Chronisch gesund geht. Aber nicht mit unserem Gesundheitssystem.

So versagt unser Gesundheitswesen

Das Faszinierende an unserem Gesundheitssystem ist, dass es 8 von 10 Deutschen an chronischen Krankheiten leiden und sterben lässt, obwohl wir genau wissen, wie wir diese Krankheiten verhüten können. Also warum tun wir's nicht?

Als Gesundheitswissenschaftler arbeite ich seit 15 Jahren an der Beantwortung dieser Frage. Viele meiner Kollegen warnen mit immer dunkler werdenden Zukunftsvisionen vor einem Tsunami aus Behandlungs- und Pflegekosten für unsere zunehmend älter, kränker und dementer werdende Bevölkerung. 

Dabei könnten wir das Zeitalter der chronischen Gesundheit bereits jetzt einläuten. Ein Zeitalter in dem  Herzinfarkt, Schlaganfall und viele Krebsarten ihre Bedeutung in der Sterbestatistik verloren haben werden. So wie die ansteckenden Krankheiten nach der Einführung der Hygiene.  Aber so, wie wir Prävention bislang machen, funktioniert sie nicht. Die Entscheidungsträger unseres Gesundheitssystems kämen zum gleichen Schluss, wären sie nicht mit einer selektiven Blindheit gegenüber unbequemen Fakten geschlagen.

Das Versagen der Prävention

Die Akteure unseres Gesundheitswesens verweisen gerne auf große staatlich finanzierte Studien, wie das US amerikanische Diabetes Prevention Program und die Look AHEAD Studie, die zeigen, wie wirksam simple Lebensstiländerungen für die Prävention der chronischen Erkrankungen sind. Worüber sie nicht gerne reden ist, wie flüchtig diese Erfolge sind. Für die meisten Teilnehmer sind anfängliche Gewichtsverluste spätestens nach 3 bis 4 Jahren wieder "aufgezehrt", und Risikofaktoren sind wieder auf dem Stand vor Studieneintritt.

Wie kann man behaupten Prävention funktioniert, wenn das Übergewicht zum Rauchen des 21. Jahrhunderts geworden ist? Wenn für jeden US Bürger, der 2011 das Rauchen aufgegeben hat, ein anderer adipös (BMI > 30) wurde? Wenn zum ersten Mal in der Menschheitsgeschichte es mehr übergewichtige als unterernährte Menschen auf dieser Welt gibt? Deren Lebensstil aus zu viel Essen und zu wenig Bewegung ist der größte Risikofaktor für die vermeidbaren kardiometabolen Erkrankungen und ihre klinischen Endpunkte: Diabetes, Herzinfarkt, Schlaganfall, Herzversagen.

Wenn also die Änderung des Gesundheitsverhaltens Krankheit verhindert, was verhindert dann die Änderung des Gesundheitsverhaltens? 

Der Aberglaube an ein willensgesteuertes Gesundheitsverhalten.

Wir alle wissen, dass Übergewicht und Bewegungsarmut ungesund sind. Trotzdem sind zwei von drei Deutschen übergewichtig und weniger als jeder fünfte bewegt sich ausreichend. Die logische Schlussfolgerung: Wenn Sie einen Lebensstil wählen, von dem Sie wissen, dass er Ihnen Krankheit und vorzeitigen Tod bringt, dann treffen Sie diese Wahl entweder mit Ihrem freien Willen, oder es ist nicht Ihr freier Wille, der Ihr Gesundheitsverhalten treibt.

Offensichtlich ist letzteres der Fall. Wie sonst können wir erklären, dass übergewichtige Kinder ihr Ess- und Bewegungsverhalten beibehalten, obwohl sie ihren Leidensdruck aus Übergewicht und Stigmatisierung als genauso schwer empfinden wie  ihre krebskranken Altersgenossen den einer Chemotherapie. Wie sonst können wir erklären, dass adipöse Erwachsene nicht abspecken, obwohl ihre Aussichten eine akademische Ausbildung, einen Job und einen Geschlechtspartner zu finden deutlich schlechter sind, als die ihrer normalgewichtigen Altersgenossen? Wie sonst können wir erklären, dass der Prozentsatz der Adipösen unter den US Bürgern in den letzten 20 Jahren um 60% gestiegen ist, während sie im gleichen Zeitraum ihre Ausgaben für Abnehmprodukte auf jährlich 60 Milliarden Dollar verdoppelt haben? Sie alle WOLLEN abnehmen, aber sie schaffen es nicht. Aus drei Gründen. 

