Monday, April 30, 2012

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?

Print Friendly and PDFPrintPrint Friendly and PDFPDF

Friday, April 27, 2012

Your shortcut to longevity.

If you don't die from an accident, a serious infection or a cancer, you'll live as long as your arteries let you. And how long they let you is all in your hands. I know this sounds over-simplified, but it's biomedical knowledge in a nutshell. Lets look at what happens in and to your arteries and what that means for keeping them in mint condition. 
Print Friendly and PDFPrintPrint Friendly and PDFPDF

Wednesday, April 25, 2012

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...
Print Friendly and PDFPrintPrint Friendly and PDFPDF

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.



F4F9V7QE32W3

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

Friday, April 20, 2012

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?

Print Friendly and PDFPrintPrint Friendly and PDFPDF

Thursday, April 19, 2012

Chronisch gesund geht doch!

In meinem vorangegangenen Beitrag habe ich erläutert, wie unser Gesundheitswesen dem Ziel der chronischen Gesundheit im Wege steht. Wie dieses Ziel erreichbar ist, ist Gegenstand meines heutigen Beitrags.
Gesundheit als shareholder value.
Anfang diesen Jahres drohte die Ratingagentur Standard & Poor's den G20 Nationen mit einer Herabstufung ihrer Ratings beginnend in 2015. Der Grund: Die bestehenden Gesundheits- und Rentensysteme werden unter der Krankheitskostenlast einer zunehmend älter, kränker und dementer werdenden Bevölkerung zusammenbrechen. Und damit das Wirtschaftswachstum ausbremsen.
Warum ist dieser Schuss vor den Bug so wichtig? Weil hier ausgesprochen wird, was schon lange hätte erkannt werden sollen: Gesundheit ist nicht nur das vielzitierte hohe Gut. Sie ist ein Wirtschaftsgut.
Ihre Gesundheit macht Sie produktiver für Ihren Arbeitgeber und profitabler für Ihre Krankenkasse und Ihren Lebensversicherer. Sobald Ihre Gesundheit im Universum des Shareholder Value auftaucht, haben Ihr Arbeitgeber, Ihre Kasse und Ihre Lebensversicherung auch finanzielle Anreize, in Ihre Gesundheit zu investieren. Und einen Anreiz, den Return-on-Investment mit Ihnen zu teilen. Im Rahmen einer Gesundheitsdividende, die Sie für Ihre Gesundheitsbemühungen belohnt. Das Schlüsselwort heißt Anreize. Fehlende Anreize sind der Grund für das Versagen der Präventionsbemühungen unseres Gesundheitswesens.
Egal ob Geld oder Anerkennung oder was auch immer Ihren Nachbarn grün vor Neid werden lässt, die treibende Kraft hinter allem menschlichen Handeln sind Anreize. Sie sind als Triebfeder unseres Handelns in unsere Hirne programmiert. In der programmiersprache des hyperbolic discounting. Wenn uns dieses Phänomen etwas gelehrt hat, dann ist es die Notwendigkeit von Anreizen, mit denen wir jene ausstechen können, die uns zu ungesundem Verhalten verführen.
Was hält unsere Firmen davon zurück, die Gesundheit ihrer Beschäftigten  massiv mit Anreizen zu fördern? Sicherlich nicht die Geringschätzung ihrer Beschäftigten. Und selten die Unberechenbarkeit des Return on Prevention. Meistens liegt es am Fehlen eines Werkzeugs, das es ermöglicht, Belohnung an jene zu verteilen, die es verdienen, und jenen vorzuenthalten, die nichts für ihre Gesundheit tun. Mit Yoga- und Betriebsportgruppen gelingt das sicherlich nicht. Dass solch ein Werkzeug im Rahmen betrieblicher Gesundheitsförderung funktioniert stellen wir gerade unter Beweis. Wir haben dieses Werkzeug entwickelt um damit auch die zweite und dritte Strategie zu realisieren.
Den eigenen Kopf überlisten
