Update: A problem with the study that I describe in this post has surfaced within the scientific community, and has even received mass-media attention. It's a technical problem of exactly the sort I warn about in the post. The only thing that's unusual here is that the problem has been called out prominently.
A new study has shown that living into your nineties and beyond is a matter of having the right genes, according to recent headlines. The technique that the researchers employed to identify the genes of long life is much the same one behind many of the discoveries of links between genes and traits or genes and disorders that we hear about frequently. To oversimplify a bit, the game involves looking at many genes in a large group of people who have some trait in common, and then trying to spot which particular genes turn up more frequently in these folks than in a large group people who don't have the trait.
I recommend not paying much attention to this study, or to most studies that purport to have identified key genes behind some important trait or disorder, and for a few reasons. First of all, this basic gene-linking technique, although an impressive one and getting better, is still beset with a variety of inherent limitations and potential flaws that often lead to simply misidentifying genes as being closely linked to a trait in most people when they are not, and misses many and possibly most of the genes that actually influence the trait. Part of the problem is that the technique is a highly statistical one based on probabilities involving all sorts of manipulations that can leave the picture convoluted and murky. In addition, the very notion that a relatively small number of genes is likely to play a huge role in determining a trait or disease risk is for the most part a mistaken one, or at best a gross oversimplification. Genes act not alone or even as a small band, but rather as a vast orchestra. Even more confusing, genes can be "turned off" so that they might as well not be there, or partly turned on so that they contribute only weakly to a trait or disease risk. What turns genes on and off? Each other, the environment, other molecules in our cells, and strips of DNA that aren't even parts of genes. It gets worse: Genes can appear in single form, or in multiple copies that increase their influence in ways most gene tests don't detect. They can pop out of their slot in the genome, replicate themselves, and then reinsert themselves somewhere else in the genome. They can flip around backwards, which also isn't detected by gene tests, even though a backwards gene can behave differently. Throw in the fact that genes can be changed by viruses, and that any protein made by a particular gene can do different things in different people, or different things in the same person at different times depending on what else is going on in the body, and you've got complexity of such staggering breadth and depth that scientists who are being honest about the situation admit they'll be lucky to make a small dent in the task of sorting it all out in their lifetimes.
Consider: A 2009 study of about 6,000 people came up with a technique for predicting the height of a person based on looking at the 54 genes most closely linked to height. The results turned out to be one-tenth as accurate as averaging the heights of both parents and adjusting for sex, a technique introduced in 1886 by statistician Sir Francis Galton. University College Dublin biomolecular researcher Helen Colhoun and colleagues have estimated that 95 percent of studies that find gene links are just plain wrong. Harvard genetics researcher Joel Hirschhorn and colleagues surveyed the medical literature on 166 published genetic links to illness that were each examined in at least two other published studies, and found that only six of the links--less than four percent--held up in all the studies. John Ioannidis of Tufts University Medical School has calculated the average odds of a gene-link study being right at one out of hundreds, or worse, depending on the disease. In the case of schizophrenia, for example, Ioannidis reckons a one out of 2,000 chance of a gene-link study being right. His estimates suggest you would have almost as good a chance of identifying some types of genuine gene links by throwing darts at a diagram of the relevant sections of the human genome as you would by reading research journals. Researchers claim their hit rate has improved quite a bit in the past few years, but we won't know the extent to which that's true for a while to come. Needless to say, all these substantial uncertainties and vagaries often get swept under the carpet in the reported findings of an exciting new study, and are almost always ignored in the mass-media reports.
None of this is to say that the study in question here didn't correctly identify many genes that may in fact in some cases be potentially important contributors to living a very long life. But even if the claim is largely or at least partly right, it's still a misleading one. When we hear it, we assume that we'll need many or most of these genes to have a good shot at a long, healthy life--and that's an absolutely unwarranted conclusion. People who live extraordinarily long lives need everything to go in their favor, including many things that may be largely irrelevant to those of us who hope to keep decent health "merely" into our 80s. Assuming we need the genes common in people who live to be 100 may be like assuming a good-performing car needs to have the components common to race cars.
