Why Medicine Might Be Wrong About Salt, Fat & BMI

Salt and fat kill you early, and your BMI tells you how early. That has been the wisdom for years, but wisdoms have an expiry date, too. Particularly medical wisdoms. Recent research says those three are probably well beyond their use-by date. [tweet this]. 

We live in interesting times. Admitted, my view of times is myopic, it's focused on the biomedical. So, I'm obviously not referring to Greece teetering on the economic brink. In biomedicine our Greeks are the cherished wisdoms about salt, fat and BMI. Similarity 1: They are not doing so well. Similarity 2: Their balance sheet screams bankruptcy. Similarity 3: Our authorities won't kick them out for fear of a domino effect.

Actually, medical history is full of interesting times. Remember, when a young doctor suggested that simply washing hands between dissecting cadavers and helping women give birth would seriously reduce the regular 1-in-five death rate from childbed fever? 

Of course, you won't remember this: the place was the Vienna General Hospital in Austria, the year was 1849 and the young doctor's name was Ignaz Semmelweis. While he didn't publish his observations, one of his students did, in the grand old dame of British medical journals, the Lancet [1]. At that time infection was known per se, but it was believed to work like this: a "peculiar morbid atmospheric influence which extends beyond the range of personal communication". Semmelweis believed in washing hands. And he had the numbers to prove his belief. After introducing a hand-washing rule in his department, childbed deaths dropped by 75%. The response of Semmelweis' peers and superiors to his challenging notion is today known as the Semmelweis reflex. Unlike Semmelweis it is very much alive. It is the reflex-like rejection of new insights because they disagree with entrenched beliefs. 

Semmelweis' observations were one of the initial steps in the development of the germ theory of disease. Three more names are attached to its development, Louis Pasteur, Robert Koch and Joseph Lister. The latter was the first to apply this new theory to surgical procedures. So, the next time you gargle with Listerine, you might want to say a silent thank you to all the men and women of science who had the guts to challenge those pompous idiots who, in true Semmelweis-reflex mode, did everything to discredit the new insights. And they usually are quite successful. Who wants to argue with a praetorian guard of honorable old professors.  In Semmelweis' case, they got him barred from medical practice, they publicly ridiculed him and ultimately drove him to insanity. All the while women continued to die in childbed. Unsurprisingly, because medical textbooks continued to teach the old views on childbed fever until the 1890s. But once germ theory, and with it hygiene, was adopted into medicine and daily life, the mortality landscape changed dramatically. Infectious diseases disappeared from the pole position of the death tables, and the 1900s witnessed the emergence of their replacements: cardiovascular disease (CVD) in all its flavors, from hypertension and atherosclerosis to heart attack, stroke and heart failure.  

Recently, potential triggers for those Semmelweis reflexes have been coming out of research, though probably not as dramatic in consequence as the infection theory. 

Salt is no evil

I have written about the potentially flawed obsession with trying to get everybody to reduce salt intake in order to reduce blood pressure and stroke in the entire population.  The latest nail in this obsession's coffin is Alderman and Cohen's review of 23 observational studies and 7 randomized controlled trials (RCT), all investigating the effects of salt intake on parameters of health [2]. The observational studies accumulated data on 360,000 participants and recorded 26,000 disease events. While 7 studies showed a direct relationship between increasing sodium and increasing CVD events, another 6 studies demonstrated the opposite: a clear inverse relationship. Two studies showed a J-shaped relationship, in which low and high intakes increased disease risk, whereas 8 studies didn't show any relationship or only inconsistent results. 

Only 9 of the 23 studies measured salt intake objectively, that is by measuring participants' urinary sodium excretion. I mention this because the other 14 studies relied on self-reported sodium intake, which is prone to recall errors. Of those 9 studies with objective measurements, only 1 showed a direct association, whereas in three studies higher intake was associated with fewer disease events. Two studies showed a J-shaped relationship and one didn't show any relation. 

Is it now wise to simply balance those scores, like in football, and let the highest scorer win the tournament? In our case the team "inverse relation" would win hands down over its competitors "direct relation" "J-shaped relation" and "no relation". Should we draw our conclusions in this way? No, science does not work this way. And it's not the way the authors chose. When they looked a little closer at the sodium intake ranges in each of the RCT's they found that the seemingly conflicting results of the observational studies could be reconciled easily. 