Wenn's ums Esesn geht lässt sich der Affe in uns kaum von dem kontrollieren, was uns zum Menschen macht: Vernunft und freier Wille. Aber egal ob Mensch oder Affe, Mutter Natur hat uns die Gabe des impliziten Lernens gegeben. Mit ihr lernen wir komplexe Aufgaben zu meistern ohne erklären zu können, wie wir das schaffen. Denken Sie ans Schwimmen oder ans Radfahren. Dies sind Beispiele für einen 6. Sinn, mit dem wir unser Verhalten präzise so steuern, dass wir weder ertrinken noch vom Rad stürzen. Warum nicht auch unser Essverhalten?  Mit einem 6. Sinn für die tägliche Kalorienbilanz schaffen Sie zwar nicht die Lust auf das Tiramisu aus der Welt, aber er hilft Ihnen zu erkennen, welche Maßnahmen notwendig sind, um Ihre Kalorienbilanz heute auf dem Kurs zu halten, mit dem Sie planmäßig Ihr Gewichtsziel erreichen. Dass es funktioniert haben wir in unserem Labor getestet. Die Idee dazu kam uns im Rahmen einer klinischen Studie, in der wir testeten, wie wir jenen Menschen zur chronischen Gesundheit verhelfen können, die am stärksten gefährdet sind: Übergewichtigen und Adipösen. Unser Probanden, die diesen 6. Sinn entwickelten, nahmen ab und hallten ihr Gewicht noch heute.     
Nun stellen Sie sich wahrscheinlich die Frage: Selbst wenn mein Arbeitgeber mir die notwendigen Anreize gibt, wie kann ich sicher sein, dass mein geändertes Bewegungs- und Ernährungsverhalten mir auch tatsächlich die chronische Gesundheit beschert? Womit wir beim letzten Punkt angekommen sind:
Die Biomedizin weiß was wirkt
Die Biomedizin kennt keine wirksamere Intervention zur Verhütung von Herzinfarkt, Schlaganfall und Diabetes als zielgerichtete Bewegung und Ernährung. Mit dieser Strategie reduzierten die Probanden des Diabetes Prevention Program das Risiko, Diabetes zu entwickeln um rund 60%. Jene Probanden die statt einer Lebensstiländerung das Medikament Metformin einnahmen, schafften nur halb so viel, 30% Risikoreduzierung.
Dass Bewegung das Risiko an chronischen Krankheiten zu sterben um 40% reduzieren kann, ist aus großen Studien bekannt. Damit ist Bewegung in ausreichender Intensität, Dauer und Häufigkeit die wirksamste Strategie zur Verhütung dieser Erkrankungen.  Auch vieler Krebserkrankungen, darunter Darmkrebs, Prostatakrebs und Brustkrebs.  Unser Gesundheitssystem aber verschleudert das Potenzial dieser Strategie, denn es ist auf die Behandlung von Krankheit ausgerichtet, nicht auf den Erhalt der Gesundheit. Solange keine Risikofaktoren messbar sind, bleiben wir aber unter dem präventiven Radar dieses Systems. So lange bis es zu spät ist. Denn wer als Mann mit 45 Jahren noch frei von Risikofaktoren ist, hat eine 97%ige Chance seinen 80 Geburtstag bei guter Gesundheit zu feiern. Liegen bereits 2 Risikofaktoren vor, wie beispielsweise Bluthochdruck und erhöhtes Cholesterin, dann schrumpft diese Chance auf 50%. Und selbst wenn Sie zu jener glücklichen Hälfte zählen, die die 80 Kerzen auf dem Kuchen ausblasen darf, werden Sie genau das wahrscheinlich nicht mehr schaffen, denn eine der chronischen Krankheiten wird Ihnen die Kraft dazu genommen haben.
Die gute Nachricht: mit den einfachen Gesundheitsverhalten - nicht rauchen, ausreichende Bewegung und kein Übergewicht - können Sie heute schon bestimmen, wie Ihre 80. Geburtstagsparty ablaufen wird.
Die schlechte Nachricht: Das alles sind keine neuen Erkenntnisse. Den Kassen sind sie genau so bekannt wie den Wissenschaftlern, die sie erarbeiten. Dass Präventionsbemühungen trotzdem nicht von den Kassen finanziert werden, hat erstaunlicherweise nichts mit Geiz oder Unvernunft zu tun, sondern mit dem Paragraphen 20 des fünften Sozialgesetzbuchs. Dort schreibt unser Gesetzgeber den Kassen eine Ausgabengrenze für Prävention vor: € 2,84 pro Versichertem pro Jahr. Offensichtlich sind die Bekenntnisse unserer Gesundheitsminister zur Prävention nichts anderes als Lippenbekenntnisse.
Es sind also nicht Defizite in Wissen oder Fortschritt, die uns das Zeitalter der chronischen Gesundheit und Langlebigkeit vorenthalten. Es ist das Versagen unseres Gesundheitssystems, das Wissen einzusetzen und damit die Gesundheit endlich als das zu behandeln was sie ist, ein Wirtschaftsfaktor. Ist das nun wirklich eine so radikale Änderung der Strategie unseres Gesundheitswesens?    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