Even if it does indeed help quite a bit to have the right genes in order to live a long and healthy life, it also helps to get a lot of other things right. What has come through from all the genetic studies more clearly than anything else is that for most of us genes really don't influence your destiny as much as, or at least any more than, your behavior does. Folks, if you want to live relatively long lives, and perhaps more importantly stay relatively healthy late into that life, there is powerful evidence that eating sensibly, exercising, breathing clean air, avoiding undue stress, and refraining from obviously bad habits such as smoking, heavy drinking and not wearing seatbelts, can for many and possibly most of us trump genes. In fact, for all we know, some of the genes that the very-long-lived had in common in this study were genes that influence healthy behaviors--in which case anyone engaging in the behaviors would get the same benefits, whether they had the genes or not.
Your fate is probably not genetically sealed--it is much more likely that your health is to a large extent under your control. Don't let announcements of marvelous gene-link breakthroughs lead you to abdicate that responsibility.
Wednesday, July 7, 2010
Thursday, July 1, 2010
The Trouble with Medications
One recent set of headlines noted that an experimental, cutting-edge drug for the difficult-to-treat disease hepatitis C isn't looking good for FDA approval because there's evidence it can harm patients without much helping them. That's terrible news for hepatitis C sufferers, of course, but most of us might just shrug, figuring that's exactly the sort of outcome we might well expect from many and perhaps most unproven, high-tech treatments that are undergoing trials. What the public is much less aware of is that the same dubious benefit-to-risk situation applies to many of the drugs that are already widely prescribed. In just the past few days we've read headlines about how the diabetes drug Avandia, which has been taken by more than a million people, has now been strongly linked by big studies to potentially fatal heart disorders and strokes. And also making the news is a smaller study that suggests testosterone gel--increasingly commonly prescribed to older men to counter some of the debilitating effects of aging, including loss of bone density, muscle mass, mobility, energy and libido--may be strongly linked to heart disorders, at least in much older men with low mobility.
This isn't just some small run of bad luck for the drug world. These sorts of problems are inherent to the very nature of drugs. Our bodies function via chemical "pathways" in which a vast number of proteins made by our genes interact with each other in ways so staggeringly complex that scientists struggle mightily to identify small pieces of the picture. When you take a drug, the hope is that it will go in and interrupt or boost some isolated part of a pathway that's contributing whatever disorder you may be suffering from. But disorders can rarely be neatly pinned down to a simple pathway, which means there isn't a clean target for the drug, which means the drug isn't likely to hit the problem head on. What's more, everyone has different genes, and even when we have the same relevant genes they may be turned "on" or "off" in different ways in different people, so that our pathways our different, which means that even when a drug is somewhat effective in one person it might not be so in another. Even worse, the drug is almost certainly affecting other pathways that are important to our health, with the effects rippling through the body in ways that may well cause harm. These basic problems are why we've seen a stream of much-hyped, widely used drugs yanked from the market after years, leaving behind a trail of people who weren't much helped, or of people who suffered or even died from the drugs. Vioxx is probably the best-known example from the past several years, but recent headlines have listed many others.
Indeed, it would be miraculous if a drug could go in, completely solve a problem, and do nothing else--virtually no drugs have ever been found that pull that trick off. Instead, the vast majority of our drugs have much messier effects on us: they sort of help some people, hurt others, and don't do much of anything for yet others. Even established, major drugs don't work on 40% to 75% of people, according to a 2005 review paper in The New England Journal of Medicine, and the variation in effectiveness and risk of side-effects tends to be much greater for newer, less-proven drugs. The picture gets even worse when you're talking about patients who are on multiple drugs, which can react with each other in any number of ways that are rarely well understood and often altogether unstudied. We don't get all this from the findings of most studies, because they tend to report averages, and are often presented in a way that make it sound as if a drug can do a lot for you, with only some chance of causing you problems. That may be sort of true, but there's really no way of getting around the fact that for most drugs you're rolling the dice to some extent as to whether the drug is going to help or hurt, if it does anything at all. There's hope genetic tests will eventually boost the odds further in your favor, but right now the claims you hear in the news that this is happening today is mostly hype, with just a few exceptions.
I want to make it clear I am in no way advocating pressuring your doctor to take you off any of your drugs--doctors admit in surveys to often succumbing to patient pressure on some drug decisions even if they don't think the decision is medically best for the patient--and I most certainly don't want anyone stopping drugs on their own. But there's no reason why you shouldn't ask your doctor to explain in more detail how likely a drug is to help, how likely it is to hurt, and why he thinks it's worth it. By the same token, you might want to know what applicable drugs she's decided aren't right for you, and why. Why shouldn't you be involved in a decision that essentially involves placing a bet on risks and benefits to your health? I always bow to my doctor's judgment, but she's willing to explain how she's arrived at it, and she's interested in getting my input when it's a matter of weighing the odds, as is usually the case with medications.
