Obesity-Cancer Link Explained By 'Gut Bug' Changes, New …

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Changes in the gut microbiome could help explain why obese mice are more likely to develop liver tumors (inset).
Credit: Eiji Hara/Japanese Foundation for Cancer Research

A long-standing question in medical science has been explaining the obesity-cancer link in humans; previous studies have shown that obesity increases the risk for many illnesses such as diabetes and cancer. But the exact biological mechanism that underlies this link has been elusive.

But now, a new study of mice microbiomes (the communities of trillions of microbes that live in the digestive tract) has revealed a DNA-damaging acid that seems to be the key molecule linking excess weight to cancer.

Researchers at the Cancer Institute at the Japanese Foundation for Cancer Research in Tokyo discovered that obesity in mice alters their microbiota — their intestinal “bug” population — which in turn leads to the unregulated production of an acid molecule called deoxycholic that can cause damage to a cells DNA and eventually cancer (e.g., liver cancer).

To uncover the elusive link, the team — led by Eiji Hara — studied two groups of mice: one lean group that was fed a normal diet, and a second group fed a fat-heavy diet (making them obese). To induce cancer in the mice (which normally don’t get much cancer) they exposed both groups to a cancer causing chemical shortly after birth.

Results of these experiments revealed the identical obesity-cancer link noted in humans: only 5% of the mice in the lean group developed cancer later in life, whereas all the obese mice did. But this result does not mean that diet itself is the primary trigger; when the team reproduced the experiment with mice that were genetically altered to become obese (though fed a normal diet), they found that these mice had an increased incidence of cancer. This seems a clear indication that it is obesity, rather than diet, that made the difference.

Pinning Down the Causal Mechanisms

The researchers found that the obese mice were more prone to live cancer and analysis of their tumors showed increased levels of key signaling molecules called pro-inflammatory cytokines which, as the name suggests, promote inflammation (note: Inflammation has been strongly correlated with tumorogenesis in many studies, but whether it is the cause, or effect, of cancer is still debated).

The team also observed that the obese mice had higher levels of deoxycholic acid (DCA), which is a cellular by-product that results when gut microbes break down bile acid (which is manufactured in the liver). The DCA has been shown previously to damage DNA and is associated with some human cancers.

With the confirmation of these two indicators (the elevated DCA and cytokine levels), the researchers next analyzed the mice intestinal tracts. Intriguingly, they observed that the obese mice were host to a different mixture of gut bugs. Specifically, they found that a type of bacteria known as gram-positive bacteria (which have a single, thick cell wall) were far more prevalent in the fatter mice.

When the team treated the obese mice with an antibiotic (vancomycin) that targets gram-positive bacteria, the result was reduced levels of DCA and a reduced incidence of cancer. Further, when they directly targeted the DCA — by slowing bile acid breakdown or stimulating more bile acid secretion into the gut — they again found a reduced incidence of cancer (and giving them increased doses of DCA brought the cancer risk back up).

“I was very surprised by the process,” Hara says. “We never expected that changes in the gut microbiota could cause the higher risk of cancer.” [source]

The gut microbiota has been the focus of intense research just in the past two years and researchers have noted many links between the composition and activity of our microbiomes and various diseases (such as inflammatory bowel disease, certain allergies, and heart disease).

These recent findings by Hara et al lend additional support to the once controversial ‘germ theory” of cancer causation: that bacteria can be primary contributors to the development of cancer (note: the helicobacter pylori bacterium was  shown to cause stomach cancer nearly a decade ago). These results may help doctors better predict — and even prevent — the disease.

However, more research is needed to demonstrate that the same mechanisms are at work in humans, who possess different cellular “micro-environments” than mice.

Results of the experiments were reported on-line June 26, 2013, in the journal in Nature.

Some source material for this post cam from the Science NOW article:‘Gut Bugs Could Explain Obesity-Cancer Link’ by Gisela Telis

 

 

Michael Ricciardi (362 Posts)

Michael Ricciardi is a well-published writer of science/nature/technology articles and essays, poetry and short fiction. Michael has interviewed dozen of scientists from many scientific fields, including Brain Greene, Paul Steinhardt, and Nobel Laureate Ilya Progogine (deceased).
Michael was trained as a naturalist and taught ecology and natural science on Cape Cod, Mass. from 1986-1991. His first arts grant was for production of the environmental (video) documentary ‘The Jones River – A Natural History’, 1987-88 (Kingston, Mass.).
Michael is also an award winning, internationally screened video artist. Two of his more recent short videos; ‘A Time of Water Bountiful’ and ‘My Name is HAM’ (an “imagined memoir” about the first chimp in space), and several other short videos, can be viewed on his website (http://www.chaosmosis.net).
Michael currently lives in Seattle, Washington.

