Friday, November 10, 2017

It's the Patient's Fault: Not

A lot of doctors don't understand how difficult it is to make major lifestyle changes of the sort that most everyone agrees will help to control type 2 diabetes. "Lose weight!" they'll say, although you may have been trying to lose weight for most of your life and not succeeding. "Get more exercise!" they'll say, even if you've been going to the gym religiously every day.

But one doctor is trying to teach medical students how difficult it is to be a type 2 diabetes patient. In  an editorial in Clinical Diabetes, Stephen Brunton describes how he tried to train medical students by asking them to give up something they loved for just one month. Just one month! Only 2 of the 40 who took part were able to comply. That means 95% failed.

Yet physicians and other medical people routinely tell diabetes patients to give up certain foods or certain behaviors not for a month, but for the rest of their lives. Is it surprising that many don't succeed?

Of course, not everyone says to newly diagnosed patients that they'll never be able to eat a doughnut again, but it's implied when they are told to eat a turkey sandwich on whole-grain bread and an apple (the favorite of nutrition writers) instead of the burgers and fries and pie that they love.

Brunton's approach isn't going to make being a type 2 diabetes patient easy. But I think patients are more apt to work with health care people who understand the problems. "Lose weight" isn't useful. Better would be to suggest keeping a food log and then looking for ways to cut back on unhealthy foods.

I once met a health care worker from Missippi who was making a booklet designed to help overweight people lose weight. She had a "before" photo of a big burger and a big order of fries, the meal taking up the whole plate. Then the booklet had a photo of what the patient should eat instead: a tiny burger and three fries, most of the plate empty. But to anyone with a huge appetite who has always eaten huge meals, a tiny burger and three fries would seem like a punishment. And they'd still be hungry. She apparently didn't understand what it was like to live with a huge appetite.

I wondered if it would work better to show a big burger without the bun and a huge mound of green beans, or some other vegetable that the patient enjoyed. That way, the meal would still take up the whole plate and would also take up room in the stomach, helping to dampen hunger.

Whatever, I think if more physicians tried to look at the problems of living with diabetes from the point of view of the patient rather than just wondering why the patients didn't improve, we'd see more progress.

"She just won't lose weight." Maybe she can't. Maybe there's something wrong with her appetite control so she's ravenously hungry all the time. It's almost impossible to not eat when you're ravenously hungry.
"He doesn't exercise." Maybe he works two jobs and commutes for two hours and just doesn't have the time or energy for formal exercise.
"I doubt that he takes his meds." Maybe he can't afford them.

Feeling that your physician understood your struggles would help a lot more than just being told to do this and give up that. No one really understands how difficult it is to live with diabetes unless it happens to them, but at least Dr Brunton is trying. Let's hope his editorial motivates some physicians to change their approach.







Thursday, November 2, 2017

Whole Grain Spinning

It's interesting how news reports of nutritional studies can spin the results, probably without the authors realizing that's what they're doing.

Take a recent report titled "Several reasons why whole grains are healthy." Now, you see a headline like that and you're apt to think "Whole grains good" and you might eat more of them, increasing your carbohydrate consumption.

Yet the article might just as well have well been titled "Several reasons why processed grains are not healthy." In that case you would be apt to think, "Processed grains bad" and eat less of them. Instead,  you might eat more whole grains, or you might eat more fish or broccoli or beef or whatever. And if you have diabetes, the latter would be more beneficial for your blood glucose levels.

The study I cited took 50 adults at risk of cardiovascular disease or diabetes and had them substitute whole grains for the processed grains they usually ate. They found that doing so reduced the amount of inflammatory markers in these adults.

I have no problem with the study or the results. Just with the way it's spun.


Wednesday, October 18, 2017

Controlling Weight

Controlling weight is affected by so many physiological factors it's sometimes difficult to keep track. Before 1994, when leptin was discovered, people thought weight control was simply a matter of willpower. Now we know better.

Most of us know that leptin is secreted by fat cells when we have had enough to eat and the fat cells are full, and the leptin turns down our appetite. Children born without leptin have voracious appetites and become obese as toddlers; when given leptin, they slim down. People with no leptin are rare, but overweight people may have leptin resistance, just as people with type 2 diabetes have insulin resistance. In both cases, levels of the hormones can be high but the body doesn't respond to them properly.

On the other hand, the hormone ghrelin is produced by the stomach when we haven't eaten, and it makes us hungry.

Now a third hormone has been discovered that increases appetite during fasting and decreases it during feeding. It has been named neurosecretory protein GL, usually referred to simply as NPGL.
This hormone not only affects appetite, but it also increases the storage of fat, even on a low-calorie diet.

Another study found a gene with the snappy name GTRAP3-18 that helps to regulate both food intake and glucose levels. Mice without this gene were both lean and hypoglycemic, and this was due to neither less activity nor an increased metabolism, but rather to eating less. The authors suggested that the gene could be a target for drugs, saying, "Eating too much or too little could actually be a genetic problem," although we know that other factors such as emotions and the food environment can play a role as well.

