Thursday, December 17, 2015

Can Viruses Cause Obesity?

Is it possible that viruses can cause obesity? I'm not talking here about what we consider common viruses like the cold virus or HIV virus that attack humans directly, but bacteriophages, which attack bacteria and can kill them.

In fact, some people are using bacteriophages, often called just phages, to treat antibiotic-resistant bacterial infections. Phages were discovered in 1915 by FW Twort in England and then in 1917 by the Canadian FĂ©lix d’Herelle but haven't been studied a lot since then in terms of human disease.

Now there is some evidence that phages in the gut can contribute to obesity.

The idea that the gut microbiome can contribute to obesity is not new. Numerous studies have shown that transferring a sample of gut bacteria from fat animals into the guts of animals raised in sterile environments will produce fat animals, and transferring bacteria from thin animals will produce thin animals.

So it was not a surprise when University of Iowa scientists showed that the weight gain that often results from use of the drug risperidone, used for psychiatric disorders, was related to the gut microbiome of mice. What is interesting is that the researchers were able to cause the weight gain not just by transferring samples of the gut microbiota, but also by transferring the gut phages alone. When they gave the mice samples of isolated phages, the mice had decreased energy expenditure and a significant increase in weight, just as they had with the drug risperidone.

The usual caveat applies. Humans don't always react like mice. For one thing, humans don't set up  housekeeping in my walls. But our physiology is also somewhat different.

Nevertheless, the idea that bacteriophages could be affecting our weight is intriguing, and further research could lead to new approaches to keeping us all thin.

Tuesday, December 15, 2015

Spinning the News

I recently posted a blogpost about how the popular press often simply regurgitates press releases publicity people at various institutions send them.

And now come two "stories" that are such blatant attempts to trump up business for a certain food -- pears -- that it's laughable. One says pear consumers weigh less than non-pear-eaters, and the other says pears are healthy.

One study was sponsored by USA Pears, the other by the Pear Bureau Northwest, which is, in their words, "a nonprofit marketing organization to promote the fresh pears grown in Oregon and Washington."

Then one paper says, and this is the shocking part, "While the body of evidence connecting pear intake and health outcomes is still limited, USA Pears has been contributing to research efforts by commissioning independent studies to learn and affirm the heath attributes of pears."

Hold on! USA Pears has commissioned research aimed at proving that pears are healthy? Presumably if the research shows that pears cause warts, they won't publish that. But that's not scientific research. Scientific research tries to ascertain the truth, not support some preconceived conclusion. So OK, in fact this ideal is often not reached. But at least you should pretend you have an open mind.

The other study concludes that "intervention studies with pears that show positive health outcomes, most likely improvements in gut health, are urgently needed." In other words, research that shows negative outcomes is not needed.

What bothers me is that this kind of "research" and the ensuing press releases do, in fact, work. Most people seeing headlines like this or hearing them read out on the evening news will only remember, "Gosh. Pears are healthy and if I eat pears I'll lose weight." In fact, when you don't have diabetes, most fruits are healthy in moderation. Each fruit is higher or lower in some nutrient, but they all contain healthy nutrients as well as sugars.

I keep those 100-calorie sugarfree canned fruits on hand to use when my blood glucose goes too low, and they do a good job of raising my blood glucose and taste good as well. But I don't expect to be a lot healthier or to weigh less as a result.

At this point, except for occasional rants like this one, whenever I see a story promoting the health benefits of a single food, I look to see who funded the study. If it's some growers' organization like USA Pears, I don't even bother reading the story. There's enough real science research to read about without wasting time on this sort of thing.

Thursday, December 10, 2015

Is There a Type 4 Diabetes?

A new type of diabetes in older people of normal weight has been proposed, and the authors suggest calling it type 4 diabetes. Well, OK, this hasn't been found in people yet, but only in mice, and mouse results often don't translated into human results, but the idea is intriguing.