Obesity is Now a Disease | Care2 Healthy Living

We, as Americans, are fat. That doesn’t mean that we are all fat; it just means that nearly 1/3 of Americans are obese and for this we pay out $147 billion annually in medical expenditures related to obesity. If this strikes you as shocking, well, this is not something that has happened overnight. Some say we have been moving toward this cataclysm of an epidemic for decades now. Some blame the fast food industry. Some blame the pervasive culture of desire and greed. Some blame the individual for just eating way too much. Blame aside, obesity is, and remains, a huge problem in this country and seems to be doing anything but going away.

As of last week, the American Medical Association (AMA) officially recognized obesity as a disease, which is a term that is made in effort to change the way the medical establishment wrestles with issues related to obesity. The labeling of obesity as a “disease” might not immediately change how doctors treat patients directly, but it will most certainly change the way obesity-related conditions are covered by insurance.

As it stands now, doctors are not readily encouraged to have the, sometimes, difficult conversations with patients about things like diet, exercise, and lifestyle decisions, not because they are awkward and difficult, but because such conversations are not reimbursed. So if the doctors don’t get paid, there is no incentive to alert a patient to their declining health. Instead doctors are driven toward conversations about procedures, rather than prevention. In the case of obesity, which is connected to everything from heart disease to diabetes, this is tragic.

Now that obesity is labeled as a disease, the hope is that there will be more of these diet and exercise conversations taking place (and paid for by insurance companies). But beyond the economics of the disease, it is hard to know how much this label will actually change. Could there be repercussions, such as more drugs created and unnecessarily prescribed? Will this label lead to more stigma? Also, by labeling obesity as a disease, will this take the focus off the food system, which markets cheap, substandard, nutritionally vacant foodstuffs to the masses at the expense of nearly everyone? Time will tell.

What do you think of this decision? Weigh in below.

Related:
Obesity Causes and Solutions

American Medical Association: Call Obesity a Disease

If insurers pay for gastric bypass surgeries and we “cure”
obesity,

There’s a rather compelling argument that the most effective
part of gastric bypass is the low carb diet they have to follow
afterward. Even after “returning to normal eating,” they recommend
avoiding popcorn, dried fruit, sodas, granola, corn and bread.

Multitasking against obesity | Harvard Gazette

Five specialists in obesity came together at Cambridge’s Royal Sonesta Hotel on Friday for a forum called “Why Is Weight Loss So Hard?” The event was part of the four-day Blackburn Course in Obesity Medicine, sponsored by Harvard Medical School (HMS) and Massachusetts General Hospital (MGH), during which experts from across the globe gathered to discuss one of America’s fastest-growing and most important health issues — the country’s increasing levels of obesity.

Complex causes

The panelists agreed on the complexity and interacting issues that underlie the crisis. Genetics and environment are just two of the many factors involved.

“The world is getting heavier,” said moderator-panelist Lee M. Kaplan, an associate professor at HMS and director of the MGH Weight Center, “and this is not a personal problem of slovenliness or laziness by the patient.”

Nadia Ahmad, former HMS instructor of medicine, now director of the Dubai Obesity Medicine Center, agreed: “There’s a lot of research to show obesity is actually a biological problem,” she said.

The causes and consequences of obesity are different in every case, Kaplan said. “Obesity isn’t the same disease in everybody. Our bodies have 20,000 genes and 4,000 are involved in weight regulation.”

W. Scott Butsch, an instructor of medicine at HMS and a doctor at MGH, and Caroline Apovian, an associate professor of medicine and pediatrics at Boston University School of Medicine, pointed to the roles of age and gender.

“As we get older our bodies change: We gain fat and lose muscle mass, which can impact health,” said Butsch.

Apovian moved from the physical — “men and women are very different about where they distribute weight” — to the psychological. Additional social pressure on women to be thin, she said, “can create psychological issues” as well as weight issues.

Environmental factors

Increases in obesity stem in part from “all the prescription medications that cause weight gain,” said Louis Aronne, clinical professor of medicine at Weill Cornell Medical College. In addition, today’s stressed person “sleeps an hour less today than 100 years ago.”