This isn't just some small run of bad luck for the drug world. These sorts of problems are inherent to the very nature of drugs. Our bodies function via chemical "pathways" in which a vast number of proteins made by our genes interact with each other in ways so staggeringly complex that scientists struggle mightily to identify small pieces of the picture. When you take a drug, the hope is that it will go in and interrupt or boost some isolated part of a pathway that's contributing whatever disorder you may be suffering from. But disorders can rarely be neatly pinned down to a simple pathway, which means there isn't a clean target for the drug, which means the drug isn't likely to hit the problem head on. What's more, everyone has different genes, and even when we have the same relevant genes they may be turned "on" or "off" in different ways in different people, so that our pathways our different, which means that even when a drug is somewhat effective in one person it might not be so in another. Even worse, the drug is almost certainly affecting other pathways that are important to our health, with the effects rippling through the body in ways that may well cause harm. These basic problems are why we've seen a stream of much-hyped, widely used drugs yanked from the market after years, leaving behind a trail of people who weren't much helped, or of people who suffered or even died from the drugs. Vioxx is probably the best-known example from the past several years, but recent headlines have listed many others.
Indeed, it would be miraculous if a drug could go in, completely solve a problem, and do nothing else--virtually no drugs have ever been found that pull that trick off. Instead, the vast majority of our drugs have much messier effects on us: they sort of help some people, hurt others, and don't do much of anything for yet others. Even established, major drugs don't work on 40% to 75% of people, according to a 2005 review paper in The New England Journal of Medicine, and the variation in effectiveness and risk of side-effects tends to be much greater for newer, less-proven drugs. The picture gets even worse when you're talking about patients who are on multiple drugs, which can react with each other in any number of ways that are rarely well understood and often altogether unstudied. We don't get all this from the findings of most studies, because they tend to report averages, and are often presented in a way that make it sound as if a drug can do a lot for you, with only some chance of causing you problems. That may be sort of true, but there's really no way of getting around the fact that for most drugs you're rolling the dice to some extent as to whether the drug is going to help or hurt, if it does anything at all. There's hope genetic tests will eventually boost the odds further in your favor, but right now the claims you hear in the news that this is happening today is mostly hype, with just a few exceptions.
I want to make it clear I am in no way advocating pressuring your doctor to take you off any of your drugs--doctors admit in surveys to often succumbing to patient pressure on some drug decisions even if they don't think the decision is medically best for the patient--and I most certainly don't want anyone stopping drugs on their own. But there's no reason why you shouldn't ask your doctor to explain in more detail how likely a drug is to help, how likely it is to hurt, and why he thinks it's worth it. By the same token, you might want to know what applicable drugs she's decided aren't right for you, and why. Why shouldn't you be involved in a decision that essentially involves placing a bet on risks and benefits to your health? I always bow to my doctor's judgment, but she's willing to explain how she's arrived at it, and she's interested in getting my input when it's a matter of weighing the odds, as is usually the case with medications.
Sunday, June 27, 2010
Breakthrough School Anti-Obesity Study Proves...Little?
If you want a wonderful illustration of the paucity of clear information with which many and possibly most health studies provide us, and in particular how hard it is to wring any sort of credible insight out of weight-loss studies, look no further than the study currently making headlines by claiming that it proved the effectiveness of school programs designed to reduce obesity.
The USA Today report on the study kept it really simple: "The health interventions significantly lowered body mass index (BMI) in children in the 85th percentile or more. Overweight or obese kids in intervention schools were 21% less likely of being obese by the end of 8th grade. The program also lowered average levels of fasting insulin and the number of students with a waist at or over the 90th percentile in intervention schools."
But the HealthDay report provided some additional information: "....The program failed to reduce the overall numbers of overweight and obese schoolchildren--those numbers fell by 4 percent over three years whether the 42 middle schools in the study had such initiatives or not, the researchers report.... [and] children from both types of schools had the same average blood sugar levels and the same percentage of students with elevated blood sugar."
OK, so let's review: The interventions made a big difference with overweight kids--but didn't make the kids much less overweight. And the interventions reduced the risk of diabetes--but didn't prevent the high blood sugar levels that are the main indicator of diabetes or pre-diabetic conditions. Got that?
