Posts Tagged ‘Diabetes’

If the members of the American medical establishment were to have a collective find-yourself-standing-naked-in-Times-Square-type nightmare, this might be it. They spend 30 years ridiculing Robert Atkins, author of the phenomenally-best-selling ”Dr. Atkins’ Diet Revolution” and ”Dr. Atkins’ New Diet Revolution,” accusing the Manhattan doctor of quackery and fraud, only to discover that the unrepentant Atkins was right all along. Or maybe it’s this: they find that their very own dietary recommendations — eat less fat and more carbohydrates — are the cause of the rampaging epidemic of obesity in America. Or, just possibly this: they find out both of the above are true.

The worst part about the way other respected people in the medical community treated Dr. Atkins is in the way they acted contemptuously towards scientific principles.

In fact, when the American Medical Association released its scathing critique of Atkins’s diet in March 1973, it acknowledged that the diet probably worked, but expressed little interest in why.

The prevailing theory, that eating more carbohydrates and fewer fats was better for health, was itself a new and untested hypothesis at one point.

The alternative hypothesis also comes with an implication that is worth considering for a moment, because it’s a whopper, and it may indeed be an obstacle to its acceptance. If the alternative hypothesis is right — still a big ”if” — then it strongly suggests that the ongoing epidemic of obesity in America and elsewhere is not, as we are constantly told, due simply to a collective lack of will power and a failure to exercise. Rather it occurred, as Atkins has been saying (along with Barry Sears, author of ”The Zone’‘), because the public health authorities told us unwittingly, but with the best of intentions, to eat precisely those foods that would make us fat, and we did. We ate more fat-free carbohydrates, which, in turn, made us hungrier and then heavier. Put simply, if the alternative hypothesis is right, then a low-fat diet is not by definition a healthy diet. In practice, such a diet cannot help being high in carbohydrates, and that can lead to obesity, and perhaps even heart disease.

Given the spectacular failure of such low fat, high carb diets to cause people to lose weight and improve their health, the medical community should have been more open to other ideas. More importantly, Dr. Atkins’ hypothesis proved correct and was easily verified after only a few years on the market.

Here is how the nonsense got started:

It was Ancel Keys, paradoxically, who introduced the low-fat-is-good-health dogma in the 50’s with his theory that dietary fat raises cholesterol levels and gives you heart disease. Over the next two decades, however, the scientific evidence supporting this theory remained stubbornly ambiguous. The case was eventually settled not by new science but by politics. It began in January 1977, when a Senate committee led by George McGovern published its ”Dietary Goals for the United States,” advising that Americans significantly curb their fat intake to abate an epidemic of ”killer diseases” supposedly sweeping the country. It peaked in late 1984, when the National Institutes of Health officially recommended that all Americans over the age of 2 eat less fat. By that time, fat had become ”this greasy killer” in the memorable words of the Center for Science in the Public Interest, and the model American breakfast of eggs and bacon was well on its way to becoming a bowl of Special K with low-fat milk, a glass of orange juice and toast, hold the butter — a dubious feast of refined carbohydrates.

The Center for Science in the Public Interest advocates neither science nor anything in the public’s interest until today. We will cover that in a future post.

According to Katherine Flegal, an epidemiologist at the National Center for Health Statistics, the percentage of obese Americans stayed relatively constant through the 1960’s and 1970’s at 13 percent to 14 percent and then shot up by 8 percentage points in the 1980’s. By the end of that decade, nearly one in four Americans was obese. That steep rise, which is consistent through all segments of American society and which continued unabated through the 1990’s, is the singular feature of the epidemic. Any theory that tries to explain obesity in America has to account for that.

Some scientists blame fast food, sedentary lives, and genes designed to store food as fat for the obesity epidemic.

This theory makes perfect sense and plays to our puritanical prejudice that fat, fast food and television are innately damaging to our humanity. But there are two catches. First, to buy this logic is to accept that the copious negative reinforcement that accompanies obesity — both socially and physically — is easily overcome by the constant bombardment of food advertising and the lure of a supersize bargain meal. And second, as Flegal points out, little data exist to support any of this. Certainly none of it explains what changed so significantly to start the epidemic. Fast-food consumption, for example, continued to grow steadily through the 70’s and 80’s, but it did not take a sudden leap, as obesity did.

Examining genetics reveals an important clue to the truth:

It is also undeniable, note students of Endocrinology 101, that mankind never evolved to eat a diet high in starches or sugars. ”Grain products and concentrated sugars were essentially absent from human nutrition until the invention of agriculture,” Ludwig says, ”which was only 10,000 years ago.” This is discussed frequently in the anthropology texts but is mostly absent from the obesity literature, with the prominent exception of the low-carbohydrate-diet books.

As our regular readers are aware, smart people easily support stupid ideas, all the more so if the new idea on the scene challenges their preconceived conception of what’s right.