The two main types of diabetes currently accepted are type 1, which is autoimmune, and type 2, which is caused by insulin resistance. Some type 1 patients have some insulin resistance and some type 2 patients have some autoantibodies, but in general types 1 and 2 have different causes.

Type 3 diabetes is what some people call Alzheimer's disease, meaning insulin resistance in the brain. Others use type 3 to mean family members of someone who has diabetes, some use it to refer to gestational diabetes, and some use type 3 to mean people whose diabetes is related to exposure to electromagnetic radiation. Definitions of type 1.5 diabetes also differ. Some use it to mean LADA (latent autoimmune diabetes of adults), which is like type 1 in older people but tends to progress more slowly. Others use it to mean people with both types 1 and 2, or "double diabetes." 

Another type of diabetes is MODY, or maturity onset diabetes of the young, which is monogenic. There are several types of MODY.

So now we may have another type of diabetes, which seems to be found in lean elderly mice in which  insulin resistance is caused not by obesity but simply by aging. The interesting thing is that this type of diabetes doesn't respond to weight loss but can be treated, at least in mice, by using antibodies to deplete the fat cells of immune cells called regulatory T cells, or Tregs. The Tregs in fat are called fTregs.

What is interesting about the Tregs is that they have been considered "good" immune cells. The Tregs control the immune system and can dampen down an immune response that is too large. There is some evidence that people with type 1 diabetes don't have enough Tregs so their immune system goes into overdrive and attacks their own tissues, including the beta cells in the pancreas.

One recent study showed that removing cells producing Tregs from people with type 1 diabetes,  culturing them in medium until they increased 1,500 fold, and then reintroducing them back into the patients produced no side effects. It is hoped that further trials show that they dampen the autoimmune attack.

But in the case of type 4 diabetes, the problem is not too few Tregs but too many in the fat cells, the fTregs. When the Salk Institute researchers, led by Ronald Evans, looked at the fTregs of obese mice with type 2 diabetes, they found that the level was lower than normal. But when they looked at the fTregs of aged lean mice with age-associated insulin resistance, they found that the levels were high (5%, compared with 0.4% in  young mice and 0.1% in obese mice). Their publication in Nature is behind a paywall, but Evans kindly sent me a copy of the full text.

When they depleted the fat of the excess fTregs by giving them a specific antibody, their metabolic abnormalities improved, glucose and insulin levels were lower, their fat cells were smaller, their serum free fatty levels were reduced to almost half of their previous levels, and they were leaner despite increased food consumption. Giving the same antibody to mice with type 2 diabetes had no effect.

As noted, this research has not yet been duplicated in humans. But the idea is exciting, because many older people diagnosed with type 2 diabetes find that weight loss has no effect. Others are diagnosed with type 2 even though they are active and of normal weight. If type 4 diabetes turns out to exist in humans, this would explain these anomalies.

Stay tuned. Evans said the research has generated a lot of interest, and I hope it's followed up in several labs, which offers the greatest possibility of confirmation.

Friday, December 4, 2015

Glucagon Again

I've written before about glucagon (here and here) and  have suggested that we need more research on alpha cells and glucagon, which sometimes seem to be ignored. Robert Unger has been writing about this for decades, but most researchers continue to focus on insulin.

In general, glucagon does the opposite of insulin. Insulin is produced by the beta cells in the pancreas and makes blood glucose (BG) levels go down. Glucagon is produced in the alpha cells in the pancreas and makes them go up. It's the ratio of the two that is important.

And now comes research showing that certain versions of the TCF7L2 gene, which are known to increase the risk of type 2 diabetes and were thought to work by inhibiting the secretion of insulin by the beta cells, may also work by making the alpha cells resistant to the action of insulin, which normally shuts them off. The senior author of the paper, Adrian Vella, kindly sent me the full text of the article.

When everything is working correctly, you eat carbohydrate and your beta cells produce and secrete insulin, which helps muscle and fat cells take up glucose. The insulin also turns down the secretion of glucagon by the alpha cells, which makes sense. Glucagon makes the liver produce and release a lot of glucose, and that's not something you want when your BG levels are already high.

