Diagnosing diabetes is a lot like trying to sculpt warm Jell-O.
At the extremes, it's pretty easy to decide if someone has diabetes or not. For example, when I was diagnosed, I was having symptoms (constant thirst and urinating a lot), my random blood glucose (BG) level was over 300 mg/dL (to convert to mmol/L divide by 18) hours after my last meal, and my next-day fasting was 269. The glucose level in my urine was so high that the hospital recalibrated its machine to make sure the result was correct.
Clearly, I was diabetic.
At the other extreme, someone with a fasting BG level of 65 who goes up to 80 after drinking a huge glucose drink and has a hemoglobin A1c level of 4.2 obviously doesn't have diabetes.
In between the extremes, there are a lot of patterns that could or could not be considered to be diabetes.
The official guidelines for diagnosing diabetes are that you should be considered diabetic if
Your fasting BG level is 126 or greater on at least two occasions (less than 100 is considered normal) or
Your BG level is 200 or greater 2 hours after starting an oral glucose tolerance test (OGTT) with 75 grams of glucose (less than 140 is considered normal) or
A random BG level is greater than 200 and you're having symptoms.
Recently, some official diabetes groups are suggesting using the hemoglobin A1c test for diagnosis, with any result of 6.5 or greater confirmed by a second test considered diagnostic.
Some years ago, the diagnostic fasting levels were even higher, as some diabetes experts felt that a diagnosis of diabetes would cause harm because of the stigma against "diabetics" and because insurance companies would refuse to insure them. More recently, people have realized that diabetic complications occur even at BG levels below these diagnostic values, and the earlier people are diagnosed, the greater their chance of preventing complications.
However, regardless of where the cutoff points are set, none of these criteria are perfect. Anyone with diabetes knows that fasting BG levels can vary from day to day, and even testing fasting levels on two different days doesn't ensure that they represent a true value.
The same may be true of the OGTT. We all know that we can eat exactly the same thing on two different days at exactly the same time and get exactly the same amount of exercise, yet one day our postprandial BG levels will be higher than the other. Furthermore, because this test is time consuming, very few physicians use it for diagnosis.
And the A1c test is affected by a lot of things, including red blood cell lifetime, which can be genetic and is also affected by various hemolytic anemias, spleen damage, or major blood loss; and abnormal hemoglobin types. Furthermore, although most labs now claim to have standardized their A1c tests, in practice there's still variation from one lab to the other.
Hence one person might have normal BG levels all day long but have an abnormal A1c result, and another person might have elevated BG levels yet have a low A1c. I know someone who had fasting BG levels above 130 but an A1c in the 4s so her doctor refused to diagnose her until things got much worse.
To further complicate things, there are various different patterns of BG abnormalities. Some people may have normal fasting BG levels but go high after meals (this was formerly called impaired glucose tolerance). Others may have high fasting levels but not go very high after meals (this was formerly called impaired fasting glucose).
Some years ago official diabetes groups decided to merge both groups into a new category called prediabetes even though some people think their risks and outcomes differ.
These aren't the only patterns one can get. Some people may have a little impaired glucose tolerance and a little impaired fasting glucose.
Some may have normal fasting BG levels, go very high after meals, but come down again quickly, so they wouldn't satisfy the official requirement for high BG levels at 2 hours after an OGTT. This and this show the variation in BG levels after a high-carb breakfast in people considered nondiabetic.
But no one knows if such wide variations in BG levels might cause complications. Some people think wide variation is worse than sustained high BG levels. Yet the people shown in the cited graphs are considered nondiabetic. Their A1c levels are in normal ranges.
Other people may have temporary increases in BG levels because of some stress, such as surgery or emotional stress, and then revert to normal BG levels.
Diet can also affect your BG levels. Someone following a low-carb diet for weight loss might have normal fasting and postprandial BG levels and normal A1c levels as long as he or she followed the LC diet. An OGTT would show the underlying diabetic defect, but most doctors don't use that test these days, especially in someone with normal fasting BG levels. And these people would be grouped with the nondiabetics if they were included in any clinical trials.
Just fasting can affect your BG levels. Fasting is the ultimate low-carb diet, and after a long fast you'll test diabetic even if you're not on a standard carbohydrate-containing diet because when you don't need them, your body stops producing carbohydrate-processing enzymes. This is called starvation diabetes.
If you've been on a very low carb diet and you're given an OGTT, you'll probably test diabetic even if you're not, for the same reason.
Some people may have abnormal BG levels because of very high insulin resistance, which can sometimes be reversed with weight loss and exercise. They also have defective beta cells that aren't able to cope with the excess demand. But if they can reduce the insulin resistance, their beta cells can cope. Many overweight couch potatoes don't have diabetes because their beta cell mass simply expands to cover the increased need.
The same situation occurs during pregnancy. In most people, the beta cell mass expands during pregnancy to cover the increased need in late pregnancy. Some people have beta cells that are unable to do this, so they are diagnosed with gestational diabetes. After the baby is born and the demand is lowered, their BG levels revert to normal.
Others may have abnormal BG levels with a lot less insulin resistance and but even wimpier beta cells. And of course there can be all kinds of combinations of these two factors.
