Showing posts with label primary prevention. Show all posts
Showing posts with label primary prevention. Show all posts

Monday, April 23, 2012

To hell with exercise



Who says that exercise is medicine? For one, the American College of Sports Medicine (ACSM) of which I'm a professional member. Then, how can I say it isn't?
Let's look first at the conventional view of the benefits of exercise. There is a large and increasing amount of evidence which clearly tells us that exercise prevents today's number 1 killer: cardiovascular disease. That is, heart attack, stroke and peripheral vascular disease. Mind you, what is common knowledge today emerged only some 50 years ago when Morris and colleagues discovered that UK bus conductors, the guys climbing up and down the double-decker London buses, had better fitness and fewer heart attacks than their all-day-seated driver colleagues [1].
In the years since then our knowledge about the effects of physical activity on cardiovascular, metabolic and mental health has virtually exploded. From this evidence the U.S. Dept. of Health and Human Services (HHS) concluded in 2008 that the most active people of the population have a 35% reduced risk of dying from cardiovascular disease compared to the least active people [2]. The WHO lists insufficient physical activity (PA) as the 4th leading cause of death world wide after high blood pressure, tobacco use and high blood glucose. What's wrong with this picture? High blood pressure and high blood glucose are known consequences of a sedentary lifestyle. So is obesity, which ranks 5th place on the WHO killer list. Which is why physical inactivity deserves top spot on that list.
What most people don't know is the way lack of physical activity causes all those diseases, from insulin resistance and diabetes to arterial dysfunction and atherosclerosis, and from there to heart attack, stroke, kidney failure. The mechanisms are extremely complex, and, while we have untangled quite some of them, there are probably a lot more to discover. I'll try to make this the subject of one of the next blog posts. 
Now you are probably asking yourself, how the hell, with all this evidence, will I ever be able to make my point that physical activity is not a medicine. Ok, here it comes: it's a matter of viewpoint. The one I'm taking is the one of evolutionary biology. Let me play its advocate and present as evidence a couple of insights.
First, our human ancestors, who had roamed this Earth as hunter/gatherers for the most part of human existence, had, by necessity, a much more physically active lifestyle. A lifestyle which required at least 1.7 to 2 times the normal resting energy expenditure [3]. [To get an idea about resting energy expenditure and physical activity levels and how they are calculated, simply follow the links to the videos.] Those ancestors' genes are what we have inherited. And these genes are exposed to a lifestyle which is vastly different from the ones under which these genes evolved. Specifically with a view to physical activity, which brings me to evidence no 2:
What we typically observe today are physical activity levels with factors of somewhere between 1.2 and 1.4 of our resting energy expenditure. That's true for most people.
Even if you were to follow the ACSM's recommendation of 30 minutes of moderate to vigorous exercise on at least 5 days per week, would you NOT reach the level of 1.7 if you are working in a typical office job or doing house work. Which means, the physical activity levels which we recommend today, do not add a behavioral type of medicine into our lives, they merely reduce the extent of a "poisonous" behavior called sedentism. It's like cutting down from 2 packs of cigarettes per day to 1 pack. Would you call this a "medicine"? Would the ACSM call that a medicine? With respect to exercise they do.
So, OK, if you had been attracted to this post in the hope of finding some excuse for not doing exercise, or some argument to get those exercise evangelists, like myself, off your back, I'm sorry to have disappointed you. No, actually, I'm not sorry. And neither will you be, if you get your physical activity level above those 1.7. Then you may just start calling exercise a medicine. Until then, chances are you will still go to hell with exercise, because you get too little of it. Certainly too little to stay out of that hell of heart disease, stroke, diabetes and many cancers.



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MORRIS JN, & RAFFLE PA (1954). Coronary heart disease in transport workers; a progress report. British journal of industrial medicine, 11 (4), 260-4 PMID: 13208943
Eaton, S., & Eaton, S. (2003). An evolutionary perspective on human physical activity: implications for health Comparative Biochemistry and Physiology - Part A: Molecular & Integrative Physiology, 136 (1), 153-159 DOI: 10.1016/S1095-6433(03)00208-3 Print Friendly and PDFPrintPrint Friendly and PDFPDF

Wednesday, April 18, 2012

Am I shittin' you? Learn to be a skeptic!

Learn to be a skeptic!

Why you cannot believe what you read about medical studies.