It turns out that it all depends on the baseline intake from which you increase or decrease your salt consumption. The safe range being actually quite large, between 2.5-6.0 g/day. Go below or above that and you will face some increased risk. Interestingly, this range is way in excess of the current authoritative recommendation of "less than 2.0g/day". What is also rarely mentioned by those "authoritative guidelines" are some other side effects of lowering salt intake. In several of those RCTs salt reduction came with an increase in blood cholesterol, insulin resistance, adrenaline secretion and sympathetic nerve activity. None of those effects is beneficial to health. That's curious because all, except for cholesterol, tend to raise blood pressure. So the net effect of salt reduction, or increase, in you is always a composite of all those biochemical responses to sodium intake change.  

Want to bet whether these insights will trigger the Semmelweis reflex in some of those who have built their career on maligning salt? On to the next subject:

Fat isn't so bad either

Khaw and colleagues wanted to know the answer to an old question: does the fat in your diet give you heart disease [3]? The belief that dietary fat and heart disease march lock-step is so ingrained that you are forgiven to wonder why anybody would spend time and effort on this question. Well, that's because a recent meta-analysis of 21 studies, following 347,000 people for 5 to 23 years, could NOT find any association between the two [4].

Since all of the previous studies had been of an observational nature, which does not allow for conclusions of causality, the researchers used data from a prospective trial which had investigated the correlation of diet with cancer outcome, the European Prospective Investigation into Cancer (EPIC)-study. They looked at the fats in the blood of 10,000 participants aged 40–79 years, and they followed them from 1993–1997 through 2011. During this period 2,424 participants were diagnosed with heart disease. From among the remaining 10,000 participants the researchers chose 4,930 disease-free controls for a comparative evaluation.  They checked whether, and how strongly, saturated and unsaturated fatty acids in the blood correlated with heart disease. 

Since the fatty acid composition in the blood mirrors dietary fatty acid intake, this is as close as you can get to a conclusion about how the intake of type of fat affects your risk of heart disease. Of course, you need to adjust for other risk factors, such as age, sex, BMI, smoking, physical activity, alcohol intake, diabetes, blood pressure, cholesterol and other known risk factors for heart disease. 

The researchers did those adjustments, and they found the saturated fatty acids to be only weakly related with heart disease. But that's not the surprising find. The real surprise was about the unsaturated fatty acids of the famous omega-3 and omega-6 persuasion. You have always heard how omega-3, the fish-oil variant is so good for your heart and the omega-6 is not. Well, listen to this: omega-6 turned out to be protective against heart disease, and omega-3 wasn't. That's contrary to our hitherto held beliefs that popping fish oil pills will make you a Methusalem, and that reducing omega-6 intake will do wonders against inflammation in your arteries. See a Semmelweis reflex on the horizon?

BMI is a useless crutch  

There is probably no other number which has become so much engrained in our medical psyche as the BMI. This relation of bodyweight over height squared is the human equivalent of a meat stamp: if it's below 25 you are the prime cut which every health insurer wants on his client list. Bring it above 30 and you are a fat and soon-to-be sick bum whom nobody wants to talk to, unless your name is John Candy. In our society where we determine the winner of a Formula-1 race with millisecond precision, we accept being stamped at-risk with the accuracy of 20/100 vision (20/20 being the normal, and 20/200 being the cut-off for legal blindness). 

The problem with BMI is, it doesn't differentiate between muscle and fat tissue, which makes a body-builder look fat, and bad, on the chart. BMI also doesn't tell you where your fat resides, on your buttocks or on your waist. The latter is certainly worse for your health than the former. Still BMI is THE number to judge you by. Maybe not any more. 

Krakauer and Krakauer have developed a new measure from looking at the numbers of the National Health and Nutrition Examination Survey (NHANES) 1999-2004, and correlating those numbers with the death statistics. They wanted to blend weight, height and body shape into a more informative indicator of disease risk. Which is why they called it A Body Shape Index, ABSI. They also wanted this number to be easy to calculate from parameters which everyone can measure. Which is why the ABSI only calls for waist circumference to be measured in addition to the BMI's parameters of height and weight. I won't bore you with the details of statistical development of this ABSI, but suffice it to say, it's been done beautifully and very thoroughly. Then, after adjusting for other known risk factors, such as age, smoking, diabetes, blood pressure and cholesterol, the authors correlated BMI, WC and ABSI with death. While WC and BMI didn't show any correlation ABSI was strongly correlated. That's surprising, given the relatively short follow-up period of 5 years. 