If diagnosing diabetes is difficult, diagnosing prediabetes is even more difficult because someone with full-blown diabetes like I had when I was diagnosed is unlikely to revert to normal no matter what they do. At that point we've lost so many beta cells that unless we figure out how to get them to regenerate, we're always going to have to be careful about our diet.
But in the prediabetes range, the probability of reverting to normal BG control is greater, especially if you're very overweight and hence are still producing a lot of insulin when you're diagnosed. Thus a diagnosis may be more vague. One month you'd qualify as prediabetic and then you'd lose some weight and you wouldn't. Then you'd regain the weight and you would.
Because of all this diagnostic vagueness, arbitrary cutoff points, and changing standards, any studies that purport to show that "diabetics" are at increased risk or decreased risk or should be taking X drug or avoiding Y practice are somewhat questionable. The older the study, the less relevant it's likely to be. In the old days they didn't even differentiate between type 1 (autoimmune; insulin requiring) and type 2.
I personally don't put a lot of trust into studies that rely on complex statistics to show some effect. You can study 10,000 patients with type 2 and show that there's a slightly better, statistically significant benefit from some treatment (usually a drug). If you're a physician interested in prescribing that drug, that suggests that the odds of success are greater if you prescribe it. (Not taking into account the biases caused by the fact that most drug studies are sponsored by drug companies that know how to manipulate data.)
But it says nothing about whether the drug will help or harm any individual patient. And as patients, that's what we want to know.
Does that mean we should simply ignore all these massive trials? I don't think so. They do tell us something; they suggest that some treatment could help or harm.
But if your doctor tells you that all "diabetics" should be taking some drug or avoiding some drug or following some other regimen and you don't think it sounds "right for you" as the TV ads are so enamored of saying, then research it carefully.
Find out if the patients in the study sound similar to you. If they were mostly elderly white men on low-fat diets and you're a young Asian woman on a low-carb diet, you might respond differently than those patients.
Diabetes comes in many flavors. Diagnosis can be arbitrary. Statements like "All diabetics should be on aspirin" are unlikely to be true, even if supported by references to some big clinical trial.
Wednesday, February 2, 2011
Sunday, January 23, 2011
Cholesterol, CVD Risk, and Type 2
Deciding whether or not to use a statin to reduce cholesterol levels can be confusing.
On one hand is the medical profession, which in general thinks statins are good things and that LDL cholesterol levels above normal ranges should be treated with statins. Recently, some have been recommending statins even for people with normal cholesterol levels but elevated levels of C-reactive protein (CRP), an indication of inflammation.
In some populations, lowering cholesterol with statins has been shown to result in lower rates of cardiovascular "events" and deaths. But some people think this isn't because of lower cholesterol levels. They suggest that the statins have some other effect as well and the lower cholesterol levels are simply a "side effect" of the drug.
At the other extreme are people who think statins are poisons. Some think no one should take a statin. Others agree they're warranted in specific populations, for example middle-aged men with previous heart attacks, but they say there's no evidence that statins help women or elderly men.
A recent Cochrane Systematic Review concluded that risks of statins are greater than benefits for those at low risk of heart disease. However, when you have diabetes, you're not considered to be at low risk.
An earlier study concluded that statins don't benefit women who have not had a heart attack and in fact may increase cardiovascular risk in this population. They say CRP levels are better predictors of heart attacks in women.
Most people agree that statins do have side effects, most commonly muscle weakness or pain, which can cause permanent damage if it's serious (rhabdomyolysis). In mild cases, taking coenzyme Q10 can sometimes help with the muscle weakness. Tendons can also be weakened by statin treatment (and treatment with other drugs like niacin that reduce cholesterol).
Beatrice Golomb of the University of California at San Diego has been studying side effects of statins and has published a comprehensive review on the topic. She says the two most common side effects are muscle weakness or pain and memory impairment.
She agrees that statin benefits outweigh risks in middle-aged men with high cholesterol and existing heart disease who tolerate the drugs, and that statins probably benefit middle-aged men with high cholesterol and "significant other risk factors for heart disease."
But she says that although those without significant risk factors for heart disease do have fewer cardiovascular deaths, there is not even a trend for lower overall death rates. In other words, fewer heart attacks and strokes but more deaths from other diseases.
Golomb says that statin benefits are not clear in middle-aged men who have heart disease or significant risks but who get side effects from statins. There is some evidence that the benefits of statins don't occur in people who get side effects.
Golomb says there is currently no evidence that statins benefit women or men over 70. They do reduce heart attacks, she says, but not overall mortality.
One problem when reading about all these studies is that different studies use different patient populations and different end points, but the news media tend to report the results without emphasizing that point.
So a drug-company-sponsored trial might be headlined as "Drug X Reduces Heart Attacks by 40%" when in fact the study showed that the drug reduced heart attacks in middle-aged men who had already had several heart attacks, had high blood pressure and high blood sugar, and smoked, and the deaths from some other disease increased with the drug. But what the public, and some physicians, will remember is "Drug X prevents heart disease."
And the confusing thing for those of us with diabetes is knowing whether or not simply having diabetes constitutes a "significant other risk factor."
Most people consider simply having diabetes to give you the same risk of cardiovascular events as people who have already had a heart attack. Is that true?