Über die Sucht aufs Essen, über entgleiste Hormone und über hyperbolische Verzinsung in unseren Hirnen geht's in meinem nächsten Blogbeitrag. Und bis dahin, schauen Sie sich doch mal an, wie Sie bereits jetzt auf den Weg zur chronischen Gesundheit und guten Figur kommen.

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Nano-encapsulated supplements. Ballyhoo or miracle drug?

When humble supplements meet ultra cool nano-technology.

I'm going to continue where I left off in my previous post: With the question:

Does nano-encapsulation improve the effect of multi-vitamin multi-mineral supplements?

When I was confronted with this question my immediate reaction was: What is wrong with old-fashioned natural delivery of vitamins, from eating fruit, and vegetables, and, yeah, eggs and meat and drinking milk, all of which are the natural carriers of vitamins and more? Is this "nano-whatever" just a cool gimmick of an industry pushing a market, which "suffers" from only moderate growth? I admit it, I have a bias.  A bias for evidence. 

And as a health scientist I also have to admit that nano-encapsulation appeared, until now, only on the very fringes of the radar screen with which I observe the thousands of studies published each year on the subject of preventable, lifestyle-dependent chronic diseases. Literally thousands! Now go to PubMed, where the US National Library of Medicine and the National Institute of Health collect and archive all of those millions of studies and papers written on anything related to biomedicine and search for the combination of the terms "nano-encapsulation" and "vitamin" and you will find the stupendous number of ...

10 papers. None of them related to the oral administration of vitamins. That settled my initial fear, that my radar might have had a blind spot. The drawback was, I can't argue the case, for or against the usefulness of nano-encapsulation, based on published evidence. That leaves me no choice than to do what we scientists are supposed to do: to come up with testable hypotheses on subjects of which we have no, or not enough, knowledge. Which is why my answer to Björn's question will admittedly, be a highly subjective one. But then, there is no clear-cut answer anywhere else to get. Beware of the types who claim to have that answer!

Now let's get the technicalities out of the way first. What does nanoencapsulation mean? It simply means to coat one substance with another at sizes ranging from 1 to 1000 nm. The purpose of doing that is to

·       deliver a drug to a specific tissue or site in an organism, where the drug is then released

·       slow down or time the release of a drug. Which is a good way of delivering Insulin via a nasal spray, a very new technique, which has shown some promise in reducing food intake in overweight women.

·       adding certain micro-nutrients, such as omega-3 fatty acids, to foods without altering the foods' textures or tastes, and to prevent degradation of the otherwise volatile micro-nutrient

·       increase the shelf-life of vitamins

·       increase the bioavailability of anti-oxidants and to prevent unwanted reactions with other food items.

There are lots of other uses in the food and cosmetics industry, but they do not concern us here.

What we want to know is, whether a nano-encapsulated vitamin supplement does its job any different from, and possibly better than, a supplement that is not so encapsulated. 

Now when you take in vitamins, with your food or with supplements, these vitamins need to travel from the mouth through your esophagus and stomach to the small intestine where they will be absorbed through the intestine's membrane. Water-soluble vitamins are typically transported via some sort of a carrier, with the exception of vitamin B12, for which specific receptors do that job. Fat-soluble vitamins require the presence of the same enzymes which fat itself requires for being absorbed. All this happens in the small intestine, the one into which the stomach empties its content. These processes are complex but well researched and known in great detail. Now, just for laughs, let's look at what the geniuses at one of the nano-encapsulation supplement producers have to say about the point where nano-encapsulated vitamins meet the small intestine.

And I quote from here (http://livethesource.com/index.php/products/dailymultivitamin):

"livethesource® nanotechnology creates a particle size small enough to be efficiently absorbed, yet not so small as to be counterproductively absorbed by the body. We use all natural plant lipids as the basis of our nano encapsulation material. The importance of this cannot be overstated. The food grade material not only is absorbed and recognized as a safe substance, but also delivers its payload in a quick, safe and efficient manner."

"small enough to be efficiently absorbed" - as opposed to what? In the intestine water-soluble vitamins are transported molecule by molecule across the intestinal barrier and fat soluble vitamins are integrated into the micelles, which are small enough to pass through this barrier. That's what happens to the vitamins in your food. No nanoencapsulation required here. I also fail to understand what could possibly be a counterproductive absorption. Either vitamins are absorbed, or they are not, but counterproductive absorption is an oxymoron.

