Missouri S&T researchers reported that adding sterculic oil to the diets of obese laboratory mice increased their sensitivity to insulin. This was due to the oil's effect on three types of microorganisms that live in the guts of the mice.
As a result, the researchers saw a "statistically significant improvement in glucose tolerance and insulin sensitivity in the obese mice," says Shreya Ghosh, a Ph.D. student in environmental engineering at Missouri S&T. The sterculic oil had no adverse affects on lean mice fed the same diet.
Sterculic oil is extracted from the seeds of the wild almond tree known as Sterculia foetida.
The research by Ghosh and her advisor, Dr. Daniel Oerther, builds upon previous studies conducted at the University of Missouri-Columbia. In those studies, sterculic oil was found to suppress the bodily enzyme stearoyl-CoA desaturase 1 (SCD1). SCD1 is associated with insulin resistance, a condition that can lead to diabetes and obesity.
Other studies have shown that obese mice deficient in the hormone leptin have a different composition of "gut microbiota" than do lean mice. (Those studies are referenced in a 2011 article in Nature Reviews Microbiology) Leptin helps regulate metabolism, and a deficiency of the hormone can contribute to obesity, says Oerther, the John and Susan Mathes Chair of Environmental Engineering at Missouri S&T.
In the Missouri S&T study, a diet supplemented by sterculic oil also correlated with lower levels of three types of gut microbiota -- Actinobacteria, Bacilli and Erysipelotrichia -- in the obese mice. It isn't clear, however, whether the lower levels of those microbiota led to the improvement of glucose tolerance and insulin sensitivity among the obese mice, Oerther says.
To perform her experiments, Ghosh studied 28 male mice -- 14 of them obese and 14 normal, and each of them five weeks old at the beginning of the study. She separated the mice into four groups and for nine weeks, fed a standard diet to one group of obese mice and one group of non-obese mice. Over the same period, she fed the same diet, supplemented with 0.5 percent of sterculic oil, to one group of obese mice and one group of non-obese mice. Ghosh recorded the weights, food consumption and glucose levels of the mice during the nine-week period.
After the nine weeks, researchers conducted a DNA analysis of the gut microbiota at King Abdullah Institute of Science and Technology in Saudi Arabia. The results confirmed correlations between the diet, improved glucose tolerance and groups of microbes. Even though the mice fed a diet with sterculic oil did not experience weight loss, both Ghosh and Oerther believe their findings could lead to new insights into controlling diabetes and weight gain.
Ghosh's research poster presentation at the ASM meeting is titled "Responses of Gut Microbiota to Sterculic Oil Supplemented Diet in Lean and Obese Mice." Her co-authors were Oerther; Dr. James W. Perfield II, assistant professor of food science at the University of Missouri-Columbia; and Dr. Pascal Saikaly, assistant professor of environmental science and engineering at King Abdullah University of Science and Technology in Saudi Arabia.
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The study, which will be presented at the American Chemical Society in Philadelphia next August, showed that the compounds in stone fruits could be a weapon against "metabolic syndrome," in which obesity and inflammation lead to serious health issues, according to Dr. Luis Cisneros-Zevallos, AgriLife Research food scientist.
"In recent years obesity has become a major concern in society due to the health problems associated to it," said Cisneros-Zevallos, who also is an associate professor at Texas A&M University. "In the U.S., statistics show that around 30 percent of the population is overweight or obese, and these cases are increasing every year in alarming numbers."
While he acknowledged that lifestyle, genetic predisposition and diet play a major role in one's tendency toward obesity, "the major concern about obesity is the associated disease known as metabolic syndrome.
"Our studies have shown that stone fruits -- peaches, plums and nectarines -- have bioactive compounds that can potentially fight the syndrome," Cisneros-Zevallos said. "Our work indicates that phenolic compounds present in these fruits have anti-obesity, anti-inflammatory and anti-diabetic properties in different cell lines and may also reduce the oxidation of bad cholesterol LDL which is associated to cardiovascular disease."
What is unique to these fruits, he said, is that their mixture of the bioactive compounds work simultaneously within the different components of the disease.