A third study found yet-another protein with a snappy name, MKK6, that affects weight by stimulating the burning of fat to generate heat. Overweight people seem to have higher levels of MKK6, which hinders the conversion of white fat cells into brown fat cells. White fat cells store fat, and brown fat cells burn fat.

A fourth study described brain cells called tanycytes that detect nutrients and tell us when we've eaten enough. Foods high in certain amino acids (the building blocks of protein) activate the tanycytes and make us feel full sooner, which is consistent with the commonly stated fact that protein is satiating. Interestingly, the receptors in the tanycytes are the same as those in the tongue that detect the umami flavor of protein foods.

The two amino acids that react the most with the tanycytes are arginine and lysine. Foods rich in these amino acids include pork shoulder, beef sirloin, chicken, mackerel, plums, apricots, avocados, lentils and almonds.

Finally, a Swiss study showed that severely obese people release fewer satiety hormones than people of normal weight because they have fewer of the intestinal cells that produce the satiety hormones than normal-weight people. Weight-loss surgery seems to increase the number of these cells.

We all know that weight loss, and especially maintenance of weight loss, is difficult. One reason is that there are so many factors involved (and I'm sure even more will be found in the future), and different people may have deficits in different systems.

In fact, an Israeli study showed that the glycemic index of various foods could vary a lot between individuals. A food that was problematic for one person might be fine for another. And for some individuals, even white bread seems to be better for blood sugar levels than whole grain bread.

Even the bacteria in your gut may affect whether or not you will lose weight on a diet with a lot of fruits, vegetables, fiber, and whole grains, according to a Danish study. So if some recommended diet doesn't work for you, it may not be that you're "doing it wrong." It may be that the diet isn't the right one for you.

What this all means is that it's up to us to take charge and find out which diets are best for our personal physiology. It's a lot more work than simply following guidelines set by some "diet expert." But it's worth the effort.

And it's encouraging that so much research is going into what factors govern appetite and fat gain or loss. In the long run, this basic research should lead to real solutions. Let's hope funds for basic research aren't cut any more in a misguided effort to save money. In the long run, figuring out the best way for people to lose weight and keep it off will save even more money from health care expenses than the costs of the research.

Wednesday, August 30, 2017

Information overload

One of my favorite cartoons, which I have pasted on my desktop computer, shows a man with a little beach pail standing on a beach while a huge wave (which looks like the woodcut "Great Wave Of Kanagawa" by Katsushika Hokusa) is about to break over him. The man is saying, "Eureka! More information."

(I can't show the cartoon here because it's copyrighted. I was going to link to the author Ted Goff's page, but he's apparently updating his website and the links don't work for now.)

This cartoon illustrates how I feel about science news these days. I get about 150 Eurekalert science press releases every day, as well as the tables of contents from a lot of journals. And it seems as if just as some fact is generally accepted, a paper comes out refuting that fact.

Also, science research is getting much more technical these days. Unless a study is commissioned by some commercial group like the the California Walnut Commission, which funds a lot of studies showing the health benefits of walnuts when some of those benefits might be found by eating similar nuts, people no longer tend to publish simple studies saying that factor X increases or decreases diabetes symptom Y. Instead the authors (often 20 or more) drill down to the molecular level and try to show that factor X increases or decreases the level of numerous cell factors that govern gene expression or hormone activity.

Unless the reader has a background in biochemistry or molecular biology, I figure the reader probably wouldn't understand these studies (sometimes I don't either), so there's no point in discussing them.

Also,  unless I think there's a major flaw in the evidence, I see no need to link to a study that has been picked up by all the news media, something like "Eating pickles and figs will make you lose 10 pounds in a week." You'll most likely see that study on the TV news anyway.

All this is a way of explaining why I'm not blogging much at the moment. But I haven't disappeared. I continue to try to keep up with new research developments, and when something both interesting and comprehensible by the average reader comes out, I'll let you know.

Hang in there. I'm trying to.

Tuesday, August 29, 2017

Is Childhood Obesity Psychological?

"Is Childhood Obesity a Psychological Disorder?" says a headline in a press release from Children's Hospital Los Angeles.

Now, many people get their information from headlines and don't read the articles. Also, a headline with a question mark suggests that the answer is Yes. If it were no, it wouldn't usually be newsworthy, akin to asking if childhood obesity were related to the name of the child's kindergarten teacher.

So this headline suggests that childhood obesity is a psychological disorder, and although there are many definitions of "psychological," a common one is "it's all in your head," meaning it's not a real disorder, and suggests that these kids are emotionally unstable and could become thin if they really wanted to.

In fact, the article focussed on brain scans of overweight or obese and normal-weight adolescents. They found that after showing the adolescents words describing various kinds of food, although the brains of all the participants were stimulated in areas that support reward and emotion, the overweight/obese ones had less activity in brain areas that support attention and self-regulation. I'd call this a brain disorder, not a psychological disorder.

As you might expect, when offered a buffet after the testing, the overweight/obese adolescents ate more than the lean ones.