Here's what apparently happened. The schools that had the interventions saw their initially overweight kids become on average very slightly less overweight over the course of the study--just enough of a drop, it seems, to push many of them from being just heavy enough to be classified as overweight to just missing being heavy enough to be classified as overweight. Voila! Not much reduction in weight (compared to height) for the overweight kids, but a significant drop in the number of them that were "officially" overweight. The interventions did little or nothing to keep kids who weren't initially overweight from becoming overweight. And there was almost no difference between what happened in the schools that had the interventions and the schools that didn't--in both schools, there was a very slight drop over the course of the study in the kids' weight (compared to height).
As for the diabetes risk, the kids in the intervention schools saw slightly lower levels of insulin in their blood, which is generally associated with a lower diabetes risk. But it's a less important indicator than blood sugar levels, which weren't improved in the intervention schools. That's a great example of how scientific findings get muddled and often outright derailed by the choice of what gets measured in a study. (It's a problem I discuss at more length in an article in the July/August 2010 issue of Discover Magazine.)
Aside from the confusing and somewhat misleading way these results were presented in the press release, and made worse in some media accounts--it seems to me an honest presentation would have simply stated up front that the interventions didn't seem to offer any clear evidence that the interventions worked--there were complicating issues in the way the study was conducted. For one thing, the intervention schools not only made changes to the food available to the kids, but it also required longer and more intense physical activity. Yes, most of us (including me) believe these two factors go hand in hand when it comes to reducing obesity. But it may be that one of these factors has a much bigger effect than the other, and it is probably the case that some schools will find it much easier to implement only one, and not the other. So studies need to try to tease these two apart. But the bigger problem, I think, is that the schools that didn't get the official interventions were given money to make whatever changes they felt like making to their nutrition and fitness programs. Who knows what these schools did with the money? We don't even know what we're comparing here.
I certainly believe we have to come up with school-based approaches to reducing the astonishingly high child obesity rates, and I applaud any effort to study how that might be done. Unfortunately, this study's results seem to join the long train of obesity study findings that cast little light on the subject. Presenting the findings in a way that makes it sound as if a marvelous breakthrough was achieved only makes things worse.
The USA Today report on the study kept it really simple: "The health interventions significantly lowered body mass index (BMI) in children in the 85th percentile or more. Overweight or obese kids in intervention schools were 21% less likely of being obese by the end of 8th grade. The program also lowered average levels of fasting insulin and the number of students with a waist at or over the 90th percentile in intervention schools."
But the HealthDay report provided some additional information: "....The program failed to reduce the overall numbers of overweight and obese schoolchildren--those numbers fell by 4 percent over three years whether the 42 middle schools in the study had such initiatives or not, the researchers report.... [and] children from both types of schools had the same average blood sugar levels and the same percentage of students with elevated blood sugar."
OK, so let's review: The interventions made a big difference with overweight kids--but didn't make the kids much less overweight. And the interventions reduced the risk of diabetes--but didn't prevent the high blood sugar levels that are the main indicator of diabetes or pre-diabetic conditions. Got that?
Here's what apparently happened. The schools that had the interventions saw their initially overweight kids become on average very slightly less overweight over the course of the study--just enough of a drop, it seems, to push many of them from being just heavy enough to be classified as overweight to just missing being heavy enough to be classified as overweight. Voila! Not much reduction in weight (compared to height) for the overweight kids, but a significant drop in the number of them that were "officially" overweight. The interventions did little or nothing to keep kids who weren't initially overweight from becoming overweight. And there was almost no difference between what happened in the schools that had the interventions and the schools that didn't--in both schools, there was a very slight drop over the course of the study in the kids' weight (compared to height).
As for the diabetes risk, the kids in the intervention schools saw slightly lower levels of insulin in their blood, which is generally associated with a lower diabetes risk. But it's a less important indicator than blood sugar levels, which weren't improved in the intervention schools. That's a great example of how scientific findings get muddled and often outright derailed by the choice of what gets measured in a study. (It's a problem I discuss at more length in an article in the July/August 2010 issue of Discover Magazine.)
Aside from the confusing and somewhat misleading way these results were presented in the press release, and made worse in some media accounts--it seems to me an honest presentation would have simply stated up front that the interventions didn't seem to offer any clear evidence that the interventions worked--there were complicating issues in the way the study was conducted. For one thing, the intervention schools not only made changes to the food available to the kids, but it also required longer and more intense physical activity. Yes, most of us (including me) believe these two factors go hand in hand when it comes to reducing obesity. But it may be that one of these factors has a much bigger effect than the other, and it is probably the case that some schools will find it much easier to implement only one, and not the other. So studies need to try to tease these two apart. But the bigger problem, I think, is that the schools that didn't get the official interventions were given money to make whatever changes they felt like making to their nutrition and fitness programs. Who knows what these schools did with the money? We don't even know what we're comparing here.