"Our work shows that the four major phenolic groups -- anthocyanins, clorogenic acids, quercetin derivatives and catechins -- work on different cells -- fat cells, macrophages and vascular endothelial cells," he explained. "They modulate different expressions of genes and proteins depending on the type of compound.
"However, at the same time, all of them are working simultaneously in different fronts against the components of the disease, including obesity, inflammation, diabetes and cardiovascular disease," he explained.
Cisneros-Zevallos said this is believed to be the first time that "bioactive compounds of a fruit have been shown to potentially work in different fronts against a disease."
"Each of these stone fruits contain similar phenolic groups but in differing proportions so all of them are a good source of health promoting compounds and may complement each other," he said, adding that his team plans to continue studying the role of each type of compound on the molecular mechanisms and confirm the work with mice studies.
The studies on the health benefits of stone fruit are funded by the California Tree Fruit Agreement, The California Plum Board, the California Grape and Tree Fruit League and the Texas Department of Agriculture. The Cisneros-Zevallos lab team in this study included Freddy Ibanez, Paula Castillo, Paula Simons and Dr. Congmei Cao.
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Researchers followed more than 3,000 people without dementia, average age 74, for more than 10 years.
At the start of the study, 23 percent of the participants had diabetes. Of the more than 2,300 participants without diabetes, 159 developed the condition during the follow-up period.
People with diabetes at the start of the study scored lower on initial tests of their thinking skills than those without diabetes. During the follow-up, participants with diabetes showed much greater declines in mental function than those without diabetes.
The study was published online June 18 in the journal Archives of Neurology.
The findings support the theory that older adults with diabetes have reduced thinking and memory skills and that poor blood sugar control may be a contributing factor, said Dr. Kristine Yaffe, of the University of California, San Francisco, and the San Francisco VA Medical Center, and colleagues in a journal news release.
The investigators said further research is needed to determine if early diagnosis and treatment of diabetes reduces the risk of mental decline and if good blood sugar control helps reduce the effect of diabetes on thinking and memory function.
While the study found an association between diabetes and mental decline, it did not show a cause-and-effect relationship.
More information
The U.S. National Institute on Aging has more about diabetes in older people.
Researchers, whose findings were published in the Journal of Clinical Oncology, found that women with diabetes who took the medication had a 25 percent lower risk of developing breast cancer over more than a decade of follow-up.
"Metformin use in postmenopausal women with diabetes was associated with lower incidence of invasive breast cancer," wrote lead researcher Rowan Chlebowski, at the Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center.
"These results can inform future studies evaluating metformin use in breast cancer management and prevention."
Metformin, also sold under the brand name Glucophage, has been on the market for many years and is generally considered safe, although five to 10 percent of patients experience side effects like nausea and bloating.
It is used by millions of type 2 diabetics every day to help control their blood sugar, and studies have shown it also shrinks lung and breast tumors in mice. Several reports show people taking it for diabetes appear to develop cancer less often.
The new study used data from about 68,000 postmenopausal women who took part in the U.S. government-funded Women's Health Initiative clinical trials.
Over nearly 12 years of observation, there were more than 3,200 new cases of breast cancer among the women.
Every year, 0.42 percent of women without diabetes developed breast cancer, compared to 0.40 percent of diabetics on metformin and 0.47 percent of diabetics taking other drugs.
After taking into account risk factors for breast cancer, the gap between women without diabetes and diabetics on drugs other than metformin vanished. But diabetics on metformin turned out to have a 25 percent lower cancer risk than their diabetes-free peers.
"This is an area of great excitement," said Pamela Goodwin, a breast cancer expert at Mount Sinai Hospital in Toronto, Canada, who wrote an editorial that appeared with the study.
"The evidence is coming together that metformin may actually have a clinically-relevant effect, but none of this is good enough to chance clinical practice just yet."
But she added that while the study is the best of its kind so far, it relies on observations instead of an actual experiment in which women are randomly selected to take metformin or not.