The problem is that when you have type 2 diabetes, not only are your insulin levels too low to overcome your insulin resistance, but your glucagon levels are too high. And for those with the high-risk version (TT) of the TCF7L2 gene (and I have the protective version, CC, according to 23&Me), one reason for this high glucagon level seems to be that the insulin doesn't turn down its production in the alpha cells. So even when you eat carbohydrate and have enough insulin, the liver keeps pouring out glucose.

The study also showed a slight decrease in insulin production in those with the high-risk version of the gene, but no difference in the effectiveness of the insulin that was produced.

The differences in glucagon levels in those with the high-risk version of the TCF7L2 gene were not enormous. Clearly, the high-risk version of the gene is not the only contributor to type 2 diabetes. But that is consistent with the idea that type 2 diabetes is caused by small effects from many genes and not just one gene, as occurs in MODY, or maturity onset diabetes of the young. That's one reason why there's so much variation in the way we respond to various factors. I may have a defect in a different gene or genes than you do.
 But this research is a reminder that alpha cells and glucagon are important contributors to the type 2 diabetes puzzle,  and genetic and environmental effects on alpha cells may turn out to be as important as the effects on beta cells. "It demonstrates a completely novel mechanism of predisposition to diabetes that could lead to novel therapies," said Vella.

Tuesday, November 24, 2015


YMMV. Or “Your Mileage May Vary.” That’s what many of us type 2 diabetes patients have discovered when it comes to diet. What works for one person may not work so well for another.

For example, some patients report that they can eat rice without a great effect on their blood glucose (BG), but potatoes make their BG levels soar. Others report the exact opposite.

One problem with such annecdotal reports is that we often don’t know how the various foods were cooked, how much the people ate, or what they ate with the foods they’re reporting on. For this reason, medical professionals tend to ignore such annecdotal results and instead rely on huge nutritional studies that usually report results only as averages, neglecting the “outliers,” or those whose results were far from the mean.

That means that if you’re an outlier yourself, the “evidence-based medicine” results from the nutritional studies, or the diet advice of some diet guru, may not apply to you, and if you try to follow this advice and don’t get good results, people may accuse you of being “noncompliant” or not doing what they told you to do.

But now it appears that even the professionals are beginning to accept that we’re all individuals with individual responses to various foods. And we now have a well-controlled study to support this view.

The study by researchers at the Weizmann Institute of Science in Israel used continuous glucose monitors to measure the BG levels of 800 healthy and prediabetic people after their meals for a week, and put this information along with what they ate, information from stool samples, and other physiological information into computers and analyzed it. They even gave them identical foods for some of their meals.

What they found was that the people differed greatly in how they responded to various foods; the glycemic index, a measure of how much your BG levels are supposed to rise after eating carbohydrate, varied among the participants. “In some cases, individuals have opposite response to one another, and this is really a big hole in the literature," said Eran Segal, the lead author of the study.

"After seeing this data, I think about the possibility that maybe we're really conceptually wrong in our thinking about the obesity and diabetes epidemic," he added. "The intuition of people is that we know how to treat these conditions, and it's just that people are not listening and are eating out of control--but maybe people are actually compliant but in many cases we were giving them wrong advice."

As an example, they cited the case of an obese woman who couldn’t lose weight despite trying hard. It turned out her BG levels spiked when she ate tomatoes, and because they’re supposed to be a healthy food (“eat more fruits and vegetables”), she was eating a lot of them  and her BG levels were spiking every day.

Not only glycemic index but other parameters resulted in different effects in different people. Some people saw increases in BG levels after meals that were unrelated to the carbohydrate content. In most people, fat reduced postprandial BG levels, but in some it had no effect.

What was especially interesting was that the variation in responses to food seemed to be linked with the microbiota, the bacteria in their guts. Although the microbiota tends to be stable throughout one’s lifetime, the researchers said they were able to alter the patients’ microbiota by controlling increases in the BG levels.