Ahmad said, “The obesity epidemic is absolutely environmentally driven,” pointing to “more processed food and people working longer hours.” Kaplan described all these factors as “a perfect storm” pushing obesity: “We work too hard; we play too little; we eat too much; our circadian rhythms are disrupted; there have been big changes in our food.” It all adds up to more weight.

Can we change our environment and lifestyle to reduce obesity? Lifestyle changes in isolation have little chance of fixing the problem, Ahmad said. “Just getting rid of sugar-sweetened beverages won’t work,” she said. We need to make better food choices, but also “reduce stress and promote more sleep,” she continued.

Kaplan agreed that there’s no “one-size fits all” remedy, but “we can decide what we eat and how much we exercise and the amount of sleep we get and how much stress we have.”

Weight management

Prescribing a weight-management program is maddeningly complex and highly individualized, said Aronne. “In some cases, it’s just trial and error.”

Diets don’t have a great track record, the panelists agreed. “No one diet has been shown to cause more weight loss than any other diet,” said Kaplan. Physicians and researchers have to do more to address the obesity epidemic, he said: “We need to do a lot more with research, with community-based care,” and other treatment options.

Ahmad was optimistic that more treatments are in the pipeline: “We’re going to have more drugs and treatments, but what you do in your lifestyle” is important too, she emphasized.



Type 2 diabetes and the diet that cured me

Why me? At 59 I was 10st 7lb, 5ft 7in, and had never been overweight. I ran and played cricket regularly and didn’t drink alcohol excessively. Yet at a routine check-up I was told that I had type 2 diabetes. In 10 years I could be dependent on insulin, it could affect my sight, feet, ears, heart and I had a 36% greater chance of dying early.

In type 1 diabetes, the body produces none of the insulin that regulates our blood sugar levels. Very high glucose levels can damage the body’s organs. Patients with type 2 diabetes, however, do produce insulin – just not enough to keep their glucose levels normal. Because I was fit and not overweight (obesity is a major risk factor in type 2 diabetes; however, a number of non-obese people, particularly members of south Asian communities, are also prone to it), my doctor told me I could control my condition with diet alone.

Desperate for information, I headed to the web, where I found a report about a research trial at Newcastle University led by Professor Roy Taylor. His research suggested type 2 diabetes could be reversed by following a daily 800-calorie diet for eight weeks.

When our bodies are deprived of normal amounts of food they consume their own fat reserves, with the fat inside organs used up first. The idea of Taylor’s diet is to use up the fat that is clogging up the pancreas and preventing it from creating insulin, until normal glucose levels return. With my GP’s blessing and a home glucose-testing kit, I began my experiment.

The diet was strict: three litres of water a day, three 200-calorie food supplements (soups and shakes) and 200 calories of green vegetables. Thanks to my doctor’s dietary guidance, and running three times a week, I had already lost a stone. Yet my glucose levels were still above 6mmol/L (millimols per litre), the upper limit for a healthy person without diabetes. According to Taylor, I had to lose a sixth of my pre-diagnosis bodyweight.

On the first full day, I weighed 9st 7lb with a healthy body mass index of 21. After reaching my target of 8st 12lb, I would be able to build myself up through exercise, as larger muscles use more energy, soaking up excess glucose before it is converted and stored as fat.

It wasn’t easy. Yet water staved off the worst hunger pangs. “If you feel hunger, celebrate the fact with a glass of water, even fizzy water,” Taylor said. By the third day, I weighed 9st 5lb.

On day four, my glucose levels had dropped to 4.6 after fasting for 10 hours overnight. It was the first time I’d ever scored a 4. But on day six, I felt really cold. It was mid-July but in the morning my fingertips were white and I had to wear a T-shirt, shirt, jumper and jacket to work. I was hungry, and just walking around the office was tiring. But I was down to 9st 3lb.

By day eight, I was being called the “disappearing man”, and began to feel a bit detached from my colleagues. While my energy levels were fine and glucose levels were 4.3mmol/L, constipation had set in, as a result of not drinking enough water. Thankfully, laxatives cured this. Taylor emailed to say my progress was so good, I  could come off the liquid diet and go back to normal foods.

By day 11, my glucose was 4.1, the lowest yet, and I was down to just 8st 13lb. The next day I treated myself to my first full evening meal of rice and fish, plus a chocolate shake to celebrate.

I waited two months to be sure, but on 24 September last year it was confirmed. Following a fasting glucose test at my surgery, my doctor declared: “The diabetes has resolved itself.” My glucose level was 5.1mmol/L, well below the diabetes mark of 6.