A recent Spanish research group says no, at least in the Spanish patient population they studied: 4410 patients aged 30 to 74 years, 2260 with type 2 diabetes and 2150 who had already had an acute myocardial infarction but no diabetes.
They found that the 10-year hazard ratios for the type 2 patients were significantly lower than those of the MI patients.
That's encouraging. So should we stop worrying about heart disease?
Definitely NO!
For one thing, other studies have had conflicting results. Some show that people with diabetes have heart disease death risks similar to those of nondiabetics who have had heart attacks; others show the opposite. Another study showed that prior heart attacks resulted in higher risks than diabetes among men 45 to 54 years old, but in older men, the risk was reversed.
As noted by the Spanish researchers, "Part of the discrepancy may stem from differences in the duration of diabetes, type of treatment, and baseline glucose control of diabetic patients included in the studies."
The cited studies also noted differences according to the age and sex of the patients. Furthermore, the results may depend on how you define diabetes.
Someone with type 2 diabetes who was diagnosed 5 years ago, controls blood glucose levels well, eats healthy foods, gets a lot of exercise, doesn't smoke, and makes sure to keep blood pressure and lipid levels in good ranges would be different from someone who is unfortunately probably more typical: a patient who just takes a pill or two, doesn't measure blood glucose levels, continues to smoke and spend most of the evening watching TV, eats mostly fast food or convenience foods, and has high blood pressure.
And the recent Spanish study was comparing diabetic patients with patients who had already had an acute MI, not with healthy people.
When we have type 2 diabetes, we're still at increased risk of heart disease, and we should do whatever we can to reduce that risk: Keep blood glucose levels down, monitor lipid levels and treat if necessary, monitor blood pressure and treat that if necessary, get regular exercise, and eat a healthy diet, although definitions of "healthy diet" of course depend on who you're talking to.
But all these studies illustrate the need to be vigilant when reading a popular press article stating that some study has shown something or other. First, see if you can read the journal article that the popular press story refers to. Even if you can't see the full text, you can usually see the abstract for free.
Find out what populations were studied, how various parameters were measured, and how the researchers define diabetes.
This takes a lot of time, and a firm grasp of statistics helps. So it can be frustrating when you're trying to earn a living or spend time on other projects and don't have time to pour through confusing research reports all day.
Sometimes the authors of drug-company-sponsored studies have used statistics to spin the results to make their drugs look more favorable. You sometimes need to comb through the methods and the statistics to see how the results have been biased. This takes a lot of time.
When you can't track all this down, don't ignore the health news, but take the health news you hear on TV or read in your local paper with a grain of salt. If your LDL cholesterol level is high, you might want to try a statin. Some people can take them without getting side effects. But be vigilant. If you get muscle weakness, try some coenzyme Q10, which Golomb says helps about 70% who have that problem. Some people recommend taking the coenzyme Q10 even if you don't have muscle problems.
But if the muscle pain or weakness persists, talk with y0ur doctor about other alternatives, like niacin. Muscle pain that progresses to rhabdomyolysis is serious.
On one hand is the medical profession, which in general thinks statins are good things and that LDL cholesterol levels above normal ranges should be treated with statins. Recently, some have been recommending statins even for people with normal cholesterol levels but elevated levels of C-reactive protein (CRP), an indication of inflammation.
In some populations, lowering cholesterol with statins has been shown to result in lower rates of cardiovascular "events" and deaths. But some people think this isn't because of lower cholesterol levels. They suggest that the statins have some other effect as well and the lower cholesterol levels are simply a "side effect" of the drug.
At the other extreme are people who think statins are poisons. Some think no one should take a statin. Others agree they're warranted in specific populations, for example middle-aged men with previous heart attacks, but they say there's no evidence that statins help women or elderly men.
A recent Cochrane Systematic Review concluded that risks of statins are greater than benefits for those at low risk of heart disease. However, when you have diabetes, you're not considered to be at low risk.
An earlier study concluded that statins don't benefit women who have not had a heart attack and in fact may increase cardiovascular risk in this population. They say CRP levels are better predictors of heart attacks in women.
Most people agree that statins do have side effects, most commonly muscle weakness or pain, which can cause permanent damage if it's serious (rhabdomyolysis). In mild cases, taking coenzyme Q10 can sometimes help with the muscle weakness. Tendons can also be weakened by statin treatment (and treatment with other drugs like niacin that reduce cholesterol).
Beatrice Golomb of the University of California at San Diego has been studying side effects of statins and has published a comprehensive review on the topic. She says the two most common side effects are muscle weakness or pain and memory impairment.
She agrees that statin benefits outweigh risks in middle-aged men with high cholesterol and existing heart disease who tolerate the drugs, and that statins probably benefit middle-aged men with high cholesterol and "significant other risk factors for heart disease."
But she says that although those without significant risk factors for heart disease do have fewer cardiovascular deaths, there is not even a trend for lower overall death rates. In other words, fewer heart attacks and strokes but more deaths from other diseases.
Golomb says that statin benefits are not clear in middle-aged men who have heart disease or significant risks but who get side effects from statins. There is some evidence that the benefits of statins don't occur in people who get side effects.
