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.

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.

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.

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.

The Glucagon Connection

Most of us understand the importance of insulin in controlling our blood glucose (BG) levels. When our BG levels get too high, we can bring them down by injecting insulin. Insulin is made in and secreted by the beta cells in the pancreas.

Many of us are also aware that another hormone, glucagon, helps bring BG levels up when they get too low. Glucagon is made in and secreted by the alpha cells in the pancreas.

In nondiabetics and people with type 2 diabetes or early type 1 diabetes, glucagon automatically gets secreted when BG levels get too low. But people with longstanding type 1 diabetes often stop producing much glucagon and need glucagon shots to bring up a serious low.

Insulin and glucagon are like the accelerator and brake on your car. And it's the ratio of the two, rather than the absolute amount, that is important. If you have almost no insulin, you might be able to have normal BG levels if you also had almost no glucagon.

In fact, a study done in 1981 in a man who had no pancreas, showed that BG levels could be maintained at about 100 without insulin as long as they didn't give the man glucagon.

The problem is that when the beta cells give out, the alpha cells don't give out as well. In fact, they often secrete even more glucagon than they would in a nondiabetic. Glucagon tells the liver to produce and secrete glucose, so the BG levels stay high even when you don't eat.

Most diabetes researchers focus on beta cells and insulin production, but some are studying the alpha cells and glucagon production as well. A recent study found that hyperglucagonemia (too much glucagon in the blood) actually precedes the decline in insulin secretion seen in diabetes.

These researchers infused rats with a lot of glucose for 10 days. After initial high BG levels, the rats adapted and maintained normal BG levels for 4 days. But then their BG levels started to go up, and by 10 days 89% of the rats had high BG levels.

This isn't surprising. The traditional view is that coping with a lot of glucose and producing a lot of insulin can "exhaust" the beta cells; this is called glucotoxicity.

But the researchers found that the rats weren't producing any more insulin than normal. Instead, their glucagon levels increased fivefold. Thus endogenous glucose production, production of glucose by the liver, was what was making the BG levels go up. And infusing them with anti-glucagon antibodies made their BG levels return to normal.

That is surprising.

The authors conclude that glucotoxicity may first manifest as alpha cell malfunction, before any deficit in beta cells and insulin secretion is seen. This is a new way of looking at how diabetes procedes.

A few months earlier, another paper showed that glutamate (or glutamic acid), an important neurotransmitter in brain and pancreas, is secreted from alpha cells along with glucagon. The glutamate contributes to beta cell destruction; it doesn't affect the alpha cells.

Hence, if you're secreting more glucagon, you'd also be secreting more glutamate, thus accelerating beta cell loss and insulin production when you needed more to oppose the extra glucagon.

The authors also found that the protein GLT1 (glial glutamate transporter 1) could protect the beta cells, and they are working on finding other beta-cell-protective compounds.

Neither of these discoveries will result in an instant cure for type 2 diabetes. The first was done in rodents, and the second was done in isolated human cells. Before they can be translated into actual diabetes treatments, they'd have to be replicated in humans, not isolated cells or rats, and treatments that turned down the alpha cells would have to be developed.

However, for decades, researchers have been studying how type 2 diabetes evolves, and they're still not sure. Of course it's all terribly complex. But is it possible people are looking in the wrong places? Maybe it's time for some new ways of looking at an old problem.

Focusing on the alpha cells is one such approach. Let's hope this work continues.

Closed Minds

I follow a low-carb (LC) diet to help control my type 2 diabetes. I can understand that this approach is very difficult for some people, and some with relatively mild type 2 can control despite eating more carbs.

But I'm always amazed at the closed-minded comments I often see in blogs of anti-low-carbers. Here's one, commenting on a photograph of a LC breakfast posted with a blog:

"There's nothing on the plate that I consider breakfast food."

The photograph seems to show bacon, ham, eggs, sausage, tomato, and mushroom.

I wonder why the poster feels that he needs special foods for breakfast. And apparently that special "breakfast food" should have a lot of carbohydrate, and little protein. That makes no sense. Most people are more insulin resistant at breakfast, and many studies have shown that blood glucose levels rise more after breakfast than after other meals. So if you feel a need for a daily allotment of orange juice, skim milk, toast, jam, and cereal, it would make more sense to eat it for supper, not breakfast.

Of course, this poster is not alone. Many people have irrational prejudices about "breakfast food." For instance, most Americans think bacon and ham are OK for breakfast. But if you say you had chicken or lamb chops, they'll think you're odd. Most Americans would consider Danish pastry or toast and jam to be suitable breakfast food. But if you say you had cheesecake or blueberry pie, they'll think you're odd.

What's the difference? Bacon, ham, chicken, and lamb are all meats. Danish, toast and jam, cheesecake, and blueberry pie are all sweetened starches.

It was the Kellogg brothers at the turn of the 20th century who pushed dry "breakfast cereals," at first primarily corn flakes, on the American public. At that time, rich people tended to eat meat and eggs for breakfast. Poor people ate starches, often boiled into porridge. Farm breakfasts tended to include a little of everything: meat, eggs, milk, pancakes, potatoes, breads, and pies. The farmers needed a lot of energy when facing long hours of backbreaking work and tended to eat the lighter meals like cereal in the evening.

By now, several generations of Americans have grown up thinking that breakfast has to include a dry cereal, often sweetened, and milk. But why do we have to mindlessly accept that there should be special "breakfast food"? We're smarter than that, aren't we?

In the rural area where I live, most people still conform to older patterns of eating. But in urban areas, it seems people are getting more creative with their meals, as described here. (The trend toward daylong snacking does not sound healthy, however, as commercial snacks are usually highly processed.) Nevertheless, the reporter reveals his underlying bias when he refers to eating nontraditional meals as "weird."

When we have diabetes, we need to eat the foods that keep our blood glucose levels down, whether they're considered "breakfast food" or "lunch food" or "dinner food." We can't let old patterns get in the way.

Lamb chops and broccoli for breakfast anyone?