I certainly believe we have to come up with school-based approaches to reducing the astonishingly high child obesity rates, and I applaud any effort to study how that might be done. Unfortunately, this study's results seem to join the long train of obesity study findings that cast little light on the subject. Presenting the findings in a way that makes it sound as if a marvelous breakthrough was achieved only makes things worse.
Monday, June 21, 2010
Why We Keep Questioning Exercise and 'Healthy' Eating
Newsflash: Exercise is good for your health. So is cutting down on high-fat meats, and on sugar and refined carbs such as white flour and white rice. Are you surprised? I'm not, personally, but it sounds as if a lot of people out there are finding these notions hard to believe, because we keep seeing health headlines that announce the latest study to discover that following these straightforward and generally well-accepted suggestions lowers the risks of various diseases, and of obesity.
Why do studies keep pounding these points home, when most people who actually care what studies have to say on these questions (as most people in America probably do not) have long since come to believe they've heard enough to make up their minds? Well, for one thing, that's how science is supposed to work--you keep validating theories with new tests, because the new tests may be better than the old ones, and might turn up different answers or at least new twists on them. And the accumulated results from many studies give scientists a much better handle on what's really going on. (The far bigger problem in science is that the vast majority of published research isn't validated at all, but that's a different story.)
Not only that, but the fact of the matter is that every so often an at least fairly credible study turns up evidence that suggests these standard healthy habits may not do as much for us as we'd like to think, and may even hurt. Thus there was the recent scientific review that suggested there is little solid evidence that any of the recommended lifestyle and nutritional habits lower the risk of Alzheimer's, even though we've been hearing that they do for years. There are studies that, in violation of what virtually everyone who has lost weight and kept it off knows, have found that exercise doesn't make any difference in controlling weight, a claim transmitted without doubt or qualification by former U.S. FDA commissioner David Kessler in his best-selling book on obesity. There are studies that find that eating a lot of saturated fat is just fine (these are pushed by the Atkins diet fanatics, of course), and others that conclude people would be thinner and healthier if they loaded up every morning on a high-carb breakfast. More than one study has found that being overweight may help you live longer.
So what's up with all that? Probably several things. First of all, bear in mind that scientists themselves have recognized (as I've documented at length elsewhere) that even most prestigiously published medical research is refuted within a few years. Research is hard enough when done impeccably, but it is in fact plagued with surprising levels of sloppiness, bias, fudging and other distorting shenanigans. So no results should be surprising--someone, somewhere will manage to screw a study up and get exciting but false results that some perfectly good journal will be thrilled to publish. In addition, different researchers who are supposed to be studying the same thing often end up measuring very different things in very different ways, and in very different sorts of people. Thus one study might conclude that a certain diet lowers the risk of, say, diabetes while another concludes it does not--simply because one of the studies measured blood-sugar levels in healthy patients while the other measured deaths from diabetes-related complications in very ill patients. (These measurement mismatches may be part of the problem with the studies that find obesity can be protective--it seems to prove so only for older patients and those with extensive heart disease, perhaps because old or sick people who are thin face greater risks from nutritional shortages than from the slower-acting ravages of obesity, or so it has been speculated.)
But there's an even more basic reason why we shouldn't be surprised that studies conflict on the healthfulness of nutrition and habits. There are thousands of factors that come into play when it comes to the ways various nutrients, habits and other environmental factors affect us, and they interact in a complex web that science may not yet have barely begun to unravel. Scientists try to tease the roles of individual factors out in their studies, but rarely can they honestly claim to have succeeded. (And let's not even get started here on the fact that they often base their claims on animal studies.)
All of these challenges conspire to distort study results and further confuse an already confusing picture. At least with exercise, satured fat and refined carbs there's a reasonably strong consensus of evidence, if not an unblemished one. That's why I'm going to keep exercising, and limiting saturated fat and refined carbs. I'm not fully confident any of that will do much for me, but at least I know I'm playing the odds.