I had stuck to the diet for just 11 days and reduced my blood sugar to a healthy non-diabetic level. It has remained that way for the past seven months.

Others have also changed their lives through the diet. Carlos Cervantes, 53 and from the US, was at death’s door when he tried it. He weighed 120kg, suffered a heart attack in spring 2011, his eyesight and kidneys were failing and he faced having an infected toe amputated. He even had fungus growing out of his ears, feeding on his ultra-high blood sugar levels. But after seeing a TV report on the Newcastle research, he started eating only 600 calories a day, replacing the supplements with not just vegetables but fruit, lean chicken, turkey, occasional bread and a daily milkshake. Two months later he had lost 40kg and 18 months later he is still free of his type  2 diabetes.Henry Cole, 67, from New Jersey, USA, did likewise. He saw a 20-second news clip on TV and took up the diet days later. He stuck rigidly to 600 calories daily from just protein (steak, chicken, turkey or fish) plus green veg, eating his one meal at 6pm most days, with coffee and calorie-counted cream for breakfast and 1.5 litres of water. His weight went down from 81kg to a stable 70kg on a now daily 1,500 cal diet, with his HbA1c level down to 5.6% from 6.9%.

Steve Vincent, 58, from Southampton, England, was diagnosed with type 2 in December 2010. He was told there was no known cure and he had an increased risk of heart attack, stroke, blindness and limb loss. He had a BMI of 29, weighed 93kg and showed an HbA1c of 10.7%. In summer 2011 he read the reversal story and went on a daily 600 calories green vegetable diet and three litres of water, for two months. At the end he was and remains diabetes-free. In December 2012 he told me: “All my blood test levels are within the normal range, and my cholesterol and blood pressure levels are now normal.” When he came off the diet he weighed just 72kg, although he has put on weight since then as he admits he has not been eating as healthily as he might, but his BMI remains at a healthy 24, and his HbA1c level is 5.5%.

Scientists are cautious, and research is continuing, but evidence is growing that the diet can indeed remove the symptoms of type 2 diabetes. The question for researchers, who are now working on identifying the type of diet that can keep diabetes at bay after reversal, is once we’ve beaten the condition, how do we improve our lifestyle so it doesn’t return? Watch this space.

• Follow Richard Doughty on Twitter at twitter.com/ricdoughty

Carbohydrates, Insulin, And Obesity

Fat, Sick  Nearly Dead

Fat, Sick Nearly Dead

Gary Taubes, co-founder of the Nutrition Science Initiative, has just published a new commentary arguing that the way we think about obesity is the result of science politics instead of good science.

The former science journalist argues in his most recent essay, published in the British Medical Journal, that we still don’t know what really causes weight gain, and that the idea that obese people just eat too much neglects much of the research done on diet and weight loss.

He also claims that the common solutions to obesity — encouraging people to eat less and exercise more — have been ineffective, because they are based on misunderstandings of why people become fat.  

Fatter people are not merely less disciplined, he has argued. And leaner people deserve no praise for their ability to keep their bodies svelte. Each of us is more or less a roll of the genetic dice, and some people are just more likely to grow chunkier than others.

The key, says Taubes, is eliminating the dietary triggers that cause our bodies to store fat in the first place. The real triggers for obesity are sugars and high-glycemic carbohydrates (such as wheat), which have been shown to stimulate the insulin response and cause our fatty tissue to accumulate more fat.

A controversial diet

Since 2002, Taubes has been publishing articles and books “Good Calories, Bad Calories,” (Knopf, 2007) and “Why We Get Fat,” (Knopf, 2010) — arguing that it is carbohydrates, not fat, that cause disease and obesity. Most of what is taken for granted by the mainstream medical and nutrition community is based on incomplete and questionable science, Taubes argues.  

Over the years, he has had his critics. His detractors say he has ignored mounds of research that contradicts his positions, his own meat-laden diet is “gross,” and some of the experts he quoted in previous work later claimed Taubes twisted their words and misrepresented their views.

Taubes quoted John Farquhar, a cardiologist at Stanford University in his first piece on obesity in the New York Times Magazine in 2002, but Farquhar later claimed his words — and those of his colleagues — had been manipulated.

“I was greatly offended at how Gary Taubes tricked us all into coming across as supporters of the Atkins diet,” Farquhar later said in a newsletter published by the Center for Science in the Public Interest.

Other scientists, like low fat-diet promoter Dean Ornish, MD, balk when Taubes says that diets low in fat and rich in carbohydrates are what really cause obesity.