What really throws me off is the "natural plant lipids" which form the "basis of our nanoencapsulation material". If water-soluble vitamins are encased in lipids (another term for fat, or fatty acids) they are not available for transport as these vitamins' carriers and receptors will not recognize them. If the nanocapsules, thanks to their fat-soluble exterior, are integrated wholly into the micelles, which transport fat and fat-soluble vitamins, then the water soluble vitamins end up in the blood in a different pathway. If the nanocapsules are dissolved in the intestine prior to their absorption, then what difference does nanoencapsulation make to the absorption process. And with "difference" I mean the difference to naturally delivered vitamins of an apple or an egg yolk which you eat.

The rest of this quote is, like most of their page, a lot of ballyhoo.

Now it's time to return to our initial question: Does nano-encapsulation improve the effect of multi-vitamin multi-mineral supplements? You probably have guessed my answer: If I had to form a hypothesis, it would be something along the line of "nano-encapsulation in itself is not expected to improve a supplement based delivery of vitamins. The potential benefit of nanoencapsulating vitamins in supplements is the potentially longer shelf life of so encapsulated products."

But this longer shelf life benefits exclusively the manufacturer, not you, the consumer. Encapsulation or not, you'll only buy a bottle of vitamin pills which you can consume before it's use-by date. Don't you?

Now that you have read my point of view on vitamin supplementation (my yesterday's post) and on nano-encapsulation of supplements, I need to tell you why my arguments may not apply to you, personally. This is an issue which plagues medicine and public health, and it is hardly recognized or being talked about. This issue is at the heart of personalized medicine and personalized prevention. Stay tuned, because I will tell you in my next post, why you should be skeptical of the interpretation of the results of any study, regardless of who interprets the results. Whether it's me or anybody else.

Stay tuned.

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Do vitamin supplements make you healthier?

The (non-)sense of vitamin supplementation?

Almost one in two American adults is a regular user of vitamin and mineral supplements, either in the form of single- or multivitamin/mineral formulations (MVMS). It all adds up to a market of US$ 9 Billion annually, or one third of the total US supplements market. Does all the pill-popping help their users to achieve better health or longevity? 

That's one question raised by Björn, one of the readers of my blog. Thanks, Björn, I wanted to write on this subject for some time. You just got me going on this a little earlier than I would have otherwise. And also thanks for the second question: Does the latest technology of delivering the drug (not to your house, but within your body to your organism's cells) via "nano-encapsulation" improve that health effect in any way? Let me try to answer these questions one by one.

When you talk about vitamins, you talk about essential micronutrients, for which the human organism has either no or only a very limited ability to produce (e.g. Vitamin D) on its own. If you want to group vitamins according to their solubility you'll find that they come in two flavors: water soluble and fat soluble. Of course, you could group them for any other biochemical characteristic, but grouping them according to their solubility makes immediate sense when you keep in mind that the fat soluble ones (A, D, E and K) can accumulate in your body's tissues, whereas the water soluble Vitamins typically can't. Whatever can accumulate, can also accumulate to the point where there is too much of it in a body's tissue. So, yes, too much of a good thing may turn into a not so good thing, as is the case for vitamins A and E for example. Or, too much of a good thing may just be flushed out of the body, as is the case with water-soluble vitamin C.

The supplement industry certainly does a good job convincing the public that supplementing one's diet with additional vitamin formulations is good for one's health. It's certainly good for the industry's bank accounts. In such cases it always pays to ask one simple question: Where is the evidence?  

In a meta-analysis of randomized clinical trials (RCT, the gold standard of clinical research methodology), the authors investigated the effects of vitamins E and A on the risk of cardiovascular disease and death in altogether 220,000 patients [1]. The effects? Zilch. The authors recommendation? The evidence does not support any recommendation for the use of Vitamins E and A. On the contrary, they found a slight increase in all-cause and cardiovascular disease mortality associated with vitamin A supplementation.