Of course, there area lot more questions to be answered before the ABSI will make it into medicine's hall of fame. The most important: Does lowering the ABSI translate into increasing health, or improving risk or extending lifespan? 

So, be prepared for quite some time to pass before your doctor tells you that your ABSI requires some serious attention. Once that happens, you might remember this post and look up the time that has passed between its publication and your encounter with the ABSI in a medical environment. You will then see that medical science grinds slowly. But ultimately it grinds. 

In this case, medical science might grind a little slower, because the ABSI isn't the brainchild of a biomedical or public health scientist. It's developer is an assistant professor in the Department of Civil Engineering of the City College of New York. 

Now, how can a civil engineer's index beat our beloved BMI when biomedicine's best brains have been laboring over a BMI replacement for years?

Great potential for a Semmelweis effect, don't you think?  [tweet this]. 

1. Routh CH: On the Causes of the Endemic Puerperal Fever of Vienna. Medico-chirurgical transactions 1849, 32:27-40.

2. Alderman MH, Cohen HW: Dietary Sodium Intake and Cardiovascular Mortality: Controversy Resolved? Am J Hypertens 2012, 25(7):727-734.

3. Khaw K-T, Friesen MD, Riboli E, Luben R, Wareham N: Plasma Phospholipid Fatty Acid Concentration and Incident Coronary Heart Disease in Men and Women: The EPIC-Norfolk Prospective Study. PLoS Med 2012, 9(7):e1001255.

4. Siri-Tarino PW, Sun Q, Hu FB, Krauss RM: Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nutr 2010, 91(3):535-546.

Routh CH (1849). On the Causes of the Endemic Puerperal Fever of Vienna. Medico-chirurgical transactions, 32, 27-40 PMID: 20895917

Alderman MH, & Cohen HW (2012). Dietary sodium intake and cardiovascular mortality: controversy resolved? American journal of hypertension, 25 (7), 727-34 PMID: 22627176

Khaw KT, Friesen MD, Riboli E, Luben R, & Wareham N (2012). Plasma Phospholipid Fatty Acid Concentration and Incident Coronary Heart Disease in Men and Women: The EPIC-Norfolk Prospective Study. PLoS medicine, 9 (7) PMID: 22802735

Siri-Tarino PW, Sun Q, Hu FB, & Krauss RM (2010). Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. The American journal of clinical nutrition, 91 (3), 535-46 PMID: 20071648

How The Media Monkeys Get You Panicked About Sitting Too Long!

From "man is made to move" to "man is not made to sit" is a very recent transition of scientific insight. Let's get our readers panicked over more than not doing exercise, is the response of the media. Here is why you should sit down and get the facts straight before jumping up in fear. [tweet this]. 

"It is now well known that spending too much time sitting down is bad for the heart, even if one takes regular exercise."

That's what the Daily Telegraph told us on 10 July this year. Behind this piece of insight is a study published by Katzmarzyk and colleagues a few days earlier. The authors investigated the question what effect the daily time we spend sitting down has on health and life expectancy. In the USA, that is. 

Maybe the Daily Telegraph lives in a different knowledge universe, but in the one where biomedical research counts, the association between sitting and heart disease is not as clear as the reporters make it out to be. Call me a fusspot, but the only study design, which allows us to draw conclusions about causality, are those where we expose a randomly assembled group of individuals to a certain intervention (in this case: sitting down for extended hours every day) and then we compare the outcome in that group with the outcome of another randomly assembled group which didn't get our intervention. Assuming the two groups didn't differ in any meaningful way from each other at the outset of our experiment, we can, at the end of it, ascribe a possible difference in outcome between the groups to our intervention. That's what I want you to keep in mind while I walk you through the study which had prompted the Daily Telegraph to tell you that sitting too long will cut your life expectancy. 

