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.
Sunday, January 23, 2011
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.
Thursday, August 5, 2010
Lipids and Diet
Low-carb and low-fat diets result in similar weight loss at 2 years when both are accompanied by comprehensive lifestyle counseling, according to a recent research project by Gary Foster and colleagues published in the Annals of Internal Medicine.
But people in the low-carb diet showed better lipid profiles after 2 years.
You have to pay to read the full text of the article, but low-carb advocate Jimmy Moore has an extensive discussion of the results including some graphs.
This study is important because it shows that various improvements in people following low-carb diets are not simply temporary. Although 2 years can't really be called long term, it's heading in the right direction.
What I find fascinating is the reaction to this article. I can't find it at all on either Science Daily or Eurekalert, both popular summaries of science news. They're always quick to report studies that say red meat is bad or low-carb diets cause problems. Why aren't they summarizing this study? Many other media outlets are, so it's not that the study is obscure.
Others have put a positive or a negative spin or a neutral spin on the study (not mentioning the better lipid profiles is actually a negative spin), some by the way they write their headlines. If you support low-carb diets, you can emphasize the fact that the lipid levels improved on that diet. If you don't, you can focus on the fact that weight loss was the same. Many people remember only the headlines; here are a few of them:
Positive:
Low-carb diets improve cholesterol long term (Medicinenet)
Low-carbohydrate diet beats low-fat diet in decreasing heart risk (Thaindian news)
Low-carb diet better for heart health than low-fat diet (The Money Times)
Neutral
Low-carb, low-fat diets tied for long term weight loss (uamshealth.com) (University of Arkansas for Medical Sciences)
Study disputes low-carb diet concerns (Philadelphia Inquirer)
Low-carb diet as good as low-fat one (Press TV)
When people do studies of "low-carb" diets that include 150 grams of carbs, low-carb supporters scream that such diets aren't really low carb (and I agree with this), that if they'd tested 50 g or 30 g or 20 g a day, they would have seen different results.
In this case, the low-fat supporters are screaming that a diet with <30% fat isn't really a low-fat diet, that if they'd limited fat to 10%, they would have seen different results.
I agree that this study would have been better if they'd tested 4 different diets: very low carb ketogenic diet (<50 g carbs), low-carb diet (50-130 g), low-fat diet (<30% fat), very low fat (<10%).
But I think the researchers were trying to compare a standard Atkins diet (the diet many people think about when they think low carb, even though there are other low-carb diets that I think are better) with "standard care," which still often means following the old Food Pyramid with 60% carbs and <30% fat.
They may also have worried that few of the study subjects would have been willing to stick to the stricter diets for 2 years or more. Even with the more moderate diets, attrition was high: 32% for the low-fat diet and 42% for the low-carb diet at the end of 2 years.
The low-fat diet was limited in calories; the low-carb diet was not.
Both groups lost weight, rapidly at first, reaching a nadir at 6 months, and then regained some of the weight, so that by the end of 2 years, they'd lost an average of 7% of their starting weight.
Interestingly, this was the goal in the Diabetes Prevention Program weight-loss study of people at high risk of developing diabetes. The DPP showed that modest weight loss (the goal of 7% was not actually reached) could reduce the risk of progressing to overt diabetes. The same phenomenon occurred in that study too: subjects initially lost weight fast, then leveled off and started regaining again.
I think we've all experienced this phenomenon. We try a new diet and are enthusiastic and follow it exactly. Then after some time we hit a plateau and we also get bored with the diet and gradually revert to our old habits.
It's also possible that the body wants to maintain a certain weight that is higher than the weight we want it to have (the set-point theory), and after some time the metabolism changes to encourage the regaining of the weight.
People will never agree on the best diet for weight loss, partly because different people do better on different diets: YMMV, or "Your mileage may vary." But the more we know about various diets and various groups of dieters, preferable for as long as possible, the better.
Like weight loss, lipid levels tend to be different in the short term than they are in the long term. For example, in this study, triglycerides rapidly decreased in the low-carb group but then went up again and by the end of 2 years were about the same as the levels in the low-fat group. LDL levels went up in the low-carb group but later went down again. Only HDL levels were consistently higher on the low-carb diet throughout the study.
It's not clear whether the fluctuating lipid levels were because after 12 weeks the people on the low-carb diet were instructed to slowly start adding back carbs until their weight stabilized. This is what Atkins told people to do. But in fact, the weights in the low-carb group continued to drop after 12 weeks and then instead of "stabilizing" started to climb.
So it's also possible that the body was adapting to a different diet and adjusting the lipid levels after a certain amount of time on the diet. Perhaps we have a "lipid set-point" as well as a weight set-point, and the body keeps trying to reach it.