Print Friendly and PDFPrintPrint Friendly and PDFPDF

Tuesday, April 17, 2012

Die Sucht aufs Essen. Warum wir dick werden obwohl wir es nicht wollen.

Unser Essverhalten wird weniger vom freien Willen und der Vernunft gesteuert, als vielmehr von autonomen Mechanismen. Den Verhaltensforschern sind sie bekannt. Den Akteuren unseres Gesundheitswesens sind sie ein Dorn im Auge. Ein Dorn, der sie mit einer selektiven Blindheit geschlagen hat für...

Die Sucht aufs Essen

Neurohormonale Mechanismen treiben den Drogensüchtigen zu seiner Droge, obwohl er die Konsequenzen seines Verhaltens kennt und fürchtet. Den Verhaltensbiologen sind diese Mechanismen seit einigen Jahren bekannt. Und auch dass Zucker dieselben Hirnzentren und Mechanismen aktiviert. Evolutionsbiologisch wichtige Mechanismen, wie wir heute wissen. Denn die Lust auf Süßes trieb unsere Urahnen zu der einzigen Nahrung, die diese Lust befriedigte: Obst und Früchte. Diese Lust war aus zwei Gründen wichtig: erstens sind unsere Speicher für Kohlehydrate, anders als die fürs Fett, sehr klein und innerhalb von spätestens 48 Stunden aufgezehrt. Zweitens liefern Obst und Früchte lebenswichtige Mikronährstoffe. Ganz im Gegensatz zu jenen Colas, Kuchen und Keksen, mit denen wir die Lust auf Süßes heute befriedigen. Für diese Lust sollten wir uns also nicht deshalb schämen, weil wir sie erst mit der Erforschung eines moralisch verpönten Verhaltens, der Drogensucht, entschlüsselt haben. Das erklärt, warum die Nahrungsmittelindustrie Zucker in allen möglichen Nahrungsmitteln versteckt, in denen wir ihn nicht vermuten. So wie die Zigarettenindustrie  ihre Tabake mit zusätzlichem Nikotin anreichert, einem der stärksten Suchtmittel überhaupt. Die Konsequenz dieser Sucht auf's Essen ist das Übergewicht. Womit wir beim zweiten Grund für das Scheitern des Abnehmens sind:

Entgleiste Hormone

Wer lange genug zu viel isst und sich zuwenig bewegt, verwandelt nicht nur seine Figur sondern auch seinen Organismus. Gemeint ist damit jene komplexe neurohormonale Vernetzung von Verdauungsapparat, Fettgewebe, Muskelzellen und jenen Hirnzentren, die Appetit, Sättigung und den Drang auf Bewegung regeln. Wer nach einem Essen, das eine vierköpfige Familie in Bangladesh ernährt hätte, der Lust auf ein Tiramisu nicht widerstehen kann, hat das auch diesem neurohormonalen Netzwerk zu verdanken. Es ist resistent geworden gegen Sättigungssignale. Wenig hilfreich ist auch, dass der Anblick des Tiramisu einen Verhaltensreflex auslöst, den wir von Boris Becker in der Besenkammer kennen. Erst mal vernaschen, bereuen kommt später. Verhaltenswissenschaftler nennen dieses Phänomen...

