How to Live Longer And Exercise Shorter?

Let's face it, if exercise was really that much fun, everybody would do it and we wouldn't be fat, diabetic or die of heart disease. So when your doctor tells you that you better start exercising, your immediate question might be: how much do I have to do? The answer is, it depends. It depends on whether you want to hear the polite version or the truth.  [tweet this].

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The one way to make you slim, fit and healthy?

That your fattening lifestyle drives health insurance costs up is nothing but a fat lie. That much I have told you in the previous post. With Marlboro Man and Ronald McDonald doing better for your health insurer's balance sheet than Healthy Living, you might think that public health should look beyond economics as an argument for health.  In this post I will tell you why they shouldn't. 

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Pass me the salt. And shut up about stroke risk.

They say, statistics lie.

That's a bad rep for a science, which has no other aspiration than that of making sense from data, of discovering an association between salt intake and stroke, of proving that the former causes the latter. Statistics is above lies. Those who interpret it are not. 

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Guess who is hiding the magic pill to longevity?

Imagine a medicine which protects you against cardiovascular disease, cancers, diabetes, depression and dementia. A medicine which works best when taken regularly and long before any symptoms of any of those diseases appear. A medicine which is cheaper than any supplement or aspirin. Would you take it?

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It's not your genes, stupid.

Imagine traveling back in time and meeting your caveman ancestor of 10,000 years ago. Imagine telling him about what life is like today: that, with the tap of a finger you turn darkness into light, a cold room into a warm one and a tube in the wall of your cave into a spring of hot and cold water. You tell him...

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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.

1.           Morris, J.N. and P.A. Raffle, Coronary heart disease in transport workers; a progress report. Br J Ind Med, 1954. 11(4): p. 260-4.

2.           Physical Activity Guidelines Advisory Committee, Physical Activity Guidelines Advisory Committee Report, 2008, U.S. Department of Health and Human Services: Washington, D.C.

3.           Eaton, S.B. and S.B. Eaton, An evolutionary perspective on human physical activity: implications for health. Comp Biochem Physiol A Mol Integr Physiol, 2003. 136(1): p. 153-9.

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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 PrintPDF

Screw Your Health?!

So, what's your excuse for not exercising enough, for smoking, for not watching your diet, for getting fatter every year, and therefore having high blood pressure, and too much glucose and cholesterol in your blood?

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How to get those vegetarian zealots off your back.

Does red meat kill you? Only in a vegetarian's dream!

Red meat is the favorite enemy of nutritionists nowadays. Their studies and publications are often (ab-)used by those evangelical vegetarian types who would love to impose their no-meat religion on the rest of us. Don't buy it. Now let me show you how you can profess your love for steak AND support it with the data from the same studies which the zealots use for their vegetarian crusades.

Earlier this year Pan et al. published a study titled "Red meat consumption and mortality" [1]. They had pooled the data of two large prospective studies, the Nurses' Health Study and the Health Professionals' Follow-up Study. Collectively these studies had followed 121,000 people, who were free of cardiovascular diseases at baseline, for more than 20 years. Altogether, the participants accumulated close to 3 million person years for observation. During the observation period close to 24,000 deaths occurred of which 6,000 were of cardiovascular causes, that is heart attack, stroke, heart failure.

The researchers discovered that for every increase of 1 serving of unprocessed red meat per day the hazard ratio of dying from any cause was 1.13 and the hazard ratio of dying from a cvd-cause was 1.2. That means for every increase of a serving of red meat per day the chances of dying from any cause and from a cvd-cause increased by 13% and 20% respectively. Those rates were a little higher for processed red meat. To put this into perspective the researchers also calculated that if all participants had eaten less than half a serving of red meat per day (42g/d), 9% of deaths in men and 7.6% of deaths in women could have been prevented. Wonderful. Sounds impressive, but it isn't for one simple reason:

Unreliable data acquisition. Just ask one question: how did the researchers know how much red meat those people ate? This question cuts to the heart of many, if not most, studies on diet-disease associations. Data on food consumption are typically acquired through food frequency questionnaires (FFQ). These FFQs ask you about your consumption of food items over the past days, weeks or even months. And as you can imagine, such recall can be terribly unreliable. So much so, that other researchers wanted to quantify this effect. So they used FFQs and compared the results with objective quantitative measurement of energy intake and protein intake [2]. And lo and behold, they discovered that if relative risks (such as the hazard ratio mentioned above) were calculated from FFQs they overestimate the true diet-disease association very severely. In fact so severe, that a hazard ratio of, say, 2 would in reality be around 1.3.