This study is interesting, but I think the headline reflects an unconscious bias against fat people, suggesting that fat children have psychological problems. If the brains of overweight people are indeed different, we should try to figure out why they're different and then figure out how to normalize them.

I'm sure there are some overweight people who overeat because of psychological traumas. But there are others who overeat because they have differences in their hunger sensations, for example the rare children who lack leptin. And there are others who don't actually overeat but have metabolisms that are superefficient at converting food into fat.

It would be nice if all weight problems had only one cause so it would be easy to fix, but that's not the case. Until we have the solutions, we should at least stop stigmatizing overweight people and instead help them heal.





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Monday, July 24, 2017

When to Measure Postmeal Glucose Levels

What's the best time to test your blood glucose (BG) after meals?

Of course that depends on what you want to learn from testing after meals. If you want to know the after-meal peak, then you should test about an hour after you eat. The peak will differ a bit with different foods; fats slow down gastric emptying, and liquids pass through faster than solids. It also can differ with different people.

So if you want to know where your own peaks are, you should test every 15 minutes or so starting about 45 minutes after eating and continuing until the numbers start coming down.

If you want to know if you're able to return to normal, or close to normal, BG levels within a few hours, then you should test at 2 or 3 hours.

"After eating" is also ambiguous. Should you test X minutes after you start to eat or after you stop eating? Again, it depends on your habits. If you wolf your meal down, it doesn't much matter. If you eat leisurely and take 30 minuts to finish a meal, then it does. What you really want to know is differences between different meals, so the important thing is to test about the same way every time. Don't compare one meal you ate in 4 minutes with another one that you took an hour to finish. Most people measure the time after starting to eat.

If you ask CDEs or your doctor when to test, they'll usually tell you to test at 2 hours. This is because most research papers about postprandial (after meal) BG numbers use the 2-hour reading. But this may not be the best.

One researcher, Antonio Ceriello, recently published a paper proposing that it's time to switch to a one-hour postprandial measurement. He kindly sent me a copy of the full text of the paper.

Ceriello says that there's evidence that the one-hour measurement has even stronger power than the two-hour measurement for identifying impaired glucose tolerance. He said this number is also related to the risk for cardiovascular complications. In vitro experiments have shown that just one hour of high BG levels is enough to cause endothelial dysfunction that can then lead to coronary vascular disease, as well as reactive oxygen species (strong oxidants), he said.

Endothelial function is worse at one hour than at two hours both during oral glucose tolerance tests and after meals, he said.

If all this isn't enough, Ceriello said short-term high BG levels can impair beta-cell function.

When I've measured BG levels in nondiabetic friends and relatives, I've sometimes found one-hour readings of 160 or so, but the numbers come down to baseline by two hours. Testing only at two hours wouldn't identify these people, who might be at risk of developing diabetes in the future.

Ceriello's recommendations apply to clinical studies, but there's no reason you couldn't measure at one hour if you so chose. The best, of course, would be to measure at both one hour and two hours if you could afford enough strips. Then you'd know which time made most sense for you.

Even if most clinicians accept Ceriello's recommendations, it will take time before they become standard. So for now most studies will continue to use the two-hour numbers. But when  you see a study mentioning postprandial (or postmeal) numbers in the future, you should check to see what they mean, if you can (abstracts may not specify).

If anyone wants references to the studies Ceriello was citing, let me know and I'll send them to you. If I get tons of requests, I'll just edit this post to put the links in.

Saturday, July 8, 2017

Of Mice and Humans

"New Research Describes the Differences Between Mice and Humans" screams a headline of an article in Eurekalert. 

Golly. I guess I'm ahead of my time because I've known the differences between mice and humans for decades. The mice are the furry ones with long tails, and the humans are the larger ones who fight and kill each other because they don't agree on politics or religion.

But once you get past the headline on Eurekalert, you find that researchers are finally accepting that mouse research often doesn't translate into human treatments. Mice have been cured of diabetes hundreds of time, but the drugs the researchers used just don't seem to work when they try them on humans. 

The problem is that it would be unethical to try new drugs on humans without some evidence that they might do something beneficial. Mice are relatively cheap to maintain, and we already know a lot about them. If we used only larger animals like pigs or dogs or monkeys, the cost of research would be even higher than it is now, and animal rights groups would protest. Very few people object to mistreating rodents.

Now researchers are beginning to find out why mouse research doesn't always translate into human cures. These researchers looked into a class of receptors found on beta cells in both mice and humans. They are called G-protein-coupled receptors (GPCRs), but the names don't matter.

What they found was that some of these receptors are found in both mice and humans, but others are not. Some are found only in mice, and others are found only in humans. If they know which ones are found in both mice and humans, future researchers can limit their research to those receptors. There's no point in spending millions of dollars on some drug that affects a receptor found only in mice! That money could instead be used to study drugs that affect both species.

Of course not all drugs target GPCRs. But a large number do. Let's hope these findings channel research into fruitful drugs, and not duds.