In my last blog post I promised to tell you why you shouldn't trust any study results, particularly when you didn't read the study yourself. It has to do with the methods of biomedical research. To make my point, I'll take the gold standard research method, the double blinded randomized controlled trial, or RCT. 
Let's say we want to test a drug, which is supposed to lower blood pressure in those who suffer from hypertension. The researchers have decided to enroll, say, 100 "subjects". That's what we typically call the people who are kind enough to play guinea pig in our studies.   
The researchers will first do a randomization of subjects into one of two groups (very often it is more than one group, but to keep it simple we will assume just two groups). What we mean with randomization is that we randomly assign each subject to one of the two groups. One group - the intervention group - will receive the drug, the other group - the control group - won't. What they get instead is a sugar pill, a placebo. 
With the randomization we want to make sure that, at the start, or baseline, both groups are indistinguishable from each other with respect to their average vital parameters. For example, if we were to calculate the mean age, blood pressure and any other variable for each group, these mean values would be not different between groups. That's important, because we want to isolate the effect of the drug. We don't want to worry at the end whether the effect, or lack thereof, was maybe due to some significant difference between the groups at baseline. 
Once the randomization is done, we organize the trial in such a way that neither the "subjects" nor their physicians and nurses know whether they get the placebo or the active drug. Both sides are blind to what they get and give, which is why this set-up is called double-blinded. That's an important feature, because a researcher often goes into a study with a certain expectation of its outcome. Either that outcome supports his hypothesis, or it doesn't. To eliminate the risk of, more or less subconsciously, influencing the study towards a desired outcome, double-blinding is very effective tool.
Fast forward to the end of our trial. We have now all the data in hand to compare the two groups. After unblinding, the researchers will compare the two groups with each other. In our example, they will compare the average, or mean, of the blood pressure values of all the individuals for each group. If the intervention group's mean value is lower than that of the control group, then it is plausible to reject the null-hypothesis, that is to REJECT the idea that the drug is NOT as ineffective as the placebo (we are, of course, assuming here that the sugar pill didn't lower the blood pressure of the control group). 

There are statistical tools to determine whether the difference between the groups may just be a chance event, or whether chance is a very unlikely explanation. We can never rule out chance completely. Now, when we are confident that it is the drug and not pure chance, which has lowered the mean blood pressure in the intervention group, we write our paper to present it in one of the medical journals. 

If the subject is a little more sexy, than just lowering blood pressure, there will sure be some journalists who pick it up and report to their readers that, say, eating chocolate makes you slimmer. I'm not kidding. This headline very conveniently went through the media shortly before Easter this year [1]. Good for Hershey who are running it of course on their webpage. And in the media it reads like it did in the Irish Times: "Good news for chocoholics this Easter. Medical Matters: No need for guilt over all those Easter eggs."    


I'm not going to comment on the media geniuses, because it's their job to put an angle on every story, so that YOU find it interesting and read their stuff. But since I'm sure you'll follow these links, just let me warn you: the chocolate study was an observational study, not an RCT. And one thing we MUST NOT do with the results of observational studies is to confuse association with causation. Only when we conduct an RCT, where the intervention group eats chocolate and the control group doesn't, might we be able to determine whether there is a causal link. And for obvious reasons we can't blind the subjects, to whether they eat chocolate or not. But I'm digressing.
Back to our blood pressure study. When we compare the group averages, everything looks very convincing. And sure enough, as researchers we are happy with the results, and we are perfectly correct, when we conclude, that this medicine does its job. 
But will it do it for you? When you are hypertensive? You might be wrong if you say "Yes". And you will be wrong more often than we, as researchers, or your doctors care to admit. For one simple reason: The variability of effect within the group. You give 50 people the same drug, and I bet with you, and I'm not the betting type, that you'll have 50 different results. 
The mean value of the entire group glosses over these inter-individual differences. Let me give you an example from a study performed on 35 overweight men, who were studied in a supervised and carefully calculated 12-weeks exercise program, with the intention of reducing body weight. The mean weight loss was 3.7 kg. That was almost exactly the amount of weight loss which the researchers had expected from the additional energy expenditure of the exercise program. But when they looked at each individual, it became clear that the group mean doesn't tell you anything about how YOU would fare in that program. 
First of all, the standard deviation was 3.6 kg. Now, a standard deviation of 3.6 kg simply tells you that approximately two thirds of the participants experienced a weight loss anywhere between 3,7 kg (the mean) minus 3.6 kg and 3.7kg + 3.6 kg, that is between 0.1 kg and 7.3 kg! That's a lot of kilos. And what about the remaining one third of those participants? They are even further from these values. In this case the greatest loser went down by 14 kg, and the biggest "winner" gained almost 2 kg. A spread of 16 kilos!
Here is the graph which shows you the change on body weight and fat for each individual participant. Which one would you be?