What does that mean for a hazard ratio which is, as in the study of Pan and colleagues, less than 1.3 to begin with? It means possibly nothing. You certainly can't conclude from these data that red meat kills you. That's what it means.  And mind you, this inaccuracy of FFQs shows up with recall periods of a few weeks. Pan and colleagues had to rely on FFQs which were conducted YEARS apart. In fact,  data acquisition based on FFQs is so flawed, that the question been raised "is it time to abandon the food frequency questionnaire?" [3]. And the authors state: "We should be very circumspect about analyses of current studies that have used FFQs for dietary assessment." That was 7 years ago. We still have those FFQs and you  still have the media telling you  how bad red meat is for you.

And I'm going to have a real nice steak now. How about you?

1.           Pan, A., et al., Red Meat Consumption and Mortality: Results From 2 Prospective Cohort Studies. Archives of Internal Medicine, 2012: p. archinternmed.2011.2287.

2.           Kipnis, V., et al., Structure of dietary measurement error: results of the OPEN biomarker study. American Journal of Epidemiology, 2003. 158(1): p. 14-21; discussion 22-6.

3.           Kristal, A.R., U. Peters, and J.D. Potter, Is it time to abandon the food frequency questionnaire? Cancer Epidemiology, Biomarkers and Prevention, 2005. 14(12): p. 2826-8.

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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?

1.           Akosah, K.O., et al., Preventing myocardial infarction in the young adult in the first place: how do the National Cholesterol Education Panel III guidelines perform? Journal of the American College of Cardiology, 2003. 41(9): p. 1475-9.

2.           Lloyd-Jones, D.M., et al., Prediction of lifetime risk for cardiovascular disease by risk factor burden at 50 years of age. Circulation, 2006. 113(6): p. 791-8.

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Are fat people just lazy?

Are fat people just lazy? Or is it in their genes?

Let's look at an unlikely place for the answer: an AA meeting. If you get up and say "My name is Jane, and I'm not really an alcoholic, I don't drink that much..." they throw you out. They welcome you back, once you say "My name is Jane and I'm an alcoholic". The same should be true for fat people. And I'm using this politically incorrect term deliberately. Because unless you wake up to the reality, you won't be able to change that reality.

 AA have long ago realized that fact. And they have a 50% long-term success rate. That is, half the alcoholics who join AA stay dry for the rest of their lives. That's way more than what public health, clinical and commercial weight loss programs achieve with obese participants. We are happy if 10% of those who enter these programs achieve a 10% weight loss AND keep it for more than 2 years. It's that bad. Is it because of the genes? A study published recently in Nature Genetics, might supply another excuse to some overweight people. But before we look at this study, let's look at some other facts first.

One thing we all know for sure: if you are overweight, you obviously have taken in more calories than you have expended. Over quite some time, because it takes a while to accumulate all those energy reserves on your waist and hips. Boils down to one of the tenets of a universal law of physics that says: Energy can neither be destroyed nor miraculously created. Not even on your hips.

Now I know all the objections raised by so many overweight people, like "But, I hardly eat anything. How can I be fat? Even my friends say, from what you eat nobody can get fat." Believe me, I've heard them all.  And my heart sinks, when I do, because I know there goes the hopeless case. The Jane who goes to AA and tells them she is different. The study published in Nature Genetics might just deliver her the next excuse. Not because the researchers tell her so, but because some media genius might just read it the wrong way. As they often do. So, let's look a what the researchers say.

The researchers conducted a meta-analysis of some 14 genome wide association studies involving altogether 14,000 children, one third of which were obese. They found 7 genetic markers which correlated with obesity and which also turned out to correlate with obesity in adults. The beauty of looking at genetics in kids is, that they haven't been exposed to decades of lifestyles which may obscure such links. 

So, the results clearly point into the direction of some genetic signature predisposing a person to become obese. But having this signature doesn't mean you'll inevitably become obese. Because most kids who have the signature are not obese. It's only that this signature shows up a little more often in the obese kids than in their non-obese peers.  And there is one more thing, you need to keep in mind. Over the past 20 years the human genetic make-up hasn't changed at all. But the obesity rate in US kids has. In fact it has tripled during that period. And health behavior has changed, too. And so did our environment.

What makes me always frustrated in all this debate about genes vs. environment vs. behavior is my scientist colleagues' and the media's inability to educate their audience about the complete picture. Genes make up the blueprint to your organism. True. But they don't make that organism. Genes make proteins, but whether they make them or whether they are silenced into not making them, that depends on epigenetics, on the interaction with your environment, and on your behavior, which again is influenced by all the others. It is a very complex relationship, and I'm afraid, genetics will not help us, to solve the obesity epidemic. But neither will the stigmatization of the obese. 