I think this study is important in the context of “diet wars.” Low carbers and low fatters and other diet gurus often act as if theirs is the only diet that will work and everyone should follow in their footsteps. Their diets do work extremely well for some people, but they don’t work for everybody.

If the Kitavans thrive on a high-carb diet, that’s the diet they should follow. If the Inuit thrive on a high-fat diet, that’s the diet they should follow. The diet you should follow may depend on the bacteria in your gut, and that may depend on your genetic heritage, although it can be somewhat altered in various ways (diet, antibiotics, etc.).

In the diabetes community, I think most people are aware of the concept of YMMV, and we’ve adopted a philosophy that takes it into consideration, namely “Eat to Your Meter.” If some food like tomatoes makes your BG levels soar, don’t eat that food. If it’s relatively benign for you, go ahead and eat it in moderation, and don’t worry if someone else says it’s no good for them.

For those without diabetes who simply want to lose weight, an analogous approach would be “Eat to Your Scales.” If you tend to gain weight when you eat certain foods, then don’t eat them.

Although most of us would agree that a diet of nothing but cheeseburgers and fries is not healthy for anyone, what is healthy is less certain. Remember YMMV and eat what works for you.

Wednesday, November 4, 2015

Parsing the Popular Press

Science, especially nutritional science, usually moves in small steps forward and then small steps steps backward and then more steps forward and a few steps sideways until we eventually arrive at the truth. One experiment or one nutritional study proves nothing. It has to be confirmed, preferably several times, in order to be accepted as true.

Unfortunately the popular press has no understanding of this. The popular press also has no understanding of statistics and what “significant” means in statistical terms. So a single study is often be blown up and spread all over the popular press. The conclusions are simplified. And if that single study confirms the average person’s preconceptions, the study will be blown up even more and simplified even more.

The obvious recent example is the study about red and processed meat and cancer.

This was a meta-analysis, and such analyses have known problems. Nutritional studies also have known problems as most of them use questionnaires, which requires people to remember how many times they ate Food X over the last week or month. I often can’t remember what I had for breakfast,  and my diet changes with the seasons and with what foods are on special that week. I haven’t the slightest idea how often I ate spinach in the last month.

Furthermore, the meat study was about only colorectal cancer (CRC). The conclusion was that “the state of the epidemiologic science on red meat consumption and CRC is best described in terms of weak associations, heterogeneity, an inability to disentangle effects from other dietary and lifestyle factors, lack of a clear dose-response effect, and weakening evidence over time.”

But the popular press ran articles with titles like “Meat as dangerous as smoking.” This is the sort of soundbite people will remember. No one will remember “weak associations” or “lack of a clear dose-response effect” even if they know what that means, or the fact that the study is limited to CRC.

Numerous diet bloggers have pointed out the limitations of this red meat study, including Zoe Harcombe and Stephan Guyenet. I don’t want to do that here, just point out how the popular press misleads the public in order to get sensational stories.

Another story that captured the attention of the popular press was a story claiming that red wine can improve cardiovascular health in people with type 2 diabetes. This is the type of story that the general public can understand, and it’s appealing to people who like to drink, so it was played large in a lot of the popular press.

These news stories are often based on just one study, and just one study proves nothing, especially if it’s a nutritional study. So the probability that further research will contradict the study the press has blown up is high. If it is, some readers (or TV watchers) decide that no health information is trustworthy and may ignore even advice based on good research that has been confirmed many times.

Here is an example of a study of chimpanzee communication claiming that their results disprove previous results by another group. And here is a study contesting the source of DNA samples supposed to be from ancient grains. They claim the results stemmed from contamination with modern grains. And here is a story refuting the idea that sitting for long periods of time is bad for your health even though you get exercise at other times.