Goodwin and her colleagues are currently running a trial to test whether metformin can help ward off new tumors in women getting breast cancer treatment. Results are expected in three to four years. SOURCE: http://bit.ly/L86p7l
(Reporting from New York by Frederik Joelving at Reuters Health; editing by Elaine Lies and Bob Tourtellotte)
With Type 2 human diabetes climbing at alarming rates in the United States, researchers are seeking treatments for the disease, which has been linked to obesity and poor diet.
Now biologists at Southern Methodist University, Dallas, report they have developed a new tool that will help researchers better understand this deadly disease.
By manipulating the diets of healthy adult fruit flies, the researchers developed flies that are insulin-resistant, a hallmark of Type 2 diabetes.
Until now, researchers largely have relied on rats, mice and other animals as model systems for exploring the metabolic and genetic changes that take place in diabetics.
The fruit fly Drosophila melanogaster has been widely deployed in labs to investigate a wide range of human diseases, from Alzheimer's to cancer. But the scientific literature hasn't documented use of the adult fruit fly for studying the metabolic disruptions that are the hallmark of Type 2 diabetes. The fruit fly's advantages include its low cost and a very short lifespan, both of which enable scientists to undertake rapid screenings in their search for new genetic and drug treatments.
The insulin-resistant fruit fly was developed in the lab of SMU biologist Johannes H. Bauer, principal investigator for the study. It was accomplished by feeding fruit flies a diet high in nutrients, said Bauer, an assistant professor in SMU's Department of Biological Sciences. That process mimics one of the ways insulin resistance develops in humans -- overeating to the point of obesity.
The lab's insulin-resistant fruit flies now can serve as a highly relevant and efficient model for studying Type 2 diabetes.
"We learned that by manipulating the nutrients of fruit flies, we can make them insulin resistant," Bauer said. "With this insulin-resistant model we can now go in with pinpoint precision and study the molecular mechanisms of insulin resistance, as well as drug treatments for the condition, as well as how to treat obesity, how to block insulin resistance and how metabolic changes from a specific diet develop. The possibilities are endless."
The researchers reported their findings in the article "Development of diet-induced insulin resistance in adult Drosophila melanogaster," published in Biochimica et Biophysica Acta -- Molecular Basis of Disease.
Two overfeeding diets, carb and protein, both result in insulin resistance
Insulin, produced by the pancreas, is the hormone that tells our cells to absorb glucose, a necessary sugar molecule that provides our body, particularly the brain, with the energy to function, make repairs, move and grow.
In Type 2 diabetes, a person is insulin-resistant because his or her cells fail to respond to insulin's signal to absorb glucose. The disregulation of glucose upsets the body's delicate internal equilibrium, causing massive disruptions in normal cellular processes. These interruptions manifest in multiple disease symptoms, making Type 2 diabetes difficult to characterize, treat and cure.
To provide a good base model organism to study aspects of this complex disease, researchers in the Bauer lab wanted to determine whether flies develop diabetes-like metabolic changes when fed different diets. The researchers developed the insulin-resistant flies in two different ways: One group of fruit flies was overfed a carbohydrate-loaded diet; a second group of flies was overfed a protein-loaded diet. In both cases, the disruption had a profoundly detrimental effect on the flies' health and physiology.
SMU biologist Siti Nur Sarah Morris, lead author on the study, said the results the researchers observed were both expected and unexpected. The researchers expected the flies to gain weight, which they did. Carb-loaded flies gained excessive weight and got fat, just like humans who overeat sweets, french fries, pasta and ice cream. Protein-loaded flies also gained weight, but upon extreme overfeeding they lost weight, just like humans who follow the popular Atkins Diet, a weight loss program in which participants eat only meat, seafood and eggs.
The researchers expected the carb-loaded fruit flies to develop insulin resistance, which they did.
In a surprising result, however, the fruit flies that overate protein also developed insulin resistance, but at a quicker and more severe rate.
"Carb-loaded flies gain weight. Protein-loaded flies gain and then lose weight. So the two diets have exactly opposite effects on metabolism," Bauer said. "But too much of either one of them causes insulin resistance. That surprised us."