Golomb says there is currently no evidence that statins benefit women or men over 70. They do reduce heart attacks, she says, but not overall mortality.
One problem when reading about all these studies is that different studies use different patient populations and different end points, but the news media tend to report the results without emphasizing that point.
So a drug-company-sponsored trial might be headlined as "Drug X Reduces Heart Attacks by 40%" when in fact the study showed that the drug reduced heart attacks in middle-aged men who had already had several heart attacks, had high blood pressure and high blood sugar, and smoked, and the deaths from some other disease increased with the drug. But what the public, and some physicians, will remember is "Drug X prevents heart disease."
And the confusing thing for those of us with diabetes is knowing whether or not simply having diabetes constitutes a "significant other risk factor."
Most people consider simply having diabetes to give you the same risk of cardiovascular events as people who have already had a heart attack. Is that true?
A recent Spanish research group says no, at least in the Spanish patient population they studied: 4410 patients aged 30 to 74 years, 2260 with type 2 diabetes and 2150 who had already had an acute myocardial infarction but no diabetes.
They found that the 10-year hazard ratios for the type 2 patients were significantly lower than those of the MI patients.
That's encouraging. So should we stop worrying about heart disease?
Definitely NO!
For one thing, other studies have had conflicting results. Some show that people with diabetes have heart disease death risks similar to those of nondiabetics who have had heart attacks; others show the opposite. Another study showed that prior heart attacks resulted in higher risks than diabetes among men 45 to 54 years old, but in older men, the risk was reversed.
As noted by the Spanish researchers, "Part of the discrepancy may stem from differences in the duration of diabetes, type of treatment, and baseline glucose control of diabetic patients included in the studies."
The cited studies also noted differences according to the age and sex of the patients. Furthermore, the results may depend on how you define diabetes.
Someone with type 2 diabetes who was diagnosed 5 years ago, controls blood glucose levels well, eats healthy foods, gets a lot of exercise, doesn't smoke, and makes sure to keep blood pressure and lipid levels in good ranges would be different from someone who is unfortunately probably more typical: a patient who just takes a pill or two, doesn't measure blood glucose levels, continues to smoke and spend most of the evening watching TV, eats mostly fast food or convenience foods, and has high blood pressure.
And the recent Spanish study was comparing diabetic patients with patients who had already had an acute MI, not with healthy people.
When we have type 2 diabetes, we're still at increased risk of heart disease, and we should do whatever we can to reduce that risk: Keep blood glucose levels down, monitor lipid levels and treat if necessary, monitor blood pressure and treat that if necessary, get regular exercise, and eat a healthy diet, although definitions of "healthy diet" of course depend on who you're talking to.
But all these studies illustrate the need to be vigilant when reading a popular press article stating that some study has shown something or other. First, see if you can read the journal article that the popular press story refers to. Even if you can't see the full text, you can usually see the abstract for free.
Find out what populations were studied, how various parameters were measured, and how the researchers define diabetes.
This takes a lot of time, and a firm grasp of statistics helps. So it can be frustrating when you're trying to earn a living or spend time on other projects and don't have time to pour through confusing research reports all day.
Sometimes the authors of drug-company-sponsored studies have used statistics to spin the results to make their drugs look more favorable. You sometimes need to comb through the methods and the statistics to see how the results have been biased. This takes a lot of time.
When you can't track all this down, don't ignore the health news, but take the health news you hear on TV or read in your local paper with a grain of salt. If your LDL cholesterol level is high, you might want to try a statin. Some people can take them without getting side effects. But be vigilant. If you get muscle weakness, try some coenzyme Q10, which Golomb says helps about 70% who have that problem. Some people recommend taking the coenzyme Q10 even if you don't have muscle problems.
But if the muscle pain or weakness persists, talk with y0ur doctor about other alternatives, like niacin. Muscle pain that progresses to rhabdomyolysis is serious.
Wednesday, December 22, 2010
Hepatokines
Most of us have heard of cytokines, signaling molecules secreted by cells that affect other cells. Examples are the various interleukins, some of which stimulate inflammation and others of which reduce inflammation. They are like text messages between cells.
When some cellular stress occurs, let's say an infection in your finger, certain cytokines are the distress signals, telling other types of cells to rush to the site and fix it. Then when things seem to be OK, different cytokines tell the cells to cool it, to stop trying to fix things (fixing involves inflammation) and let the site get back to normal.
Fat cells used to be considered boring blobs of stored calories, with no interesting functions. Then they discovered that fat cells also secreted signaling molecules, which they termed adipokines. One of the most widely known adipokine is leptin.
Hormones are also signaling molecules, and some people debate about which signaling molecules should be called cytokines or adipokines and which should be called hormones. Traditionally, hormones were considered to be molecules secreted by one organ that affected other organs. For example, beta cells secrete insulin, which has effects all over the body.
Cytokines were considered to be hormonelike molecules secreted by numerous cells throughout the body that affected immune system cells. Adipokines were considered to be hormonelike molecules secreted by fat cells. In both cases, a certain type of cell rather than a certain organ secretes the signaling molecules. And unlike hormones, which are usually synthesized and then stored within the cell for rapid release when needed, cytokines tend to be synthesized only when needed.