Taubes said in an interview with Business Insider that he is not trying to push a diet, he simply wants the scientific and medical community to widen the discussion on the actual causes of obesity and the reliability of the available research.

In this recent paper, Taubes points to forgotten scientific research that he claims supports his long-held contention that spikes in insulin levels caused by sugar and starches are really what balloon our waistlines. 

A controversial history

Taubes claims the alternative “insulin hypothesis” has its own long but neglected history and was once a serious alternative to the conventional “calories in, calories out” theory that has dominated nutrition science since the mid-20th Century. 

Most scientists — even diehard fans of the energy balance hypothesis (a.k.a the “calories in, calories out” theory) don’t really know where it came from, or that there ever was an alternative theory, Taubes said.

The conventional “energy balance” hypothesis is a tautology, Taubes claims. People eat too much, so they become obese.  But obese people must take on more calories to sustain their weight, so obese people eat too much because they are obese.

Taubes claims that an alternative theory, proposed by German and Austrian scientists in the early 20th century, may do a better job of explaining how our bodies accumulate and store excess fat, and why some people grow so much fatter than others.  

Wilhelm Falta and Gustav Von Bergmann were among the first researchers to argue that underlying biological factors — not just what we eat — regulate how fat we get.

They argued that obesity was a “hormonal, regulatory disorder” and not simply the result of eating too much or exercising too little. However, American health and nutrition science in the years that followed WWII ignored these ideas.

Taubes thinks it is time to revive their theories.

Bodily Chemistry

In our bodies, insulin spikes when we eat something that signals to fat tissue to store the sugar in our blood as fat. Falta believed that more insulin means more sugar being turned into fat, making us fatter.

“When insulin was injected into both diabetic dogs and humans in the laboratory as early as the 1920s, they would put on weight and fat,” Taubes said. 

Gustav Von Bergmann — for whom Germany’s highest honor in medicine is named — was another scientist working on a slightly different problem, but it led him to a similar conclusion. 

He was working on the problem of not only why some people gained weight more than others, but why people gain weight in different places. He came up with the concept of lipophilia (literally, “love of fat”).

Some cells are “lipophilic” than others, Von Bergmann thought. Those tend to gather more fat than other fat cells.

People that are “constitutionally predisposed to fatten” (we would now say genetically) have cells that are more lipophilic. This, thought Von Bergmann, was also the reason we tend accumulate fat in certain places and not others (the belly and not the forehead, for example).

So, if some fat cells were gathering more than their “fair share” of energy consumed (i.e. calories eaten), this must mean that other parts of the body were being deprived of energy and the body would compensate by growing hungry or tired.  

“If you discuss insulin regulating fat accumulation, you are pretty much stuck with carbohydrates [sugars and starches] in the diet being the problem,” Taubes said.

The effect of the war

This notion would later prove unpopular with the handful of men who dominated American obesity research in the second half of the 20th Century and was, in some cases, literally erased from the scientific literature.

Later scientists were interested in and supported many of Falta and Von Bergmann’s ideas, says Taubes. But anti-German sentiment in the aftermath of WWII and the rise of English as the language of science left this research largely forgotten.  

“Pre-war, they would discuss different hypotheses to explain what they were seeing and the observations that supported them and the studies that were done that supported them and the studies that didn’t support them,” Taubes said. “It was a very scientific approach. And then post war it became all about energy balance, and gluttony and sloth, and there’s nothing left to discuss, nothing left to question. So even the type of dialogue changes. It ceases to be a scientific dialogue after the war.” 

By the 1960s, most of the people studying obesity in the United States were psychologists and psychiatrists. Obesity was treated as a mental disorder, not a physiological one.  

“They’re not trying to figure out why fat cells accumulate too much fat, they are trying to figure out why people eat so much or exercise so little,” Taubes said. “It’s all this energy balance conception, as opposed to the simple question, why do you put too much fat in your fat cells?”

“The more I understood this, the crazier it seemed,” Taubes said. “We had this disorder of excess fat accumulation, and yet researchers write entire papers, journalists write entire books that never actually discuss what regulates the amount of fat that goes in and out of fat cells. It would be like writing a book about why there are giants and dwarves, without ever discussing growth hormones and growth hormone receptors and other regulators of human growth.”  

Taubes cites other research from the 1960s that shows the hormone insulin is responsible for how much fat cells accumulate.  

Had American scientists been aware of Falta’s and Von Bergmann’s ideas, they might have been able to knit them together into a single coherent alternative to the dominant energy balance hypothesis.