Why do studies keep pounding these points home, when most people who actually care what studies have to say on these questions (as most people in America probably do not) have long since come to believe they've heard enough to make up their minds? Well, for one thing, that's how science is supposed to work--you keep validating theories with new tests, because the new tests may be better than the old ones, and might turn up different answers or at least new twists on them. And the accumulated results from many studies give scientists a much better handle on what's really going on. (The far bigger problem in science is that the vast majority of published research isn't validated at all, but that's a different story.)
Not only that, but the fact of the matter is that every so often an at least fairly credible study turns up evidence that suggests these standard healthy habits may not do as much for us as we'd like to think, and may even hurt. Thus there was the recent scientific review that suggested there is little solid evidence that any of the recommended lifestyle and nutritional habits lower the risk of Alzheimer's, even though we've been hearing that they do for years. There are studies that, in violation of what virtually everyone who has lost weight and kept it off knows, have found that exercise doesn't make any difference in controlling weight, a claim transmitted without doubt or qualification by former U.S. FDA commissioner David Kessler in his best-selling book on obesity. There are studies that find that eating a lot of saturated fat is just fine (these are pushed by the Atkins diet fanatics, of course), and others that conclude people would be thinner and healthier if they loaded up every morning on a high-carb breakfast. More than one study has found that being overweight may help you live longer.
So what's up with all that? Probably several things. First of all, bear in mind that scientists themselves have recognized (as I've documented at length elsewhere) that even most prestigiously published medical research is refuted within a few years. Research is hard enough when done impeccably, but it is in fact plagued with surprising levels of sloppiness, bias, fudging and other distorting shenanigans. So no results should be surprising--someone, somewhere will manage to screw a study up and get exciting but false results that some perfectly good journal will be thrilled to publish. In addition, different researchers who are supposed to be studying the same thing often end up measuring very different things in very different ways, and in very different sorts of people. Thus one study might conclude that a certain diet lowers the risk of, say, diabetes while another concludes it does not--simply because one of the studies measured blood-sugar levels in healthy patients while the other measured deaths from diabetes-related complications in very ill patients. (These measurement mismatches may be part of the problem with the studies that find obesity can be protective--it seems to prove so only for older patients and those with extensive heart disease, perhaps because old or sick people who are thin face greater risks from nutritional shortages than from the slower-acting ravages of obesity, or so it has been speculated.)
But there's an even more basic reason why we shouldn't be surprised that studies conflict on the healthfulness of nutrition and habits. There are thousands of factors that come into play when it comes to the ways various nutrients, habits and other environmental factors affect us, and they interact in a complex web that science may not yet have barely begun to unravel. Scientists try to tease the roles of individual factors out in their studies, but rarely can they honestly claim to have succeeded. (And let's not even get started here on the fact that they often base their claims on animal studies.)
All of these challenges conspire to distort study results and further confuse an already confusing picture. At least with exercise, satured fat and refined carbs there's a reasonably strong consensus of evidence, if not an unblemished one. That's why I'm going to keep exercising, and limiting saturated fat and refined carbs. I'm not fully confident any of that will do much for me, but at least I know I'm playing the odds.
Sunday, June 13, 2010
Do Blood-Pressure Pills Cause Cancer?
Blood-pressure pills appear to be linked to higher risks of cancer, according to a big review study making headlines. Should these results be at least a little worrisome to you if you're on one of these medications? In my opinion, yes--it's worth discussing with your doctor. (Please don't stop taking your pills on your own.) This study has many of the earmarks of more trustworthy research. It's a meta-study, which means it looked at the results from several previous studies, so that if some of the studies were troubled there's still some hope the results from the better studies will partly compensate for those problems. The studies were randomized, controlled trials, which means the people in them were randomly assigned to either take the medication in question or not take it, which can eliminate a lot of the problems studies run into. (I'm oversimplifying, but that's the basic idea.) And the studies were large, totaling some 60,000 patients, so there shouldn't be as big a chance for statistical flukes as there would be in small studies. None of these characteristics guarantee reliable findings, but they can all help.