One might conclude that no scientific studies are worth reading about because next week someone will claim the opposite. That’s not true. Often studies are confirmed by other researchers. It’s just that we have to interpret any studies as tentative, and especially if they’re funded by a group that sells the product, for example, a study by the US Gloopyberry Association showing that gloopyberries reduce cholesterol levels when you eat the equivalent of five pounds a day. The popular press would run stories with headlines like “Gloopyberries reduce cholesterol,” and people would buy more gloopyberries, which of course is why the Gloopyberry Association funded the study.

Many of the foods we eat have effects on the compounds in our blood, especially when eaten in excess, and most of them have never been tested. In fact, some of them might have a greater effect on cholesterol than the gloopyberries but we won’t know until someone studies them in reasonable amounts, and this requires funding for the study.

Derek Lowe has a blogpost about another problem with popular press articles. That is the tendency to label the results of studies as “breakthrough” or “miracle” cures when in fact they represent baby steps on the way to the solution of some problem. Most articles by science news organizations like Science Daily or Eurekalert are simply press releases from the institutions whose scientists did the experiments. Quite often you’ll see two or even three articles about the same research, each one emphasizing the researchers from their institution.

Their job is to put the best possible spin on their institutions, and “breakthrough” studies are a good way to do this. They also provide suggested headlines, which these science news sites usually use. Easier than writing their own.

The popular press then reads the Science Daily or Eurekalert stories and simplifies even more and that’s what most people read or hear on the evening news.

So what can we as intelligent readers do? We can’t ignore all these studies. But we have to file them away as “interesting and perhaps with some truth in them.” Then we can wait to see if the work is confirmed.

This isn’t as exciting as thinking that eating gloopyberries will solve all our problems and do our taxes for us. But it’s closer to reality. We can’t control the popular press. But we can control our reactions to the popular press articles. Sometimes ignore is the best solution, I think.

Thursday, October 22, 2015

New Book Is Out

This is blatant self-promotion, which I hate, but I thought I should let people know that the third edition of my book "The First Year: Type 2 Diabetes" is out. Official publication date is November 1, but it seems to be shipping from Amazon now.

I'm now recommending that people with type 2 diabetes try a low-carb diet first, as it helps with both blood glucose control and weight loss, and they'll find less opposition from their health care team today than they would have in 2007, when the second edition was published. Then if for some reason the LC diet doesn't work for a particular person, that person can try other approaches. But the LC diet should be, as Richard Feinman says, "the default diet."

Other updates include discussion of the new drugs now available, insurance availability because of the Affordable Care Act, discussion of ketosis-prone diabetes (Flatbush diabetes), networking via social media, new sweeteners, and updated references. David Mendosa's chapter "Searching the Internet is completely new.

Saturday, October 10, 2015

Does Insulin Resistance Protect the Heart?

We think of insulin resistance as a bad thing. But could it sometimes be a good thing?

Christopher Nolan and colleagues think so. And some others agree.

These researchers argue that under conditions of "overnutrition," meaning eating more than your body requires, insulin resistance (IR) is a protective mechanism that keeps the heart cells from taking up too much glucose. We need glucose, but we also know that glucose can be toxic when it's present in excess.

However, we tend to think of blood glucose (BG) levels as being the only important factor. In fact, the glucose levels inside cells are also important. In general, when BG levels are high, the levels inside the cell are also higher than normal because of mass action. Hence the body has evolved a mechanism to protect some tissues, mostly skeletal and cardiac muscle, from taking up too much glucose when the BG levels in the blood are high. This is insulin resistance, and it means the extra energy is diverted to fat instead.

However, not all cells require insulin to take up glucose, and hence IR won't protect these tissues. Such tissues include the endothelial cells that line our blood vessels and may be one reason high BG levels contribute to vascular disease. Thus reducing BG levels when they're too high is essential for good health.

But how we reduce BG levels may also be important. Some treatments like the drug metformin reduce the amount of glucose the liver produces through gluconeogenesis and ships out into the blood. This should be beneficial.