Let's first look at the background to the authors' research question, which was "To determine the impact of sitting and television viewing on life expectancy in the USA" [1]. Over the past 60 years we have accumulated a vast body of evidence for the benefits of physical activity on health. The results of this research are reflected in every guideline on how and how much we should exercise. You could say "made to move" is written all over our genes. Only very recently are we discovering a sub-clause, written in small-print, saying "man is not made to sit", which we interpret to mean that cramming movement into a brief period of time every day doesn't help us much if sitting around is what we do for the rest of the day. Katzmarzik and Lee simply wanted to extract from the available evidence how a violation of this newly discovered sub-clause impacts our health and longevity.

So, they set out to identify all the studies from which reliable data could be gleaned about the effects of sitting and television time on the risk of dying. Only 5 studies matched those criteria. From these they pooled the relative risk results into a meta-analysis. Then they looked at the sedentary behaviors of the U.S. population. For that purpose they consulted the data of the National Health And Nutrition Surveys (NHANES), and they also looked at the latest life tables for this population as published by the World Health Organization (WHO). We don't need to go into the statistic intricacies of the procedure. They are a very thorough and methodical attempt at coming up with an educated guess about the impact of extended sitting on the life expectancy of a population. By way of analogy: the authors threw all those data into the statistics blender and came up with what we call the population attributable fraction, or PAF, which tells you how many deaths (or disease cases) could be avoided in a population if the risk factor or exposure were eliminated, in our case, the exposure being extended sitting time. 

Fast forward to the results, which the authors comment as follows: "The results of this study indicate that limiting sitting to less than 3 hrs/day and limiting television viewing to less than 2 hrs/day may increase life expectancy at birth in the USA by approximately 2.0 and 1.4 years respectively, assuming a causal relationship." That's what I like about the authors, whose work I have been following for quite some time. They point out that this conclusion is only valid UNDER THE ASSUMPTION that sitting and dying early are causally related. They also go on to emphasize that this is "...a theoretical estimate..." (emphasis in italics by the authors) and that "This should not be interpreted to mean that people who are more sedentary can expect to live 1.4 or 2.0 years less than someone who does not engage in these behaviours as much." That's obviously addressed at those media types who, of course find it far more sexy to tell you that spending too much time on your butt cuts down your life expectancy. 

Now, instead of picking the raisins out of this nicely done study, I want to walk you briefly through the 5 studies from which the authors extracted their results. After that, you can still judge for yourself how much trust you want to put into the Daily Telegraph interpretation. 

The first of the 5 studies was conducted by the same lead author, Dr Katzmarzyk. It was a study of 17,013 adults of the 1981 Canada Fitness Survey (CFS) who had been followed for up for 12 years [2]. At baseline, the survey participants had been asked, among other things, about their time spent sitting. Death from cardiovascular and other causes were the outcome measure. In such a study it wouldn't make sense to simply correlate sitting time with death. After all, there are a lot of other factors which determine our demise. Age being one of them. My chances to die in the next 12 years are quite a bit greater if I'm 70 than if I'm 35. So, believe me when I say that the authors adjusted as much as possible for such factors. And it is this "as much as possible" where we begin to find hairs in the soup. 

First of all, cardiovascular disease (CVD) is a main cause of death today. So, we should account for all those people who already had CVD when they entered the study. But that's not as simple as it sounds. CVD has a mean streak in that it remains asymptomatic for years, often decades, before it hits you with a heart attack or stroke. So, eliminating those cases who had reported such events at baseline, doesn't mean our survey participants had a clean bill of cardiovascular health.  At the average age of over 40, there will certainly have been quite a number of people who had such silent stages of CVD. The principal manifestation of "silent" cardiovascular diseases are those atherosclerotic plaques which narrow the arteries and arterioles. While the authors used the PAR-Q (physical activity readiness questionnaire) which asks, in five questions, about symptoms of CVD, silent CVD would have flown below that radar. So, not accounting for those silent cases may, in all likelihood, have biased the results. Think about it, if those with silent CVD don't move as much, simply because exercising causes them discomfort (which happens when narrowed arteries don't supply enough blood to a working muscle, or heart), it is not the sitting time, but the silent CVD which correlates with an earlier death. 