The glycemic-index concept and the idea that starches can be absorbed into the blood even faster than sugar emerged in the late 70’s, but again had no influence on public health recommendations, because of the attendant controversies. To wit: if you bought the glycemic-index concept, then you had to accept that the starches we were supposed to be eating 6 to 11 times a day were, once swallowed, physiologically indistinguishable from sugars. This made them seem considerably less than wholesome. Rather than accept this possibility, the policy makers simply allowed sugar and corn syrup to elude the vilification that befell dietary fat. After all, they are fat-free.

David Ludwig, M.D., Ph.D., the Harvard endocrinologist, runs a pediatric obesity clinic.

He does not recommend the Atkins diet because he says he believes such a very low carbohydrate approach is unnecessarily restrictive; instead, he tells his patients to effectively replace refined carbohydrates and starches with vegetables, legumes and fruit. This makes a low-glycemic-index diet consistent with dietary common sense, albeit in a higher-fat kind of way. His clinic now has a nine-month waiting list.

Note the common themes prevailing here which are evident in other areas, and which will continue to pop up again and again:

  • Government stepping in with ambiguous evidence in an effort to provide a solution to a problem which may not exist. Government bureaucracy increases to handle this new “problem”, which requires increasing tax revenue.
  • Smart, very educated people unable to see past the end of their noses, even when doing so means accepting common sense.
  • The “experts” offer all sorts of advice which revolve around the idea that John Smith, typical citizen, cannot be held responsible for his actions. For example, “it’s not your lack of self control that’s making you fat, just blame the fast food industry for making food too cheap and delicious”.

Replacing individual responsibility with reliance on government is something which has been going on this country for several decades, and is coming to a head over the recent universal government healthcare bill. The only cure is for citizens to pay attention and to remain ever vigilant against encroaching tyranny.

Many experts do not see cradle to grave reliance on government as a flaw, but as a desirable goal. They truly believe that the average American is a moron unable to handle serious decisions, perhaps slightly smarter than cabbage. It is that brand of “we know what’s best for you” elitism which may bear the greatest responsibility for the obesity epidemic.

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Beta cells are in a part of the pancreas called the islets of Langerhans. They are responsible for producing insulin, without which the body cannot metabolize sugar. Currently, diabetics must inject insulin to enable proper digestion.

On Thursday, a team of European and American researchers showed that pancreatic cells in diabetic mice could be reprogrammed into beta cells by turning on just one gene, called Pax4.

The latest scientific research involves finding which gene(s) are responsible for instructing a cell in the pancreas to become a beta cell. If the beta cells which die out in diabetics could be replaced by using the body’s own mechanisms, then insulin injections may become a thing of the past.

They found that the gene converted so-called alpha cells — which normally made a hormone called glucagon — into beta cells that made insulin. Beta cell levels were eight times higher in treated mice than in untreated control subjects, according to the study published in Friday’s edition of the journal Cell.

There are still issues to be worked out, such as why it works a little too well in very young mice and not older ones. This is an important milestone, and the next part of this research should be to determine the on/off switch so the gene is only active for exactly the right amount of time.

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Researchers at the Salk Institute for Biological Studies have uncovered the connection between obesity and insulin resistance. Their explanation reveals how thin people too can become insulin resistant.

It had been well established that obesity promotes insulin resistance through the inappropriate inactivation of a process called gluconeogenesis, where the liver creates glucose for fuel and which ordinarily occurs only in times of fasting.

The researchers investigated the possibility that stress induced other changes to take place on the cellular level, specifically in the endoplasmic reticulum, a protein factory.

“When a cell starts to sense stress a red light goes on, which slows down the production of proteins,” explains Montminy. “This process, which is known as ER stress response, is abnormally active in livers of obese individuals, where it contributes to the development of hyperglycemia, or high blood glucose levels. We asked whether chronic ER stress in obesity leads to abnormal activation of the fasting switch that normally controls glucose production in the liver.”

Now, for the hard science portion of this lecture:

Glucose production is turned on by a transcriptional switch called CRTC2, which normally sits outside the nucleus waiting for the signal that allows it to slip inside and do its work. Once in the nucleus, it teams up with a protein called CREB and together they switch on the genes necessary to increase glucose output. In insulin-resistant mice, however, the CRTC2 switch seems to get stuck in the “on” position and the cells start churning out glucose like sugar factories in overdrive.Surprisingly, when postdoctoral researcher and first author Yiguo Wang, Ph.D., mimicked the conditions of ER stress in mice, CRTC2 moved to the nucleus but failed to activate gluconeogenesis. Instead, it switched on genes important for combating stress and returning cells to health. On closer inspection, Wang found that in this scenario CRTC2 did not bind to CREB but instead joined forces with another factor, called ATF6a.

What’s more, like jealous lovers CREB and ATF6a competing for CRTC2’s affection—the more ATF6a is bound to CRTC2, the less there is for CREB to bind to.

Although the detailed answer paints a complex picture, the main point is that high levels of glucose in the blood leads to insulin resistance. Understanding precisely how those mechanisms work will lead to better treatments in the future.

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