This effect is what you do not see when you don't read the studies. And in most studies, it isn't made obvious either. 
Which is why, you shouldn't be surprised to learn that most major drugs are effective only in 25-60% of their users [2]. The same goes for weight loss drugs and interventions, for almost everything we study in biomedicine. 
That's not a problem for us in public health. Because a drug, which works in 60% of the patients, helps us reduce the burden of disease in our population. Public health is not interested whether you are one of the 60% or not. But you are. And that's why I believe not only medicine, but also prevention must be individualized.
 Which is why the GPS to chronic health, which I currently develop, is all about helping you find your individual path to your health objectives.
Why not have a look at it, and maybe even try it out? 

References


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Wednesday, April 11, 2012

When risk scores for heart attack really suck!

When risk scores really suck.

If you are a man aged 55 or younger, or a woman aged 65 or younger and have had your risk for heart attack and stroke profiled recently, chances are your doctor told you that you have a low risk. So you probably walked out of her clinic, seeing no reason to change your lifestyle. Now here I am, the party pooper, who is going to rain on your parade. How so?
Well, first off, those risk scores, like the Framingham score used in the US and the PROCAM score used here in Germany, typically look at things like cholesterol, blood pressure, blood sugar, smoking status, age and gender. From these values the scores determine your 10-year forward risk. Conventionally, if your chances of suffering a heart attack, stroke or any other of the cardiovascular diseases endpoints is less than 10% for that 10-year period, yours is categorized as low-risk. If it was in excess of 20%, you would be considered a high-risk person, and anything in between is called moderate risk. Now here is the problem: of the women who are hospitalized for their first heart attack at an age younger than 65, typically none would have scored as high-risk even a day before the event [1].  In fact, 95% of these women would have flown under the risk radar in the low-risk altitude.
How come, you may ask. To understand the reason you need to know how heart attacks and strokes happen. Most of them are the result of a blood clot being formed at the site of a ruptured plaque (those fatty streaks) in one of your arteries. Traveling downstream these clots may be dissolved or they may be not. If they get stuck some place downstream, blocking the supply of blood, and thereby of oxygen, to your heart or brain tissue, a heart attack or stroke occurs. But most plaque ruptures do not cause a heart attack or stroke. There is a large element of chance involved. Fact of the matter is, we can't really predict which plaques will cause a heart attack or stroke. We can't even say whether a stable or a so-called vulnerable plaque will still be stable or vulnerable in a few months down the line. They can change their status. Which means, even if your doctor was able to map all the plaques in all the arteries throughout your body, he still wouldn't be able to tell you exactly your risk. How much less accurate will his risk prediction be when he uses risk factors which just correlate somewhat with plaque burden, such as cholesterol? There you go.  
Which is why you should not look at 10-year risk, but at lifetime risk. For a woman that risk stands at roughly 40% once she has reached the age of 50 [2]. Men, by the way have a 52% risk at that age. But here is the kicker: being free of any of the risk factors (those of the Framingham or PROCAM variety) at that age, means a dramatically lower lifetime risk of 8% and 5% for women and men respectively.
So here you are. Your doctor has just sent you off with a low-risk assurance for the next 10 years, even though 2 of your risk factors are elevated. You walk out of his clinic with a strong sense of invulnerability and no real motivation to change your lifestyle and to get those two risk factors back into the green zone. That's why risk scores really suck. When they rain on your parade later on it's a lot worse than if I, the party pooper, do it right now. Don't you think?


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Friday, April 6, 2012

How to get to chronic health. With three steps into the age of chronic health and longevity.

Into the age of chronic health.

My yesterday's post was all about what's holding us back from achieving chronic health for everybody. Today I want to look at the three important steps we can do right now to enter the age of chronic health and longevity. 

Incentivize health! 