Overfed flies had shortened lifespans, differences in fertility
In other findings, carb-loaded flies experienced a profound decline in egg-laying, a measurement of fertility. In contrast, protein-loaded flies first experienced increased egg-laying, but the extreme diet led to decreased egg laying. Both diets led to shortened longevity, the scientists reported.
"The high-protein flies looked frail and unhealthy. They moved less, almost as if sedated," Morris said. "The fatter flies on the high-carb diet had massively decreased fertility; they flew less but still tried to move."
While both diets resulted in insulin resistance, differences were remarkable.
"The carb data imply a linear relationship between carb levels and health. The more carbs, the more weight, the more sugar storage and fat, the more insulin resistance and the less fertility," Bauer said. "But with protein, this relationship becomes parabolic, meaning all readouts go up, then come down again. The decreased storage we liken to a catabolic state that is primarily destructive for the body's optimum metabolic functioning, such as the ketosis typically seen in people eating Atkins-type diets."
Besides Morris and Bauer, other authors on the study were SMU students Claire Coogan, Khalil Chamseddin and Santharam Kolli. Other co-authors, from Pennington Biomedical Research Center, Baton Rouge, La., are Jeffrey N. Keller, director, Institute of Dementia Research & Prevention, and Sun Ok Fernandez-Kim. The research was funded by the National Institute on Aging.
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The phrase “death by snacking” is not too far from the truth, especially if a person is overweight and struggles to lose weight. Two new studies confirm the dangers of snacking, something I have been adamant about since the release of Mastering Leptin in 2002.
Both studies appeared recently in the American Journal of Clinical Nutrition. The first followed 29,206 U.S. men who were free of metabolic disease for 16 years. It found that skipping breakfast was associated with a 21 percent increased risk for developing type 2 diabetes, which is why the Leptin Diet tells you to start your metabolic engines with a high protein breakfast. This study also confirmed the relationship between a high BMI Body Mass Index. BMI is a statistical measurement of body weight based on the person's height and weight. It does not actually measure the body fat percentage but provides an estimation of a healthy body weight. Normal BMI for adults ranges from 18.5-24.9, snacking, and the risk for type 2 diabetes.
Another controlled human study found that snacking caused a loss of the ability to sense fullness, resulting in consumption of larger and larger snacks. Snacking appears to induce a repetitive strain injury to your taste and pleasure system, making them numb to normal intake.
The more food you eat, the fatter you are likely to become, which is news to nobody. Figuring out how to feel satisfied on less food is the trick. This is why following the Five Rules of the Leptin Diet is so important.
When you do not have leptin working to your advantage then leptin entry into your brain is decreased while leptin levels in your blood elevate, a problem known as leptin resistance. In addition to leptin, the other important hormone made by your fat is adiponectin Protein hormone that modulates metabolism including glucose and fatty acid catabolism. High levels are associated with low body fat. . Both of these hormones are made in tandem when you are metabolically healthy. Once you develop leptin resistance, then your adiponectin Protein hormone that modulates metabolism including glucose and fatty acid catabolism. High levels are associated with low body fat. levels decline. This causes insulin resistance and increased risk for type 2 diabetes.
It is just as important when you eat as what you eat. It isn’t just an issue of how many calories you consume; it is also an issue of how efficiently you can metabolize the calories you do consume. Eating in harmony with leptin is by far the best way to improve metabolic efficiency.
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Talrige undersøgelser samt direkte observation fortælle os, at en person, der spiser hurtig sandsynligvis vil være fedt. En ny undersøgelse udvider denne bemærkning til den øgede risiko for type 2 diabetes. Undersøgelsen fandt, de hurtigste spise 2 1/2 gange mere sandsynligt at udvikle type 2 diabetes.
En sund person tager det 10 minutter for et passende beløb af fødevarer til at oprette et fuld signal i din hjerne. Du kan spise en masse ekstra fødevarer i 10 minutter. Når du begynder at vinde vægt fuld signal systemet i din hjerne yderligere uanvendeligt, hvilket betyder, at du sandsynligvis at spise alt i syne så hurtigt, som du kan.