The Present Situation

Taubes concludes his latest essay by calling much of the current experimental research “flawed” and “substandard science” and says he has founded the Nutrition Science Initiative to perform independent, skeptical research into the real cause of obesity.

What is lacking is a body of randomized, controlled studies that evaluate which diets actually work. He believes observational studies are pseudo-science. 

“They’re basically conventional wisdom confirmation machines,” he said. “If you think about who eats a mostly plant-based diet, it’s not poor Asian emigres, who aren’t in these studies anyway.”

“They’re people who think that a vegetarian lifestyle is a healthy lifestyle. They are health-conscious individuals, and if you actually look at the data they are a higher socio-economic status, they are better educated, they smoke less than meat eaters.”

“Like a comparison a friend of mine said, you’re basically comparing Berkeley vegetarians who eat at Alice Waters’s Chez Panisse once a week after yoga practice to redneck truck drivers from West Virginia on the town at Denny’s.”

“On one level, if you are looking at experimental evidence from clinical trials we know that obese and diabetic individuals do much better on diets that have a lot fat and saturated fat in them,” Taubes said.

To truly be effective, a study would have to select randomized groups of people, put each group on a different diet and then follow them for several years to see how they do.

To this end, Taubes is launching the Nutrition Science Initiative, in the hope of sponsoring objective scientific research into the causes of obesity. He hopes to conduct such studies there.   

But such experiments would also require a high-degree of compliance: sticking to any diet for 10 years or more can be tough.

His own diet, as reported on his blog, closely resembles the controversial Atkins Diet. By ditching sugars and starches for meat and cheese, Taubes believes some dieters predisposed to getting fat can keep the insulin trigger at bay, and thus prevent fatty tissue from absorbing energy. 

“I do indeed eat three eggs with cheese, bacon and sausage for breakfast every morning, typically a couple of cheeseburgers (no bun) or a roast chicken for lunch, and more often than not, a ribeye or New York steak (grass fed) for dinner, usually in the neighborhood of a pound of meat. I cook with butter and, occasionally, olive oil (the sausages). My snacks run to cheese and almonds. So lots of fat and saturated fat and very little carbohydrates. A deadly diet, according to Dr. Oz.”

SEE ALSO: 
THE FAST DIET: Get Thin Quick By Starving Yourself Two Days A Week

Dangerous Diabetes preventable

Diabetes Mellitus is one of the major chronic diseases which can be prevented. The study was conducted to assess the carbohydrate intake of type 2 diabetic female patients of age from 45 to 50 years at diabetic clinic of Services Hospital, Lahore. The tools used for data collection were anthropometric measurements, biochemical analysis, clinical signs and dietary data. The findings of the study are; BMI of selected diabetic patients reflects that the majority patients (54 per cent) are overweight. HbA1C value of selected diabetic population is 9.0 per cent which indicated a high blood sugar level and poor management and control of diabetes. Multiple clinical signs and symptoms are present among diabetic patients. Hypertension is found to be the most common health problem in patients with type 2 diabetes. A strong family history and gestational diabetes history relates to the onset of type 2 diabetes. Majority patients have less than basal energy expenditure k-calorie intake. Majority patients have more than 3 meals with snacks in a day. An important finding is that carbohydrate intake of diabetic patients is 156g/day while requirement is for 200g/day. Fibre consumption is unsatisfactory in diabetic patients.