But there's a lot of overlap between cytokines and hormones, and some people think it's time to stop trying to classify the numerous new signaling molecules that seem to be discovered every week. The important thing is what they do.
Recently a new type of cellular "kine" has been proposed: the hepatokine.
A protein called selenoprotein P is produced in the liver and transports the trace mineral selenium from the liver to the cells that need it. These researchers found that selenoprotein P concentrations are higher in people with type 2 diabetes than they are in healthy people, and they proposed that overproduction of selenoprotein P in the liver causes insulin resistance and type 2 diabetes. Their research results were consistent with this hypothesis.
Interestingly, their results suggested that selenoprotein P works via AMPK, which is also affected by the diabetes drug metformin.
They said their research "raises the possibility that the liver functions as an endocrine organ by producing a variety of hepatokines and that the dysregulation or impairment of hepatokine production might contribute to the development of various diseases."
Whether or not selenoprotein P turns out to be vital in causing type 2 diabetes, I find this paper fascinating because it gives us a new way of approaching diabetes: looking for important modulators in a new place. Sometimes takes a shakeup of traditional ideas in order to make breakthroughs.
If there are adipokines and hepatokines, might there not also be musculokines or myokines? Skelatokines or osteokines? Or other "kines" in places no one has thought to look?
Maybe the tongue produces signaling molecules when it tastes different kinds of foods. We know that the sight, smell, and even thought of food can trigger nervous signals that affect gastric and insulin secretion (the cephalic phase of digestion). Why not small molecules as well?
Progress in genetic research is proceeding rapidly, but we still don't know what really causes type 2 diabetes. Perhaps these new ideas will stimulate new research that will come up with something that will help us prevent this epidemic disease.
When some cellular stress occurs, let's say an infection in your finger, certain cytokines are the distress signals, telling other types of cells to rush to the site and fix it. Then when things seem to be OK, different cytokines tell the cells to cool it, to stop trying to fix things (fixing involves inflammation) and let the site get back to normal.
Fat cells used to be considered boring blobs of stored calories, with no interesting functions. Then they discovered that fat cells also secreted signaling molecules, which they termed adipokines. One of the most widely known adipokine is leptin.
Hormones are also signaling molecules, and some people debate about which signaling molecules should be called cytokines or adipokines and which should be called hormones. Traditionally, hormones were considered to be molecules secreted by one organ that affected other organs. For example, beta cells secrete insulin, which has effects all over the body.
Cytokines were considered to be hormonelike molecules secreted by numerous cells throughout the body that affected immune system cells. Adipokines were considered to be hormonelike molecules secreted by fat cells. In both cases, a certain type of cell rather than a certain organ secretes the signaling molecules. And unlike hormones, which are usually synthesized and then stored within the cell for rapid release when needed, cytokines tend to be synthesized only when needed.
But there's a lot of overlap between cytokines and hormones, and some people think it's time to stop trying to classify the numerous new signaling molecules that seem to be discovered every week. The important thing is what they do.
Recently a new type of cellular "kine" has been proposed: the hepatokine.
A protein called selenoprotein P is produced in the liver and transports the trace mineral selenium from the liver to the cells that need it. These researchers found that selenoprotein P concentrations are higher in people with type 2 diabetes than they are in healthy people, and they proposed that overproduction of selenoprotein P in the liver causes insulin resistance and type 2 diabetes. Their research results were consistent with this hypothesis.
Interestingly, their results suggested that selenoprotein P works via AMPK, which is also affected by the diabetes drug metformin.
They said their research "raises the possibility that the liver functions as an endocrine organ by producing a variety of hepatokines and that the dysregulation or impairment of hepatokine production might contribute to the development of various diseases."
Whether or not selenoprotein P turns out to be vital in causing type 2 diabetes, I find this paper fascinating because it gives us a new way of approaching diabetes: looking for important modulators in a new place. Sometimes takes a shakeup of traditional ideas in order to make breakthroughs.
If there are adipokines and hepatokines, might there not also be musculokines or myokines? Skelatokines or osteokines? Or other "kines" in places no one has thought to look?
Maybe the tongue produces signaling molecules when it tastes different kinds of foods. We know that the sight, smell, and even thought of food can trigger nervous signals that affect gastric and insulin secretion (the cephalic phase of digestion). Why not small molecules as well?
Progress in genetic research is proceeding rapidly, but we still don't know what really causes type 2 diabetes. Perhaps these new ideas will stimulate new research that will come up with something that will help us prevent this epidemic disease.
Wednesday, November 24, 2010
Preconceptions . . . Again
Maybe it's a waste of time to point out the biased preconceptions one sees in various science journals; most of the intelligent people I assume are the primary readers of this blog can spot them for themselves. But they annoy me so much I can't not point them out.
The latest one occurred in an article titled "Overweight Primarily a Problem Among Wealthier Women in Low To Middle-Income Countries" and published in the American Journal of Clinical Nutrition.
Researchers at the Harvard School of Public Health reported that in less affluent countries, being overweight is more common among women with higher incomes (they studied only women). In contrast, in more affluent countries like the United States, obesity is associated with poverty.