Hyperbolic discounting

Discounting heißt Abzinsung. Was der Verhaltensforscher darunter versteht, ist die Art, wie unser Gehirn intuitiv den Gegenwartswert eines erwarteten zukünftigen Nutzens ermittelt. Vor die Wahl gestellt, entweder 120 Euro in 6 Monaten geschenkt zu bekommen oder 100 Euro in 5 Monaten, entscheiden sich die meisten Menschen für die 120 Euro. Was aber, wenn ich Ihnen 100 Euro jetzt bar auf die Hand biete oder 120 Euro in einem Monat? Die meisten Probanden ziehen die sofort verfügbaren 100 Euro vor. In beiden Fällen ist die Differenz die Gleiche, nur Sie bewerten sie intuitiv anders. Dieser Effekt ist mit dem Wörtchen "hyperbolisch" beschrieben, einer mathematischen Formel die sich von der exponentiellen Form der Abzinsung unterscheidet, auf der wir unser Banken- und Wirtschaftssystem aufgebaut haben.
Dank der hyperbolischen Abzinsung greifen Sie morgen doch wieder zum Tiramisu, obwohl Sie heute Stein und Bein schwören, dass Ihnen der Gesundheitsgewinn in der ferneren Zukunft wirklich mehr wert sei als der Lustgewinn nach dem Mittagessen morgen. Und genauso funktioniert nicht nur das menschliche Gehirn sondern auch das von Tauben, Mäusen und Affen. Das zeigt, im Laufe der Evolution muss sich die hyperbolische Abzinsung als wirksames Werkzeug fürs Überleben bewährt haben. Andernfalls hätte Mutter Natur es nicht über Millionen Jahre in die Hirne ihrer Spezies programmiert. Heute müssen wir mit diesem Erbe in einer Umwelt zurechtkommen, deren Gestaltung wir Mutter Natur aus der Hand genommen haben. 
Dem Aberglauben an die Vernunft und den freien Willen als Treiber unseres Ess- und Bewegungsverhaltens hätten diese Erkenntnisse schon seit mehr als 10 Jahren den Wind aus den Segeln nehmen müssen. Haben sie aber nicht. Wohl weil es einfacher ist, den Dicken und chronisch Kranken die Schuld für ihren Zustand zu geben, als sich zu fragen, wie das Produktions- und Werbeverhalten einer Nahrungsmittelindustrie, von Nestle bis zu MacDonalds, zu reglementieren sei.
Und wie kann ich nun behaupten, dass das Zeitalter der chronischen Gesundheit greifbar ist?
Aus drei Gründen: weil sich die Börsen für das Thema zu interessieren beginnen, weil wir unser Hirn überlisten können, und weil wir die notwendigen Werkzeuge aus den Gesundheitswissenschaften haben. 
Dazu mehr im nächsten Beitrag. Und falls es Ihnen bis dahin langweilig werden sollte, können Sie ja schon mal einen Blick auf unser Navi zur chronischen Gesundheit werfen.   Print Friendly and PDFPrintPrint Friendly and PDFPDF

Monday, April 16, 2012

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.
Print Friendly and PDFPrintPrint Friendly and PDFPDF

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.
Print Friendly and PDFPrintPrint Friendly and PDFPDF

Friday, April 13, 2012

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. 



Print Friendly and PDFPrintPrint Friendly and PDFPDF

Thursday, April 12, 2012

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?


Print Friendly and PDFPrintPrint Friendly and PDFPDF

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?


Print Friendly and PDFPrintPrint Friendly and PDFPDF