Earlier this year Standard & Poor's told the G20 economies:  Get prevention to work or we will downgrade your triple A rating by latest 2018. Because your economies won't be able to deal with the costs for treating your sick, demented and frail population. Of course Standard & Poor's phrased it more politely but the message was all the same.  Why is that so important? Because it's the first step to making everybody realize that your chronic health is not just this often proclaimed "higher good", it is an economic asset. It makes you more productive for your employer, and less costly for your health and life insurer. Once your health shows up in the shareholder value universe, employers have an incentive to invest into it. And they have an incentive to share with you in the form of a health dividend. The keyword here is incentive. The lack of it is what ails our current health care strategies. Because until now we have failed to incentivize people's prevention efforts. Think about it: Whether it's status or money or anything else that turns your neighbors green with envy, the driving force behind all human endeavors is the prospect of incentives. It's hardwired into our brains. It's why everybody's efforts to achieve chronic health needs incentives, too. As we have seen, the prospect of being healthy in a distant future can't beat the siren call of a humble tiramisu, or of the drag on a cigarette, or of staying on the sofa instead of jogging through the Park. So, if the phenomenon of hyperbolic discounting has taught us anything, it is the need for incentives with which to beat those that lure us into unhealthy behaviors.
What holds our companies and insurers back from incentivizing health big time? Certainly it is not unwillingness, and rarely is it uncertainty about the size of the returns on investment. It is rather the lack of a tool with which to direct incentives to where they are deserved and to withhold them from where they are not. A tool which helps you to express, in objectively measurable terms, not only your health but also your efforts and achievements of preserving it. We are currently testing the first prototype of such a tool. We started to develop it with this and two more goals in mind. The first is to help you to...  

Outfox your brain!

As you have learned above, the evolutionary ape in us is well protected against any interference of free will and reason, the two things that make us human. But whether human or ape, we all have the ability to develop a 6th sense for mastering any skill which improves our chance of survival, makes our life easier or more enjoyable. In your case, think swimming, think cycling, think keeping your in-laws out of your hair. So we thought, how about a 6th sense for your daily calorie balance? We thought, if you knew it intuitively, at any moment, and before it shows on your bathroom scale, you would effectively know your metabolic state. With that knowledge you will be able to correct and to keep that balance always in line with your weight targets. This intuitive knowledge does not eliminate the craving for the tiramisu. But it enables you to recognize the need for taking some compensatory measure and to select the appropriate size of that measure.  This idea was borne out of the results of a new web-assisted intervention which we developed and tested in Germany with the aim to institute lasting behavior change in adults at elevated risk for chronic disease. Once the participants of our clinical trial showed signs of mastering this 6th sense, they also started to drop their dress sizes. And they still keep those dress sizes down.
Now, I can hear your question: Even if, say, my employer pays me a monthly or quarterly health dividend, in the form of money or annual leave or whatever floats my boat, how can you be so sure that my new lifestyle of eating right and exercising right will bring me chronic health and longevity? Which brings me to the last point. 

Take Biomedicine's most powerful tools!

Let's just look at how your chances play out. If, at age 45, you are free of any risk factors, you stand a 97% chance of making it through to your 80th birthday in good health. If, however, you already have 2 risk factors, such as hypertension and elevated blood sugar, for example, those chances shrink to a mere fifty-fifty. And even if you are among the lucky half, who will see those 80 candles on their cakes, chances are that you won't blow them out under your own steam. Because one of those nasty chronic diseases will have taken that last piece of strength and dignity away from you. The good news is that simple health behaviors - physical activity, dietary and smoking behaviors - determine which version of the party, if any, will apply to you. In fact, biomedicine currently knows no intervention which prevents disease and promotes longevity better than physical activity and dietary behaviors. There is one caveat, though: these simple behaviors need to be tailored to your individual health profile, which also means to your genotype AND your phenotype. 
Which is why my colleagues and I are building an intervention matching feature into the tool I mentioned earlier. It will give you the means to match your individual health and risk profile with the physical activity and dietary strategies most suitable for your profile. We call this tool the GPS to chronic health and longevity. It takes its coordinates on the landscape of health from your vital functions and keeps you right on track towards your health goals.
It is the engine which we hope will give you the power of mapping and following your personal path into the age of chronic health and longevity. After all, nobody deserves the indignity of a stroke or a heart attack and the disabilities that come as a consequence. 
I firmly believe we are only a tiny step away from the age of chronic health and longevity. To that tiny step you can contribute.  Just visit me at indiegogo until 31st of May. 
I'm looking forward to meeting you there. 
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Thursday, April 5, 2012

The three hidden barriers to chronic health, weight loss and weight maintenance.