It's worth noting that some articles describing this new study report that the study found that people on the drugs have a one percent higher risk of getting cancer. But other articles say the findings indicate risks go up on average about 10 percent, and for lung cancer a whopping 25 percent. The seeming contradiction here is due to the media's ongoing, near-complete and deeply problematic failure to specify and make clear the difference between absolute risk and relative risk. When your absolute risk of contracting a disease goes up by, say, ten percent, it means that, for example, if your risk of the disease was 14 percent, it is now 24 percent (14 plus 10), a big difference. When your relative risk goes up by ten percent, then if it was 14 percent, it is now around 15 percent (14 plus ten percent of 14)--not such a big difference. So in this example, an increase in relative risk of about 10 percent translates to an increase in absolute risk of a mere 1 percent. Research institutions typically want the public to be impressed with the importance of their results, so they often emphasize to the press relative risk, which is a generally misleadingly high number. But in this case--perhaps because there is concern that people on blood-pressure pills will overreact and stop taking them--there seems to be more interest than usual in reporting the change in absolute risk, which tends to be a very low number. Assuming you don't carry any special risk factors for lung cancer (such as smoking), you only have a tiny chance of getting it, and if you add on the apparent increased risk from blood-pressure pills, you now have a slightly less-tiny chance of getting lung cancer. Still, your chances of getting cancer of any type aren't so tiny, and a one percent increased absolute risk is nothing to sneer at. A percentage here, a percentage there, and pretty soon you're taking years off your life.
If you read about the study, you might note that even though the study found an increased risk for blood-pressure-pill takers of getting cancer, it didn't find an increased risk of them dying from it. Unfortunately, you shouldn't take this as reassuring. Most cancer studies fail to convincingly link increased risk factors to mortality, usually simply because it tends to take people many years to die of cancer (if they do die from it, that is), and studies usually don't go on long enough to follow people to their graves. (That's another reason, by the way, that researchers love running studies on mice instead of people--they're conveniently short-lived. We humans can be annoyingly enduring, from a medical-research point of view.)
Talk to your doctor about it. It may be that if you were just on the borderline of high blood pressure but have special risks for cancer, she may want you off the pills. But if your doctor feels your risks from uncontrolled high blood pressure outweigh the possible slightly increased risks of cancer turned up by this study, I'd trust him. In the unlikely chance your doctor doesn't know what you're talking about when you ask about this study, I myself would tell him that I'd be happy to sit there and wait while he looked the study up.
It's worth noting that some articles describing this new study report that the study found that people on the drugs have a one percent higher risk of getting cancer. But other articles say the findings indicate risks go up on average about 10 percent, and for lung cancer a whopping 25 percent. The seeming contradiction here is due to the media's ongoing, near-complete and deeply problematic failure to specify and make clear the difference between absolute risk and relative risk. When your absolute risk of contracting a disease goes up by, say, ten percent, it means that, for example, if your risk of the disease was 14 percent, it is now 24 percent (14 plus 10), a big difference. When your relative risk goes up by ten percent, then if it was 14 percent, it is now around 15 percent (14 plus ten percent of 14)--not such a big difference. So in this example, an increase in relative risk of about 10 percent translates to an increase in absolute risk of a mere 1 percent. Research institutions typically want the public to be impressed with the importance of their results, so they often emphasize to the press relative risk, which is a generally misleadingly high number. But in this case--perhaps because there is concern that people on blood-pressure pills will overreact and stop taking them--there seems to be more interest than usual in reporting the change in absolute risk, which tends to be a very low number. Assuming you don't carry any special risk factors for lung cancer (such as smoking), you only have a tiny chance of getting it, and if you add on the apparent increased risk from blood-pressure pills, you now have a slightly less-tiny chance of getting lung cancer. Still, your chances of getting cancer of any type aren't so tiny, and a one percent increased absolute risk is nothing to sneer at. A percentage here, a percentage there, and pretty soon you're taking years off your life.
If you read about the study, you might note that even though the study found an increased risk for blood-pressure-pill takers of getting cancer, it didn't find an increased risk of them dying from it. Unfortunately, you shouldn't take this as reassuring. Most cancer studies fail to convincingly link increased risk factors to mortality, usually simply because it tends to take people many years to die of cancer (if they do die from it, that is), and studies usually don't go on long enough to follow people to their graves. (That's another reason, by the way, that researchers love running studies on mice instead of people--they're conveniently short-lived. We humans can be annoyingly enduring, from a medical-research point of view.)
Talk to your doctor about it. It may be that if you were just on the borderline of high blood pressure but have special risks for cancer, she may want you off the pills. But if your doctor feels your risks from uncontrolled high blood pressure outweigh the possible slightly increased risks of cancer turned up by this study, I'd trust him. In the unlikely chance your doctor doesn't know what you're talking about when you ask about this study, I myself would tell him that I'd be happy to sit there and wait while he looked the study up.