I think this is intuitively obvious. When it's difficult to get enough food, then only richer people will obtain enough calories to become fat. When food is plentiful but starchy and fatty food is cheaper than meat and vegetables, then the poorer you are, the more apt you are to be fat.
A famous photo of an emaciated boy holding out a bowl and begging for rice, while behind him a fat (by the standards of those days) merchant woman sits among huge bags of rice, illustrates this. The boy isn't counting calories; he's starving.
So initially, I found the study pretty ho-hum. Then I came on this attempt at an explanation:
"The researchers theorize that these findings could be due to a number of factors, including that women in higher income groups are more likely to have diets richer in animal fats than lower-income women."
In other words, they started with the assumption that obesity (and probably all the other ills of a "Western" diet) stem from too much animal fat. So that must surely be the explanation here too.
Couldn't it also be because the richer women were able to buy white bread and jam instead of fiber-filled vegetables the poorer people probably grew themselves?
They do make a couple of other suggestions:
"Also, cultural norms in developing countries may favor fatty body shapes among wealthier women. Richer women are also less likely than poor women to engage in regular physical labor."
I'm sure the difference in physical work does make a difference. But if cultural norms in developing countries favored fatty body shapes among wealthier women (as a sign that you could afford a lot of food), wouldn't you think the same would be true among poor people as well? Wouldn't poor people want to look as if they were rich?
Sometimes the logic in nutrition papers boggles my mind.
The latest one occurred in an article titled "Overweight Primarily a Problem Among Wealthier Women in Low To Middle-Income Countries" and published in the American Journal of Clinical Nutrition.
Researchers at the Harvard School of Public Health reported that in less affluent countries, being overweight is more common among women with higher incomes (they studied only women). In contrast, in more affluent countries like the United States, obesity is associated with poverty.
I think this is intuitively obvious. When it's difficult to get enough food, then only richer people will obtain enough calories to become fat. When food is plentiful but starchy and fatty food is cheaper than meat and vegetables, then the poorer you are, the more apt you are to be fat.
A famous photo of an emaciated boy holding out a bowl and begging for rice, while behind him a fat (by the standards of those days) merchant woman sits among huge bags of rice, illustrates this. The boy isn't counting calories; he's starving.
So initially, I found the study pretty ho-hum. Then I came on this attempt at an explanation:
"The researchers theorize that these findings could be due to a number of factors, including that women in higher income groups are more likely to have diets richer in animal fats than lower-income women."
In other words, they started with the assumption that obesity (and probably all the other ills of a "Western" diet) stem from too much animal fat. So that must surely be the explanation here too.
Couldn't it also be because the richer women were able to buy white bread and jam instead of fiber-filled vegetables the poorer people probably grew themselves?
They do make a couple of other suggestions:
"Also, cultural norms in developing countries may favor fatty body shapes among wealthier women. Richer women are also less likely than poor women to engage in regular physical labor."
I'm sure the difference in physical work does make a difference. But if cultural norms in developing countries favored fatty body shapes among wealthier women (as a sign that you could afford a lot of food), wouldn't you think the same would be true among poor people as well? Wouldn't poor people want to look as if they were rich?
Sometimes the logic in nutrition papers boggles my mind.
Saturday, November 13, 2010
Free Full Text
Mary Ann Liebert, Inc, publisher of many journals, is offering free full text of their diabetes-related journals through the end of November. The offer is in recognition of World Diabetes Day.
The three journals are Diabetes Technology & Therapeutics, Metabolic Syndrome and Related Disorders, and Childhood Obesity.
I've often seen abstracts in the first journal and wished I could read the full texts, but access was too expensive. So this is a good chance to download the articles that interest you, if any.
The three journals are Diabetes Technology & Therapeutics, Metabolic Syndrome and Related Disorders, and Childhood Obesity.
I've often seen abstracts in the first journal and wished I could read the full texts, but access was too expensive. So this is a good chance to download the articles that interest you, if any.
Friday, October 22, 2010
Are Parasites in Charge?
Parasites can influence the behavior of the organisms they inhabit.
For example, mice infected with the protozoan Toxoplasma gondii, the organism that causes toxoplasmosis, become lethargic and lose their fear of cats, the primary host of the parasite
Clearly, in a cat-infested environment, such mice don't last very long. And the cats that eat the infected mice become infected themselves and then spread the eggs (oocysts) through their feces.
The behavior modification caused by other parasites in other organisms are even more bizarre.
So, could human behavior also be influenced by some of the parasites we all carry? Some people think yes.
Our guts are filled with bacteria. Many of these bacteria are beneficial. For example, gut bacteria produce most of the B vitamin biotin that we need. Other bacteria can cause obvious harm, for example, gut inflammation, pain, and diarrhea. The diarrhea benefits the bacteria because it increases the probability that other people will come in contact with the abundant fluid and become infected themselves.
Effects on behavior could be more subtle. We know that animals infected with rabies virus behave differently. They become more aggressive and tend to bite. Because the virus colonizes the salivary gland, such bites pass the infection on.
But why am I babbling about all this, interesting though it might be?
It's because I'm wondering if it's gut bacteria that program some people to eat more than normal, causing obesity. Why would the bacteria do that? Well, the more you eat, the more food there will be in the gut, which means the more the bacteria could grow.