Some drugs like the glitazones seem to increase the number of new and active fat cells, which can take fatty acids and glucose out of the blood. This reduces the BG levels but also can lead to weight gain.

However, other drugs like insulin, or the sulfonylureas that make us secrete more of our own insulin, overcome the IR and hence force more glucose into the muscle cells. This will reduce our BG levels and make us and our physicians happy. But in the long run, is it damaging the heart cells? That's what Nolan and colleagues argue. And it could be one reason that reducing BG levels doesn't have a huge effect on heart disease.

In other words, treatments designed to overcome what is believed to be the primary cause of type 2 diabetes (in addition to genetics) may not be the best for everyone. And research into new drugs that would reduce IR might not be as useful as research into other types of treatment.

Nolan and colleagues argue that such treatments are especially harmful for people with massive IR who require massive amounts of insulin to overcome it. And if this subset of patients are harmed by intensive treatment with IR-reducing drugs, then the results of clinical studies that included such patients would be unclear. Some patients would be helped and others would be harmed.

This could explain the results of the ACCORD trial, which some interpreted to mean that aggressive BG lowering was harmful. Later analysis showed that those who were harmed were those who got aggressive treatment but it wasn't effective. In other words, the harm caused by the drugs was not offset by the benefit of lower BG levels.

Unfortunately, the best approach, according to Nolan and colleagues, is to focus on the other cause of type 2 diabetes: overnutrition. This is not good news for those of us born with excessive appetites. It's very difficult to eat less when your body is screaming for more food. But it's one reason many people with huge appetites find that low-carbohydrate diets are useful. Such diets tend to reduce appetite because the high fat content slows down gastric emptying so you feel satisfied for hours after eating. This doesn't happen to everyone, but it does occur with most. It did with me.

Unfortunately, too many people diagnosed with type 2 diabetes want to be able to take a pill and continue to eat the standard American diet that everyone else eats. This may work in the short term, but Nolan and colleagues argue that such an approach causes harm in the long term.

What if a new drug that reduced IR to normal came on the market. Would I take it? I used to think this would be my dream drug, letting me eat like all my friends and neighbors. But now I'm having second thoughts. As so many research papers conclude, "More research is needed." Let's hope some of that research addresses the question of IR as harmful or protective.

Researchers don't routinely measure glucose levels inside cells, but technology is advancing so quickly that this might become feasible and affordable in the future. Also useful would be techniques for measuring IR in different tissues. For example, IR in fat would keep you thinner, but it would also reduce fat's ability to take up some of the excess glucose for storage as fat.

More research is needed.

Monday, October 5, 2015

Low Carbohydrate Diet and Fiber

A recent blogpost at Optimising Nutrition pointed out that it's difficult for some people to get enough fiber on low-carbohydrate diets. Many people do well on very low carb diets without added fiber, but some do not.

I thought it would be relevant to point out that the Four Corners Diet, previously the GO Diet, was designed to emphasize fiber as well as monounsaturated fats and low carbohydrate levels. The original name of the diet stems from the names of the two physicians who worked it out, Jack Goldberg and Karen O'Mara. They tried it on a small group of patients, with good results.

Back in the early part of this century, I felt the diet was the healthiest one out there for people with type 2 diabetes, so I worked with them to add some comments about the beneficial effect of the diet for type 2, and it was published as the Four Corners Diet, emphasizing low-carb, high-fiber, high-mono fat, and what we called pharmafoods, foods with health benefits beyond their macronutrients. These include fermented foods like yogurt or kefir as well as foods containing antioxidants, cancer-inhibiting compounds, phytoestrogens, and cholesterol reducers.

Goldberg was the first person to point out that yogurt and kefir have less carbohydrate than the milk from which they're made, and he even tested the carb count in yogurt and showed that you can subtract 1 gram of carb for every ounce, so a cup of milk, with about 12 grams of carbs, would result in only 4 grams of carbs in well-fermented yogurt and kefir. (The counts can vary a bit depending on when you stop the fermentation. Sour is best as it has the least amount of carbohydrate.)