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The combination of blood sugar controlling strategies (diet, medications and exercise) is followed by only a small percentage of patients. Majority patients are complying with a prescribed diet plan. Reasons for non compliance are also observed. The diet plan provided to diabetic patients is unsatisfactory and based on improper distribution of k-calorie between carbohydrate, protein and fat. It is recommended that balanced diet with adequate kilo calories and proper distribution of carbohydrates should be provided to the diabetic patients to prevent many health problems.
AWARENESS is needed on the management of diabetes.
ENCOURAGE patients to lead a normal healthy life and assure them that it is a manageable problem.
WEIGHT MAINTENANCE should be achieved for a good glycemic control.
OBESITY is the major risk factor and weight maintenance should be part of school education.
FAMILY HISTORY is also a major contributing factor and people should be screened and encouraged to adopt a lifestyle to delay the onset of diabetes.
EDUCATION LEVEL is an important factor for the better management and treatment of diabetes.
INDIVIDUAL NUTRITIONAL COUNSELING and nutrition education with special reference to patient’s carbohydrate intake is needed for much better control of glycemic levels; individualizing patient’s own variables, i.e. sex, age, body weight parameters, cooking methods, eating patterns and their lifestyles.
PROPER MEAL SPACING should be introduced to the patients for the best glycemic goals to achieve.
FLEXIBILITY in eating patterns should be encouraged to the patients, by providing them more food choices of selection with the same (amount) grams of carbohydrates.
PROPER DISTRIBUTION OF CARBOHYDRATE regarding quantity and quality be encouraged. Such low-calorie recipes should be developed that focus on complex carbohydrates, high fiber and low to moderate fat, and modified diets that help to produce a low-glycemic load after a meal and ultimately beneficial for improving blood sugar levels.
Much attention is needed in the control of portion sizes by the use of measuring cups, and with the visual aids, rather than written documentations for majority of illiterate patients so that the focus on amount is achieved for all diabetic patients.
Household chores; a part of physical activity was also ignored by diabetic patients. Such types of physical activity should be encouraged for diabetic patients.
Diabetes is a lifelong problem and must be managed and controlled to avoid complications. Every diabetic clinic must have a qualified dietitian in the health care team.
This is an excerpt from the Ghazala Pervez Zaman-supervised thesis of the writer, a Punjab University MSc Food and Nutrition student.

White blood cell enzyme contributes to inflammation and obesity

Imbalance between an enzyme called neutrophil elastase and its inhibitor causes inflammation, obesity, insulin resistance, and fatty liver in mice and humans—providing a new therapeutic target for these health conditions

Many recent studies have suggested that obesity is associated with chronic inflammation in fat tissues. In a new study, researchers discovered that an imbalance between an enzyme called neutrophil elastase and its inhibitor causes inflammation, obesity, insulin resistance, and fatty liver disease. This enzyme is produced by white blood cells called neutrophils, which play an important role in the body’s immune defense against bacteria.

The researchers found that obese humans and mice have increased neutrophil elastase activity and decreased levels of α1-antitrypsin, a protein that inhibits the elastase. When the team reversed this imbalance in a mouse model and fed them a high-fat diet, the mice were resistant to body weight gain, insulin resistance (a precursor to type 2 diabetes), and fatty liver disease. Their study appears April 2 in Cell Metabolism.

“The imbalance between neutrophil elastase and its inhibitor, α1-antitrypsin, is likely an important contributing factor in the development of obesity, inflammation, and other health problems. Shifting this balance—by either reducing one or increasing the other—could provide a new therapeutic approach to preventing and treating obesity and several obesity-related conditions,” said Zhen Jiang, Ph.D., assistant professor at Sanford-Burnham and senior author of the study.

What happens when you reduce neutrophil elastase levels

This study began when Jiang and his team noticed that neutrophil elastase levels are particularly high and α1-antitrypsin levels are low in a mouse model of obesity. Then they saw the same thing in blood samples from human male volunteers.

To further probe this curious neutrophil elastase-obesity relationship, the researcher turned once again to mouse models. They found that mice completely lacking the neutrophil elastase enzyme don’t get as fat as normal mice, even when fed a high-fat diet. Those mice were also protected against inflammation, insulin resistance, and fatty liver. The same was true in a mouse model genetically modified to produce human α1-antitrypsin, which inhibits neutrophil elastase.

Normal mice on a high-fat diet were also protected against inflammation, insulin resistance, and fatty liver when they were given a chemical compound that inhibits neutrophil elastase. This finding helps validate the team’s conclusions about neutrophil elastase’s role in inflammation and metabolism and also suggests that a medicinal drug could someday be developed to target this enzyme.

Mechanism: how neutrophil elastase influences inflammation and metabolism

How do high neutrophil elastase levels increase inflammation and cause weight gain and other metabolic problems?

Jiang and his team began connecting the mechanistic dots. They discovered that neutrophil elastase-deficient mice have increased levels of several factors, including adiponectin, AMPK, and fatty acid oxidation. These are known for their roles in increasing energy expenditure, thus helping the body burn excess fat.

###

This research was funded by a Sanford-Burnham start-up fund, the American Diabetes Association (grant 7-11-BS-72), U.S. National Institutes of Health (National Institute of Diabetes and Digestive and Kidney Diseases grant R01DK094025), and U.K. Medical Research Council (grant U117512772).