There is some evidence that gut bacteria are related to obesity: overweight people tend to have different types of bacteria than normal-weight people. And some animal studies showed that transferring the gut bacteria from mice prone to metabolic syndrome into normal mice caused the normal ones to develop metabolic syndrome too.
So this idea that gut bacteria are associated with obesity is not new. Whether the bacterial population causes the obesity or the obesity provides a gut environment friendly to certain types of bacteria, or perhaps both in a vicious circle, has not yet been definitively proved.
A recent study reported at the Stockholm meeting of the European Association for the Study of Diabetes showed that transplanting fecal matter from thin people into obese people with prediabetes did not result in any weight loss. However, the recipients did see their insulin resistance decrease.
Clearly, obesity, type 2 diabetes, and gut populations are related somehow. One possibility is that certain bacteria are especially efficient converters of food and fiber into compounds that can easily be taken up in the gut, essentially adding calories to whatever we eat.
But I'm wondering if there's more than a metabolic effect. I wonder if the gut bacteria, like the parasites that change behavior in mice and spiders, are subtly changing the behavior of their hosts.
If the bacteria made the hosts feel sluggish, they wouldn't want to move around a lot and burn off calories. If the bacteria made the hosts hungry all the time, they would eat more than they needed to maintain their weight.
The bacteria could then happily munch on the extra calories, rapidly multiply, and infect other people.
Is this really true? No one knows. But the idea intrigues me.
For example, mice infected with the protozoan Toxoplasma gondii, the organism that causes toxoplasmosis, become lethargic and lose their fear of cats, the primary host of the parasite
Clearly, in a cat-infested environment, such mice don't last very long. And the cats that eat the infected mice become infected themselves and then spread the eggs (oocysts) through their feces.
The behavior modification caused by other parasites in other organisms are even more bizarre.
So, could human behavior also be influenced by some of the parasites we all carry? Some people think yes.
Our guts are filled with bacteria. Many of these bacteria are beneficial. For example, gut bacteria produce most of the B vitamin biotin that we need. Other bacteria can cause obvious harm, for example, gut inflammation, pain, and diarrhea. The diarrhea benefits the bacteria because it increases the probability that other people will come in contact with the abundant fluid and become infected themselves.
Effects on behavior could be more subtle. We know that animals infected with rabies virus behave differently. They become more aggressive and tend to bite. Because the virus colonizes the salivary gland, such bites pass the infection on.
But why am I babbling about all this, interesting though it might be?
It's because I'm wondering if it's gut bacteria that program some people to eat more than normal, causing obesity. Why would the bacteria do that? Well, the more you eat, the more food there will be in the gut, which means the more the bacteria could grow.
There is some evidence that gut bacteria are related to obesity: overweight people tend to have different types of bacteria than normal-weight people. And some animal studies showed that transferring the gut bacteria from mice prone to metabolic syndrome into normal mice caused the normal ones to develop metabolic syndrome too.
So this idea that gut bacteria are associated with obesity is not new. Whether the bacterial population causes the obesity or the obesity provides a gut environment friendly to certain types of bacteria, or perhaps both in a vicious circle, has not yet been definitively proved.
A recent study reported at the Stockholm meeting of the European Association for the Study of Diabetes showed that transplanting fecal matter from thin people into obese people with prediabetes did not result in any weight loss. However, the recipients did see their insulin resistance decrease.
Clearly, obesity, type 2 diabetes, and gut populations are related somehow. One possibility is that certain bacteria are especially efficient converters of food and fiber into compounds that can easily be taken up in the gut, essentially adding calories to whatever we eat.
But I'm wondering if there's more than a metabolic effect. I wonder if the gut bacteria, like the parasites that change behavior in mice and spiders, are subtly changing the behavior of their hosts.
If the bacteria made the hosts feel sluggish, they wouldn't want to move around a lot and burn off calories. If the bacteria made the hosts hungry all the time, they would eat more than they needed to maintain their weight.
The bacteria could then happily munch on the extra calories, rapidly multiply, and infect other people.
Is this really true? No one knows. But the idea intrigues me.
Friday, October 15, 2010
Popular Press Spins
When I was in graduate school, way back in the 1960s, almost every news report about some scientific finding ended by trying to explain why this finding would help to cure cancer. This was the era of the War on Cancer, and scientists hoped that relating their research to curing cancer would increase their chances of getting big research grants.
In the virus course I took with Jim Watson, the exams usually included a question in which we had to explain why some newspaper report of a scientific finding was wrong, that it actually would have nothing to do with cancer. They were fun questions.
Today, instead of trying to show how new studies can help to cure cancer, most popular press stories I see suggest that the findings provide a new target for new drugs, probably hoping to increase their chances of getting funding from drug companies.
Many of the stories appearing in popular science releases like Eurekalert and Science Daily are written by PR people at the institutions where the research is done. Their goal is to call attention to their institutions, professors, and funding sources as well as to the research itself. As a result, usually more than half of the articles is garbage.
When I was a newspaper editor, we'd get tons of press releases like this, and part of our job was to rewrite them without the self-promoting garbage. But these science news sites don't do this. Most of them simply print the press releases verbatim; you can read exactly the same stories on myriad sites.