Unfortunately, the book was published just as a low-carb trend had peaked and was coming down, so the book did not do well. However, that's a benefit for you, as you can now get a used copy for a penny plus shipping.

I still think the diet is the healthiest out there. And all the suggested menus include nutritional analysis of carbs, fiber, net carbs, and percentage mono fat. The suggested 7-day starting menus work up slowly to a lot of fiber, but by day 7 you'd be getting 28 grams of fiber, close to the recommended minimum unless you're a man under 50 years, in which case the minimum is 38 grams.

So if you want both low-carb and sufficient fiber, it would be worthwhile to look into this book.

Saturday, October 3, 2015

Is Insulin a Red Herring?

Yes, I know: Insulin is essential for life. People who don't produce enough insulin have to take insulin shots to stay alive. And by carefully matching their food with their insulin, they can live long and happy lives, albeit lives that are more difficult than those of people who don't need extra insulin.

However, controlling diabetes through diet and insulin -- even with the "artifical pancreas" that does some of the calculations for the patient --  is not enough for most people. We want a cure. Both type 1 and type 2: We want a cure.

What is a cure? Different people define cure differently. Some sellers of the "miracle cures" that you can find on the Internet seem to define cure as having lower blood glucose levels than you had when you started. Some people define cure as not taking any drugs, even though you might have to go on a strict low-carb diet in order to do so. Dr Richard Bernstein defines cure as having a normal glucose tolerance test. I agree with him.

There's certainly no lack of studies of insulin. I just searched PubMed, which showed almost 13,000 articles with insulin in the title published so far in 2015, and more than 30,000 papers about diabetes.

But we still don't have a cure.

Is it possible that because insulin is so important for diabetes, and essential for controlling it, it's drawing attention and research funding away from other compounds that might be less important for control but more important for prevention or cure?

Don't ask me what these compounds would be. If I knew I'd be famous. But some people feel that hormones like glucagon play a big role, and more and more are studying this hormone (about 1300 papers in 2015). How about somatostatin (621 articles), which inhibits the release of both insulin and glucagon, as well as having effects on other hormone systems?

It wasn't that long ago that we didn't know about leptin (identified in 1990s), which plays a large role in obesity. Could there be other yet-undiscovered hormones out there that would be the key to preventing diabetes and maybe even reversing it once it's manifest? Could the focus on the essential-for-life hormone insulin be blinding us to the effects if other, more obscure hormones?

I'm probably wrong, but it never hurts to wonder.

I'm Back

As of October 1, I am no longer blogging for Health Central, and I hope to use the increased time to revive this blog. I doubt that anyone is still reading it, but writing my thoughts down helps me to organize them, so I will try to do so.

I'm interested in new ideas, new ways of looking at type 2 diabetes, and new research, rather than flogging old ideas or getting involved in what I call Diet Wars. I think too many diet blogs tend to preach to the converted rather than trying to come up with new ideas that might help us all in the obesogenic diabetogenic environment in which most of us live.

Re diets: I believe strongly in low-carb diets for people with type 2 diabetes, but I also recognize that we all have different genes, different food preferences, different financial situations, and different family situations, and there are some patients for whom another diet might work as well. Nevertheless, I think the LC diet should be what Richard Feinman calls "the default diet." Unless there are strong reasons to start with something else, you start with a LC diet, and if that doesn't work for you, you can try something else.

Some people say no one can stick to such a diet for very long. I've been on one for almost 20 years, and Richard Bernstein for even longer than that. As I stack wood I'm listening to an audiobook about medical myths. He repeats this argument and suggests that to lose weight you should just "eat healthy." I don't know any overweight person who has managed to lose and keep the weight off by using such an approach. The people who use that approach are usually thin people who don't have diabetes.

In the next post I will discuss the idea that insulin resistance, as well as body fat, may be protective for our health.