In another 2007 review on the subject, published in the American Journal of Clinical Nutrition, its author came to the same conclusion, stating that "Results to date are not compelling concerning a role for MVMs in preventing morbidity or mortality from cancer or CVD." [2] The two largest trials on Vitamin A and E supplementation in smokers, the Finnish Alpha-Tocopherol Beta-Carotene (ATBC Trial) and the US Carotene and Retinol Efficacy Trial (CARET) enrolled 29,000 and 18,000 smokers. In the Finnish trial, supplementation with Vitamin A increased the risk for lung cancers by 18% within a 5 to 8-year observation period [3]. And the US trial was halted after 2 years for the same reason: a 28% increase in lung cancer risk, a 26% increase in risk for dying from cardiovascular disease [4]. In 22,000 healthy men who had been observed for 12 years, supplementation with vitamin A showed neither benefit nor harm [5].  

So where is the evidence for you to believe that buying Vitamin E and A supplements will make you healthier and live longer? Maybe I'm blinded by a perverse distrust of everything a sales man tells me, but I can't see it.

So, how about multi-vitamins? In the group of people with the highest take-up rate of multivitamins: post-menopausal women? Again, the authors of a study which pooled the data from the Women's Health Initiative trial and observational study cohorts, come to the same conclusion "the WHI CT and OS cohorts provide convincing evidence that multivitamin use has little or no influence on the risk of cancer or CVD in postmenopausal women." [6].

Not even for infections is there any evidence that MVMS have any protective effect on those most vulnerable, the elderly [7]. 

Of course, keeping all this in mind, the nagging question remains: would there be an effect if only the delivery of the drug in the human body was improved? After all, if vitamins are essential for survival, and if vitamin supplementation does not improve health, then there are several possible reasons for this observation. For instance, we might get enough vitamins from our food, and adding vitamins has simply no effect. Or, maybe we have vitamin deficiencies but the supplements are ineffective in delivering their vitamin loads.

Which brings us to Björn's second question: "Does nano-encapsulation improve the effect of MVMS?

And may I add my nagging question: Or is "nano-whatever" just a cool gimmick of the industry to push a market, which currently grows only moderately? In the next post (Monday 16. April) I'll try to answer this question. So, stay tuned. 

1.           Vivekananthan, D.P., et al., Use of antioxidant vitamins for the prevention of cardiovascular disease: meta-analysis of randomised trials. Lancet, 2003. 361(9374): p. 2017-23.

2.           Prentice, R.L., Clinical trials and observational studies to assess the chronic disease benefits and risks of multivitamin-multimineral supplements. American Journal of Clinical Nutrition, 2007. 85(1): p. 308S-313S.

3.           The Effect of Vitamin E and Beta Carotene on the Incidence of Lung Cancer and Other Cancers in Male Smokers. New England Journal of Medicine, 1994. 330(15): p. 1029-1035.

4.           Omenn, G.S., et al., Effects of a combination of beta carotene and vitamin A on lung cancer and cardiovascular disease. N Engl J Med, 1996. 334(18): p. 1150-5.

5.           Hennekens, C.H., et al., Lack of Effect of Long-Term Supplementation with Beta Carotene on the Incidence of Malignant Neoplasms and Cardiovascular Disease. New England Journal of Medicine, 1996. 334(18): p. 1145-1149.

6.           Neuhouser, M.L., et al., Multivitamin Use and Risk of Cancer and Cardiovascular Disease in the Women's Health Initiative Cohorts. Archives of Internal Medicine, 2009. 169(3): p. 294-304.

7.           El-Kadiki, A. and A.J. Sutton, Role of multivitamins and mineral supplements in preventing infections in elderly people: systematic review and meta-analysis of randomised controlled trials. BMJ, 2005. 330(7496): p. 871.

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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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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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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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Chronic Health at indiegogo.com

We have just launched our crowd funding campaign for Project Chronic Health on www.indiegogo.com/adiphea.

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The daily super stimulus to prevent diabetes, or maybe not?

The daily super stimulus to prevent diabetes, or maybe not?

Today a newly released case report in the British Medical Journal caught my attention: "Towards creating a superstimulus to normalise glucose metabolism in the prediabetic: a case-study in the feast-famine and activity-rest cycle". Normalizing glucose metabolism in the prediabetic person means nothing less than preventing diabetes in those at high risk. Naturally I sought enlightenment. 

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What weight loss?
You have probably heard one or the other diet guru claiming that manipulating the nutrient composition of your diet will make you lose weight. Well, for those of you, who stubbornly cling to the notion that excess weight is simply a matter of too many calories-in vs. too few calories-out, here is the good news: You are right, after all. It really doesn't matter.
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