Regardless of the reasons for these shifts, in order to really understand how diets affect various heart health risks, we need longer-term data. Foster and colleagues have made a valuable first step. Perhaps even longer studies will follow.
But people in the low-carb diet showed better lipid profiles after 2 years.
You have to pay to read the full text of the article, but low-carb advocate Jimmy Moore has an extensive discussion of the results including some graphs.
This study is important because it shows that various improvements in people following low-carb diets are not simply temporary. Although 2 years can't really be called long term, it's heading in the right direction.
What I find fascinating is the reaction to this article. I can't find it at all on either Science Daily or Eurekalert, both popular summaries of science news. They're always quick to report studies that say red meat is bad or low-carb diets cause problems. Why aren't they summarizing this study? Many other media outlets are, so it's not that the study is obscure.
Others have put a positive or a negative spin or a neutral spin on the study (not mentioning the better lipid profiles is actually a negative spin), some by the way they write their headlines. If you support low-carb diets, you can emphasize the fact that the lipid levels improved on that diet. If you don't, you can focus on the fact that weight loss was the same. Many people remember only the headlines; here are a few of them:
Positive:
Low-carb diets improve cholesterol long term (Medicinenet)
Low-carbohydrate diet beats low-fat diet in decreasing heart risk (Thaindian news)
Low-carb diet better for heart health than low-fat diet (The Money Times)
Neutral
Low-carb, low-fat diets tied for long term weight loss (uamshealth.com) (University of Arkansas for Medical Sciences)
Study disputes low-carb diet concerns (Philadelphia Inquirer)
Low-carb diet as good as low-fat one (Press TV)
When people do studies of "low-carb" diets that include 150 grams of carbs, low-carb supporters scream that such diets aren't really low carb (and I agree with this), that if they'd tested 50 g or 30 g or 20 g a day, they would have seen different results.
In this case, the low-fat supporters are screaming that a diet with <30% fat isn't really a low-fat diet, that if they'd limited fat to 10%, they would have seen different results.
I agree that this study would have been better if they'd tested 4 different diets: very low carb ketogenic diet (<50 g carbs), low-carb diet (50-130 g), low-fat diet (<30% fat), very low fat (<10%).
But I think the researchers were trying to compare a standard Atkins diet (the diet many people think about when they think low carb, even though there are other low-carb diets that I think are better) with "standard care," which still often means following the old Food Pyramid with 60% carbs and <30% fat.
They may also have worried that few of the study subjects would have been willing to stick to the stricter diets for 2 years or more. Even with the more moderate diets, attrition was high: 32% for the low-fat diet and 42% for the low-carb diet at the end of 2 years.
The low-fat diet was limited in calories; the low-carb diet was not.
Both groups lost weight, rapidly at first, reaching a nadir at 6 months, and then regained some of the weight, so that by the end of 2 years, they'd lost an average of 7% of their starting weight.
Interestingly, this was the goal in the Diabetes Prevention Program weight-loss study of people at high risk of developing diabetes. The DPP showed that modest weight loss (the goal of 7% was not actually reached) could reduce the risk of progressing to overt diabetes. The same phenomenon occurred in that study too: subjects initially lost weight fast, then leveled off and started regaining again.
I think we've all experienced this phenomenon. We try a new diet and are enthusiastic and follow it exactly. Then after some time we hit a plateau and we also get bored with the diet and gradually revert to our old habits.
It's also possible that the body wants to maintain a certain weight that is higher than the weight we want it to have (the set-point theory), and after some time the metabolism changes to encourage the regaining of the weight.
People will never agree on the best diet for weight loss, partly because different people do better on different diets: YMMV, or "Your mileage may vary." But the more we know about various diets and various groups of dieters, preferable for as long as possible, the better.
Like weight loss, lipid levels tend to be different in the short term than they are in the long term. For example, in this study, triglycerides rapidly decreased in the low-carb group but then went up again and by the end of 2 years were about the same as the levels in the low-fat group. LDL levels went up in the low-carb group but later went down again. Only HDL levels were consistently higher on the low-carb diet throughout the study.
It's not clear whether the fluctuating lipid levels were because after 12 weeks the people on the low-carb diet were instructed to slowly start adding back carbs until their weight stabilized. This is what Atkins told people to do. But in fact, the weights in the low-carb group continued to drop after 12 weeks and then instead of "stabilizing" started to climb.
So it's also possible that the body was adapting to a different diet and adjusting the lipid levels after a certain amount of time on the diet. Perhaps we have a "lipid set-point" as well as a weight set-point, and the body keeps trying to reach it.
Regardless of the reasons for these shifts, in order to really understand how diets affect various heart health risks, we need longer-term data. Foster and colleagues have made a valuable first step. Perhaps even longer studies will follow.
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