Into The Age of Chronic Health
The most amazing thing about modern health care systems is that they let most of us die from chronic diseases which we know how to prevent. So why don't we?
As a public health scientist I have devoted the past 15 years of my life to answering this question. Many of my colleagues outdo each other with doom and gloom predictions of aging societies buckling under the economic burden of aging related diseases. I believe that the age of chronic health and longevity is about to begin. With you. And with a radically new approach to make the prevention of heart attacks, strokes diabetes and cancers finally work.     
Because, until now, it doesn't. But don't just take my word for it, let's look at some of the facts first:
You have probably heard that obesity is the new smoking. In fact for every American who stopped smoking in 2011 another one became obese.   
Today, for the first time in human history there are more overfed than malnourished people walking this planet. And their lifestyles of too much food and too little exercise have become the number one risk factor for the number one chronic disease and killer: cardiovascular disease with its most well-known end points - heart attack, stroke and heart failure. With nasty other diseases on the side: diabetes, kidney failure and certain cancers.
You probably also heard about major studies, like the U.S. government funded Diabetes Prevention Program, and the Look AHEAD trial, which proudly, and correctly, report weight loss and major reductions in cardiovascular risk factors among participants in the lifestyle arms of these trials. What you don't hear so often, is that within 3-4 years after enrollment, most participants will have regained not only most of their weight but also all their risk factors.
Ok then, lifestyle change prevents disease. But what prevents lifestyle change?
Why is it that over the last 30 years of public health efforts we have not seen a demonstration of any program that results in a clinically meaningful weight loss that can be maintained for more than 2-3 years in the majority of participants and at low cost?  That's the question which Dr. Richard Khan threw at an assembly of public health advocates, who had gathered earlier this year under the event's message "Prevention works!".  Dr. Khan, who teaches medicine at the University of North Carolina, was the chief scientific officer of the American Diabetes Association for 25 years. The man certainly knows what he is talking about. 
Now think about the implication. If you chose a lifestyle of which you know might increase risk of disease and premature death, then you make that choice either willingly or it is not your free will which makes that choice.
My money is on the latter. Because how else could we explain that an obese child maintains her fattening habits despite experiencing the same psychological agony as a child with cancer? How else could we explain that obese adults maintain their bulk when it significantly reduces their chances of getting an academic education, a job and a mate? How else could we explain that over the past 20 years the obesity rate in the US went up by 60% when, during the same period, Americans doubled their spending on weight loss products to US$ 60 billion annually? They WANT to lose weight, but they don't. The explanations are called addiction, hormones and hyperbole.  
Food addiction
The neurohormonal architecture which drives an addict to crave and consume his drug, despite knowing and hating the consequences, is exactly the same architecture that keeps us going for the sweet, fatty and salty stuff in restaurants, hawker centers and vending machines. Does that explain, why the food industry adds sugars to so many foods in which you least expect it? You bet. In fact we shouldn't be afraid of calling ourselves food addicts, because this is what Mother Nature intended us to be all along. With this addiction she drove our ancestors for millions of years to what is naturally sweet in the natural human habitat: fruits. They deliver not only the carbohydrates for which we have very little storage capacity in our bodies and without which our brain can't function. Fruits also pack a punch of essential micronutrients. Unlike the cokes and cakes and cookies which deliver more sugar than we need and no other nutrients with it.  
Hormones
Once you have changed your figure into the shape of a beached whale, you will also have changed the way the hormones of your gut and of your fat tissue work. It's a rather complicated picture unfolding in the labs of biomedicine, but one emerging theme is a colossal malfunction of the satiety and appetite signaling pathways. Instead of feeling full, you are now ready to add a tiramisu to a lunch that would have satiated a family of four in rural Bangladesh.
Hyperbole
Actually it's called hyperbolic discounting, and it's a simple mathematical formula, which behavioral scientists have found to neatly describe why we will still grab that tiramisu tomorrow even though we swear today that we won't. It has to do with how we more steeply discount the relatively larger but more distant reward of staying healthy against the relatively smaller but immediate reward of enjoying the tiramisu. It doesn't operate only in humans. The behaviors of rats, pigeons and apes, for example, follow the same formula. Which means, Mother Nature must have found out early during evolution that this principle is a recipe for survival in her species. We simply inherited this survival tool.   
With all these issues stacked in favor of an ever expanding population of chronically ill people, why do I believe that we might be close to the age of chronic health and longevity? For three reasons: Because Wall Street is getting into the act, because we can outfox our brain, and because biomedical science has got the tools ready.
How we will enter the age of chronic health is the subject of the next episode, so stay tuned!
In the meantime, visit my crowd funding campaign, watch the videos, recommend the campaign to your friends and, if you like what you see, participate in our chronic health project: www.indiegogo.com/adiphea

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