Vi kan nu sige, at dette er en fast track at blive type 2 diabetic. Langsommere, har nogle samtale. Hvis du er overvægtige og har tendens til at være en hurtig Æderen, tage en 10 minutters pause fra spise når du er halvdelen gjort med en normal størrelse måltid. Give signalet vaklende fuld en fighting chance!
Det tager store viljestyrke at stoppe spise efter du har forbrugt en normale antal kalorier (generelt 400-600 kalorier pr. måltid afhængigt af dine aktiviteter). Hvis du vil vide, hvordan nutty signalet fuld er blevet, skubbe væk fra tabellen efter en normal del og gå gøre noget andet. Vær opmærksom på hvor lang tid det tager for signalet fuld at vise.
Være glad, hvis det viser inden for 10 minutter som middel til at løse dit defekt fuld signal er blot et spørgsmål om sinker. Mange overvægtige mennesker, det er 20 minutter og én time – kan folk spise en masse af fødevarer de ikke behøver på denne tid.
Som du få i bedre harmoni med leptin, øge din hjerne plasticitet med næringsstoffer og øvelse dit normale fuld signal kan få tilbage på sporet. Det kan tage tid for din hjerne at få sorteret. I mellemtiden kan viljestyrke være forskellen mellem succes og fiasko. Blot forståelse at signalet fuld er i en funk har tendens til at hjælpe; du forstår mindst del af arten af den tiger, du forsøger at tæmme. Spise langsommere er et nyttigt skridt i den rigtige retning.
Andel:Vanedannende art Compulsive spise
Spiser du, hvad du ved du bør spise?
Fødevarer afhængighed og Stress spise mekanisme, der identificeres
Spiser du leve eller spise to Die?
Andre vægt tab nyheder
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Patrick Tso, PhD, professor in the UC Department of Pathology and Laboratory Medicine, has published research on the ability of apoA-IV to reduce blood sugar levels and enhance insulin secretion.
The results appear the week of May 21, 2012, in the online early edition of Proceedings of the National Academy of Sciences.
ApoA-IV is secreted by the small intestine in response to fat absorption. Previous studies have shown apoA-IV to be elevated in humans following gastric bypass -- coinciding with improvement in symptoms for diabetes.
The Tso team found that mice deficient in apoA-IV had impaired glucose tolerance (insulin was not secreted to move glucose from the blood stream). These mice also developed diabetes when continuously fed a high-fat diet. When injected with apoA-IV, these same mice showed improved insulin response to glucose, despite a diet high in fat.
Tso's team also tested the response to injected apoA-IV in diabetic mice and found it reduced glucose levels among that group as well.
Tso says their research shows apoA-IV to behave similar to an incretin -- a gastrointestinal hormone causing an increased release of insulin after eating to combat the onset of elevated blood glucose. Two well-known incretins that have been used in the development of existing diabetes medications include gastric inhibitory peptide (GIP) and glucagon-like peptide-1 (GLP-1).
"The problem with both of these incretins is that they are short-lived -- lasting only for minutes -- and are quickly inactivated by an enzyme," says Tso. "They have also been linked to hypoglycemia, or low blood sugar, when administered when the body has a low glucose concentration. The challenge is to find something safer with a longer half-life."
Tso says apoA-IV has a long half-life (between seven and eight hours) and that tests in his lab showed it to have no effect on glucose levels when administered at low glucose concentrations. Instead, he says, it seems to function to normalize glucose.
The University of Cincinnati has licensed this research finding to a startup biotech company, Apofore Corporation, formed by HealthCare Ventures of Cambridge, Mass. Apofore will further study apoA-IV in humans in an effort to develop a novel diabetes therapeutic.
Tso's research was supported by grants from the National Institute of Diabetes and Digestive and Kidney Diseases of the National Institutes of Health.
Co-authors include Sean Davidson, PhD, Tammy Kindel, Alison Kohan, Silvana Obici, PhD, Fei Wang and Stephen Woods, PhD, all from the University of Cincinnati; and Kathryn Corbin and Craig Nunemaker of the University of Virginia, Charlottesville.
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A better understanding of the body's response to indulgent eating could lead to new approaches for treating diabetes and metabolic syndrome. High-fat foods can contribute to obesity, which increases the risk for developing type 2 diabetes.