An example from Science Daily:
"Researchers at the University of Edinburgh report a new experimental compound that can improve memory and cognitive function in aging mice. The compound is being investigated with a view to developing a drug that could slow the natural decline in memory associated with aging.
"With support from the Wellcome Trust Seeding Drug Discovery award, the team has identified a preclinical condition that they hope to take into human trials within a year."
Note that in the first two paragraphs they've mentioned the institution, the potential for drug development, and the funding source. They haven't mentioned what we all want to know: what this compound is. You have to slog through a lot of other boring stuff before they'll reveal that. Some stories even list all the researchers, their degrees, and their positions at the university before they'll tell you what the new finding actually was.
Here's another one:
"University of Michigan scientists have identified events inside insulin-producing pancreatic cells that set the stage for a neonatal form of non-autoimmune type 1 diabetes, and may play a role in type 2 diabetes as well. The results point to a potential target for drugs to protect normally functioning proteins essential for producing insulin."
In this case the PR people managed to make the institution the first word of the article.
You may say, "So what!" and that's partially true. We just have to learn to skim most of these articles to get to the crux of the story. And these popular press releases are important in alerting us to new journal articles that we'd probably never know of otherwise. Most of the press releases do have links to the original articles, although in many cases we can only read the abstracts unless we want to pay.
But I think the important thing is to remember that these articles are written by PR people whose goal is different from our goal. Their goal is to publicize their institution and overemphasize the importance of the research there. Our goal is to understand as completely as possible how good the evidence supporting the claims in the summary article is.
Whenever possible, I try to get the full text of an important article. I don't make the effort for what I consider less important ones. Time is not infinite. I once spent 2 days researching the science behind a story about using lettuce and some complex molecular biology to give people insulin by eating lettuce. Most of the popular press summaries didn't really understand what the research showed.
But if I spent 2 days researching every article I read, I wouldn't be able to read very many, and in the long run I'm hoping that having a surface acquaintance with a lot of research will be more useful than having an in-depth acquaintance with just a little.
I'm sure most of you are already aware of the way the press spins news about science research. But it never hurts to examine it again.
It's a reader-beware situation out there.
In the virus course I took with Jim Watson, the exams usually included a question in which we had to explain why some newspaper report of a scientific finding was wrong, that it actually would have nothing to do with cancer. They were fun questions.
Today, instead of trying to show how new studies can help to cure cancer, most popular press stories I see suggest that the findings provide a new target for new drugs, probably hoping to increase their chances of getting funding from drug companies.
Many of the stories appearing in popular science releases like Eurekalert and Science Daily are written by PR people at the institutions where the research is done. Their goal is to call attention to their institutions, professors, and funding sources as well as to the research itself. As a result, usually more than half of the articles is garbage.
When I was a newspaper editor, we'd get tons of press releases like this, and part of our job was to rewrite them without the self-promoting garbage. But these science news sites don't do this. Most of them simply print the press releases verbatim; you can read exactly the same stories on myriad sites.
An example from Science Daily:
"Researchers at the University of Edinburgh report a new experimental compound that can improve memory and cognitive function in aging mice. The compound is being investigated with a view to developing a drug that could slow the natural decline in memory associated with aging.
"With support from the Wellcome Trust Seeding Drug Discovery award, the team has identified a preclinical condition that they hope to take into human trials within a year."
Note that in the first two paragraphs they've mentioned the institution, the potential for drug development, and the funding source. They haven't mentioned what we all want to know: what this compound is. You have to slog through a lot of other boring stuff before they'll reveal that. Some stories even list all the researchers, their degrees, and their positions at the university before they'll tell you what the new finding actually was.
Here's another one:
"University of Michigan scientists have identified events inside insulin-producing pancreatic cells that set the stage for a neonatal form of non-autoimmune type 1 diabetes, and may play a role in type 2 diabetes as well. The results point to a potential target for drugs to protect normally functioning proteins essential for producing insulin."
In this case the PR people managed to make the institution the first word of the article.
You may say, "So what!" and that's partially true. We just have to learn to skim most of these articles to get to the crux of the story. And these popular press releases are important in alerting us to new journal articles that we'd probably never know of otherwise. Most of the press releases do have links to the original articles, although in many cases we can only read the abstracts unless we want to pay.
But I think the important thing is to remember that these articles are written by PR people whose goal is different from our goal. Their goal is to publicize their institution and overemphasize the importance of the research there. Our goal is to understand as completely as possible how good the evidence supporting the claims in the summary article is.
Whenever possible, I try to get the full text of an important article. I don't make the effort for what I consider less important ones. Time is not infinite. I once spent 2 days researching the science behind a story about using lettuce and some complex molecular biology to give people insulin by eating lettuce. Most of the popular press summaries didn't really understand what the research showed.
But if I spent 2 days researching every article I read, I wouldn't be able to read very many, and in the long run I'm hoping that having a surface acquaintance with a lot of research will be more useful than having an in-depth acquaintance with just a little.
I'm sure most of you are already aware of the way the press spins news about science research. But it never hurts to examine it again.
It's a reader-beware situation out there.
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