What we need, is a way to help those who recognize their fatness as a resolvable reality, resolve it. That's why I'm working on the GPS tochronic health, because I know that once the health behaviors put you on track to chronic health and longevity, your overweight problem will resolve automatically. As a side effect. But only if the obese person works with us. 

So did that answer the question? You decide for yourself.    PrintPDF

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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How to admire obese people? The Token Fat Girl

Yesterday, on a whim, I started searching the web for sites where obese people present themselves and how they deal with obesity. My expectation was:  I won't find much. Boy was I wrong. In fact I was so wrong, that I decided to discuss some of the outstanding people whose sites I have seen. Before I get to The Token Fat Girl, let me explain why I didn't expect to find what I found:

There is a stigma attached to being overweight. Interpersonal and work related discrimination against overweight people pervades our society [1]. Whether it's finding a sex partner or a salary, if you are female and have a BMI north of 30, your weight alone reduces your chances compared with a peer of normal weight. And don't think for a moment that my colleagues from the health and medical sciences are free from such bias. One in 4 nurses reports being repulsed by obese patients [2], and exercise science students show a strong bias against obese people, equating obesity with laziness [3]. The frequently used before-after portraits of successful weight reducers have been found to reinforce the belief that weight loss is a matter of volition, which in turn reinforces the stigmatization of the overweight [4]. This bias has become so pervasive in our society that even obese people themselves now endorse the fat=lazy equation [5]. Uncharacteristically for my otherwise more colloquial blog I include here the references to my statements. For one simple reason: To take the wind out of the sails of those who would otherwise eloquently try to summarily refute my statements.  

Now, what's my point? With this type of agony load, wouldn't we rightly expect the obese person to simply change her lifestyle if this change was really up to her free will - her volition - to make? Yes we would. The fact that most obese people really WANT to be slim but never seem to get there should, however, make us question the power of free will over our health behaviors, particularly the dietary and exercise behaviors. Let me illustrate that point a little more.

If the volition-behavior assumption was true, children would change their fattening behaviors once the agony load from being obese crosses a threshold at which they would be motivated to actively pursue weight loss. This agony load is indeed high for the obese child. In fact it has been found to be equal to that of child cancer patients receiving chemo therapy [6]. Yet the percentage of obese children and adolescents has more than tripled over the past 40 years.

So my question to the stigmatizers, to those who believe in the fat=lazy equation, is: if obesity was a result of behavior, and if health behavior is a matter of choice, then why do children and adults choose to be ostracized, stigmatized and victimized?

Obviously our health behaviors are driven by something more powerful than volition alone. I will address this issue in a separate blog entry.

What I want to highlight here is the extraordinary guts of people like The Token Fat Girl, who proudly present themselves and address their weight openly and publicly. Not only is her courage admirable, but so is the frankness with which she approaches her life. I quote from her site: " I've struggled with being overweight or obese my entire life and while I don't agree that I can be obese and healthy, I do believe that it shouldn't stop me from living a pretty decent life." Here is a girl with an admirable sense of reality. A girl with that attitude would certainly solve her weight issues if those were solvable by volition only. 

This issue is at the core of my work. I have a pretty clear model about what drives our health behaviors. That model was part of my dissertation work. I also believe that our strategy of helping people to train a 6th sense for their daily calorie balance is a promising alternative to diets and weight loss fads. I would love to enroll people like the Token Fat Girl into our chronic health project. So if you know somebody who fits this description, give them my contact.  

   

1.           Carr, D. and M.A. Friedman, Is obesity stigmatizing? Body weight, perceived discrimination, and psychological well-being in the United States. J Health Soc Behav, 2005. 46(3): p. 244-59.

2.           Puhl, R. and K.D. Brownell, Bias, Discrimination, and Obesity. Obesity Res, 2001. 9(12): p. 788-805.

3.           Chambliss, H.O., C.E. Finley, and S.N. Blair, Attitudes toward obese individuals among exercise science students. Med Sci Sports Exerc, 2004. 36(3): p. 468-74.

4.           Geier, A.B., M.B. Schwartz, and K.D. Brownell, "Before and after" diet advertisements escalate weight stigma. Eat Weight Disord, 2003. 8(4): p. 282-8.

5.           Wang, S.S., K.D. Brownell, and T.A. Wadden, The influence of the stigma of obesity on overweight individuals. Int J Obes Relat Metab Disord, 2004. 28(10): p. 1333-7.

6.           Schwimmer, J.B., T.M. Burwinkle, and J.W. Varni, Health-Related Quality of Life of Severely Obese Children and Adolescents. JAMA, 2003. 289(14): p. 1813-1819.

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