Original paper:

Mansuy-Aubert, V., Zhou, Q., Xie, X., Gong, Z., Huang, J., Khan, A., Aubert, G., Candelaria, K., Thomas, S., Shin, D., Booth, S., Baig, S., Bilal, A., Hwang, D., Zhang, H., Lovell-Badge, R., Smith, S., Awan, F., Jiang, Z. (2013). Imbalance between Neutrophil Elastase and its Inhibitor α1-Antitrypsin in Obesity Alters Insulin Sensitivity, Inflammation, and Energy Expenditure Cell Metabolism, 17 (4), 534-548 DOI: 10.1016/j.cmet.2013.03.005

ResearchBlogging.org

Diet 'just as good as op' for diabetes

It has long been known that patients who undergo gastric operations to curb eating see a dramatic improvement in their diabetes.

But patients with Type 2 diabetes who simply follow the same strict diet as that after surgery are just as likely to see a reduction in their blood glucose levels.

The report was released by researchers at UT Southwestern Medical Centre in Dallas.

Invokana (canaglifozin) For Type 2 Diabetes Approved By FDA

Editor’s Choice
Main Category: Diabetes
Also Included In: Regulatory Affairs / Drug Approvals
Article Date: 31 Mar 2013 – 0:00 PDT

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The FDA has approved Johnson Johnson’s Invokana (canaglifozin) tablets, to be used with exercise and diet, for adults with type 2 diabetes to improve glycemic control.

Type 2 diabetes affects approximately 24 million Americans. Patients eventually tend to have complications from high blood sugar levels, including kidney damage, nerve damage, blindness and heart disease.

Mary Parks, M.D., director of the Division of Metabolism and Endocrinology Products in the FDA’s Center for Drug Evaluation and Research, said:

“Invokana is the first diabetes treatment approved in a new class of drugs known as sodium-glucose co-transporter 2 (SGLT2) inhibitors. We continue to advance innovation with the approval of new drug classes that provide additional treatment options for chronic conditions that impact public health.”

Invokana stops the kidney from reabsorbing glucose, increasing glucose excretion, and reducing blood glucose levels in patients with diabetes who have excessively high blood glucose levels.

Richard Aguilar, M.D., Medical Director, Diabetes Nation LLC and the Diabetes Care Foundation, said “Patients with type 2 diabetes struggle managing their blood sugar, and nearly half of adults with type 2 diabetes do not achieve recommended levels of glucose control, increasing their risks for potentially life-threatening complications. Invokana is thought to work differently than other currently-available medicines because it reduces blood glucose by acting on the kidneys as a ‘glucuretic,’ increasing the loss of glucose in the urine. What has historically been viewed as a sign of diabetes – glucose in the urine – may also reflect the efficacy of a new and unique approach to treatment.”

Invokana’s safety and efficacy were assessed in nine clinical trials involving 10,285 type 2 diabetes patients. Patients on Invokana experienced improved A1c levels and fasting blood sugar (plasma glucose) levels. In Phase III studies, Invokana was also associated with reductions in body weight and systolic blood pressure.

Invokana has been studied as therapy to be taken on its own, and also in combination with, pioglitazone, sulfonylurea, metformin and insulin.

Invokana should not be used for patients with:

  • Type 1 diabetes
  • Diabetic ketoacidosis – ketones in their urine or blood
  • Severe renal (kidney) impairment
  • End stage kidney disease
  • On dialysis

According to the FDA, Janssen Pharmaceuticals, Inc. (part of Johnson Johnson) will have to carry out post-marketing studies:

  • A cardiovascular outcomes trial to check for liver abnormalities, photosensitivity reactions, adverse pregnancy outcomes, malignancies, severe hypersensitivity reactions, and serious cases of pancreatitis.
  • A bone safety study
  • Two studies on children under the Pediatric Research Equity Act (PREA). These should include a safety and efficacy study and a pharmacokinetic and pharmacodynamic study.

The following side effects were reported during the Invokana trials: urinary tract infection and vulvovaginal candidiasis.

Invokana’s diuretic effect can cause a sudden fall in blood pressure when the patient stands up (postural or orthostatic hypotension) – symptoms include fainting or dizziness. This is more common during the first twelve weeks of therapy.

Invokana is made by Janssen Pharmaceuticals, Inc., Titusville, N.J.

One month ago the FDA approved Nesina (alogliptin) tablets, Oseni (alogliptin and pioglitazone) tablets, and Kazano (alogliptin and metformin hydrochloride) tablets, to improve blood sugar control.

Written by Christian Nordqvist

Copyright: Medical News Today

Not to be reproduced without permission of Medical News Today

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MediLexicon International Ltd © 2004-2013 All rights reserved.
MNT (logo) is the registered trade mark of MediLexicon Int. Limited.