The researchers learned a key protein called Bcl10 is needed for the free fatty acids -- which are found in high fat food and stored in body fat -- to impair insulin action and lead to abnormally high blood sugar.
In the laboratory study, mice deficient in Bcl10 were protected from developing insulin resistance when fed a high-fat diet. The findings will be published May 31 in Cell Reports.
Insulin helps control blood sugar, but insulin resistance can lead to the abnormally high blood sugar levels that are the hallmark of diabetes. Insulin resistance can occur as part of metabolic syndrome, a cluster of conditions that increase the risk for type 2 diabetes and heart disease.
As millions of Americans become overweight and obese, type 2 diabetes and metabolic syndrome are on the rise.
"The study also underscores how very short-term changes in diet such as high-fat eating for only a few days, perhaps even less, can induce a state of insulin resistance," says senior study author Peter C. Lucas, M.D., Ph.D., associate professor of pathology at the University of Michigan Medical School.
Researchers began by investigating how free fatty acids induce inflammation and impair insulin action in the liver. It's thought the liver is a major target for the harmful effects of free fatty acids.
In the liver, free fatty acids undergo metabolism to produce diacylglycerols prior to inducing the inflammatory response. Diacylglycerols also activate NF-B signaling which has been linked with cancer, metabolic and vascular diseases.
The team of researchers concluded that Bcl10 is required for fatty acids to induce inflammation and insulin resistance. In the study, Bcl10-deficient mice showed significant improvement in regulation of blood sugar.
"We were surprised to learn that Bcl10, a protein previously known for its critical role in immune cell response to infection, also plays a critical role in the liver's response to fatty acid," says Lucas.. "This is an example of nature co-opting a mechanism fundamental to the immune system and using it in a metabolic organ, in this case, the liver."
"These findings reveal a new and important role for Bcl10 and could lead to novel ideas for treating patients with metabolic syndrome and type 2 diabetes," says co-senior author Linda M. McAllister-Lucas, M.D., Ph.D., associate professor of pediatric hemotology/oncology.
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A team led by Dr. Tony Lam and Dr. Danna Breen, a post- doctoral fellow in the lab of Dr. Lam, used a rat model to study novel nutrient-sensing signals in the jejunum, located in the middle of the intestine. Dr. Lam and his team demonstrate that duodenal-jejunal bypass surgery activates novel nutrient-sensing signals in the jejunum and rapidly lowers blood sugar levels in non-obese rats with uncontrolled diabetes. DJB surgery is a type of bariatric surgery which excludes the duodenum and proximal jejunum, the first section of the small intestine, and instead redirects food into the distal jejunum, the middle to last section of the intestine. This latter section of the intestine, as demonstrated by Dr. Lam and his team, can sense glucose and signal to the brain to let the liver know that it must lower glucose production, leading to better control of blood sugar in the diabetic rats.
The study showed for the first time that a surgical intervention induces a rapid glucose-lowering effect in non-obese type 1 uncontrolled diabetic rats, independent of a reduction in food intake and body weight as well as changes in blood insulin levels.
The research was published in a paper entitled, "Jejunal nutrient sensing is required for duodenal-proximal jejunal bypass surgery to lower glucose levels in uncontrolled diabetes," in the May 20, 2012 on-line edition of the international journal Nature Medicine.
"We report that shortly after a meal, the influx of nutrients into the jejunum of DJB surgical diabetic rats activates novel sensing mechanisms to lower blood sugar levels. Importantly, this occurs in the presence of insulin-deficiency and is independent of weight loss," says Dr. Lam, who holds The John Kitson McIvor (1915 -- 1942) Endowed Chair in Diabetes Research and the Canada Research Chair in Obesity at the Toronto General Research Institute and the University of Toronto. He is also Associate Director of Research at the Banting and Best Diabetes Centre at the University of Toronto.
Currently, patients with Type 1 diabetes lower their glucose through insulin injections (usually several times a day) and must regularly monitor blood glucose levels. High or uncontrolled glucose levels can result in damage to eyes, nerves and kidneys and increase the risk of heart attack, stroke, blindness, erectile dysfunction, foot problems and amputations. Many laboratories around the world are in a race to find alternative and effective ways in which to lower and better control glucose levels because of the severe complications which can result from high sugar levels.
Dr. Lam's laboratory is a world pioneer in exploring the role of the gut in regulating blood sugar. "The gut is an easier and therefore more promising therapeutic target in regulating blood sugar than the brain or liver, due to their potential side effects, " says Dr. Danna Breen, who is the lead author in the study. Dr. Breen adds that this type of surgery may potentially have therapeutic value in lowering glucose (sugar) levels in non-obese individuals with type 2 or 1 diabetes, but that many more years of future studies are required to determine whether this approach is effective and safe in humans who have diabetes.
In healthy individuals, insulin is a hormone whose primary role is to regulate blood sugar. It is produced by cells located on the pancreas in response to sugar intake, and it acts to bring blood sugar to appropriate levels, allowing the body to have the energy it needs to function properly. In persons with type 1 diabetes, the pancreas does not produce insulin, resulting in elevated blood sugar levels due to lack of insulin which cannot signal to the liver to reduce sugar production. People with type 1 diabetes need to take daily insulin shots and carefully monitor their blood sugar levels.
"If new medicines or surgical interventions can be developed that stimulate this sensing mechanism in the gut, we may have an effective and alternative way of slowing down the body's production of sugar, thereby lowering blood sugar levels in diabetes," says Dr. Lam, who is also an Associate Professor of Medicine and Physiology at the University of Toronto. Other ongoing studies of Dr. Lam's lab reveal novel molecular targets in the gut that effectively lower blood sugar in obesity and type 2 diabetes.
Studies reported in the New England Journal of Medicine this year have challenged medical therapy as the prevailing method of treating patients with type 2 diabetes. Two studies reported that bariatric surgery induced remission in severely obese patients with type 2 diabetes, and was associated with significant improvement in metabolic control over and above medical therapy, both conventional and intensive. An accompanying April 26, 2012 editorial by Drs. Zimmet and Alberti, states that "surgeons may now be able to claim greater success in achieving metabolic control," in these patients, although long-term studies with greater numbers of patients still need to be completed. No studies have yet reported on surgical interventions as treatments for patients with type 1 diabetes.
"More than two million Canadians have diabetes. Diabetes is an epidemic in Canada and around the world that is growing at an alarming rate," says Dr. Philip M. Sherman, Scientific Director of the Institute of Nutrition, Metabolism and Diabetes at the Canadian Institutes of Health Research. "Since many people are undergoing bariatric surgery in an attempt to manage morbid obesity and the associated health problems, such as diabetes, it is critical that we understand how it works. The Canadian Institutes of Health Research is pleased to support Dr. Lam's work which increases our understanding and may offer a new approach to managing morbidity and premature mortality resulting from this illness."
Working with rats, Drs. Lam, Breen and colleagues designed and performed a series of elegant experiments on two different groups of rats: rats whose insulin-producing pancreatic islet cells were destroyed by toxins; and genetically-altered rats which experienced spontaneous autoimmune destruction of islet cells -- similar to what happens in humans with type 1 diabetes.
Non-obese rats induced with uncontrolled diabetes or autoimmune type 1 diabetes had an experimental DJB surgery, a variation of the Roux-en-Y gastric bypass, the most common surgical method currently used to treat obese patients. Two days after DJB surgery, blood sugars were normal in the insulin-deficient diabetic rats.
Dr. Breen emphasized that further studies need to be undertaken to determine the long-term effects of this intervention in rodents, as well as to ensure the safety and efficacy of this procedure in humans.
Other researchers involved in the study include Brittany A. Rasmussen, Andrea Kokorovic and Grace W.C. Cheung from the Toronto General Research Institute and the Department of Physiology, University of Toronto; and Dr. Rennian Wang, from the Departments of Physiology and Pharmacology, University of Western Ontario.
The work was funded by the Canadian Institutes of Health Research, as well as a fellowship from the University Health Network and the Banting and Best Diabetes Centre, University of Toronto.
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