On to the 2nd study: Author Patel and colleagues looked at 123,216 adults, aged 60+, of the CPS-II nutrition cohort, who had been followed up for 14 years [3]. Again the results support an association between sitting time and CVD mortality, but, again, silent asymptomatic disease had not been assessed. Interestingly, in this study the association was far stronger in women than in men. Tellingly, age 60+ is also the age at which women start to "catch up" with their male peers in respect to CVD risk.

In the third study, Dunstan and colleagues had looked at the correlation between television viewing time and death among 8,800 adults aged 50+ with a median follow-up period of 6.6 years. In contrast to the previous 2 studies, the authors were able to adjust for known CVD risk factors such as hypertension, blood lipids, blood glucose and diabetic status. Those who reported sitting in front of the TV for more than 4 hours per day, had a 50% higher risk of dying from any cause and an 80% higher risk of dying from CVD causes. But adjusting for risk factors of CVD is not the same as adjusting for CVD. 

In the fourth study, Stamatakis and colleagues had looked at the data of 4512 people, aged 57+, of the Scottish Health Survey, who had been interviewed in 2003 and followed up until 2007. Those who had reported watching more than 2 hours of TV per day had an increased risk of CVD events (not of CVD death), and only those who had reported watching TV for more than 4 hours per day had a statistically significant risk increase of dying from any cause.

In the fifth and final study Wijndaele investigated the data of 13,197 adults aged 60+ of the EPIC study cohort. Those people had been assessed at the 1998-2000 baseline and followed up for 9.5 years. Like in the other 4 studies, the association between increased TV viewing time and all-cause and CVD death was evident. This observation prompted the authors to say that: "Given the high prevalence of excessive TV watching, ...  these results indicate the importance of public health recommendations aimed at decreasing TV time and possibly overall sedentary behaviour." So, will throwing away your TV make you live longer? 

You'll probably appreciate the difference between Wijndaele's and Katzmarzyk's way of interpreting essentially similar results. I personally go with Katzmarzyk's more careful interpretation. It does not outright assume a causal correlation to exist. There are still too many question marks. For example: We know that self-reported physical activity, self-reported screen time, well, self reported anything, is inherently fraud with over- and under-reporting of facts. Dunstan and colleagues were adamant at pointing out that this couldn't have affected their results. But when you look at how well, or how poorly, their questionnaire really performs, you will be forgiven to be less enthusiastic than the authors. Use that questionnaire twice on the same person to assess same-level PA, and chances are you'll get two different answers. That's not just me being the party pooper, it has been confirmed in validation studies which have shown, at best, only a moderate level of agreement between two rounds of questioning (the parameter is the intraclass correlation coefficient, or ICC) [4]. If repeated questioning is already fraud with inconsistencies, how large, do you think, such inconsistencies will be between the answers of any given respondent and his actual physical activity level? 

So, what are we to make of all this? I can only give you my personal opinion. I tend to believe that there is a threshold volume and intensity of DAILY physical activity, which protects you against the effects of extended sitting time. Only we can't see this level in the 5 discussed studies for obvious reasons. Their ways of assessing PA were not accurate enough.

I have to admit, that my belief is biased: I don't know about you, but less than 3 hours of sitting time appears unachievable for most of us today. And while I'm working at a desk, which allows me to alternate between standing and sitting, seen through the lenses of these 5 studies, I still have what those studies proclaim to be a risk factor for premature death: extended sitting time. But I also do exercise on a daily basis at an intensity and with a volume which far exceeds what 90% of the population is doing. That's why I love to think of this effort as being CVD-protective. This belief is founded in a large body evidence which essentially says: exercise triggers biochemical reactions and mechanisms with a vast array of protective effects. In a dose-dependent way. 

Fortunately, I'm able to measure the effects of my personal dose of exercise in my health lab. And from doing the same thing for our clients, I happen to know that everyone is unique in his response to intervention, be that exercise or diet or a pharmacological treatment. Which is why I am quite confident when I tell you not to lose any sleep over those attention grabbing headlines. Especially, when they suggest cause-effect relationships from studies which simply can't establish such relationships. In the case at hand, none of the 5 studies could have adjusted for pre-existing silent CVD. CVD is a cause of premature death and, as I have argued, it can be a reason for people to avoid exercise and spend more time sitting, simply because exercise causes them discomfort. So, here is my question: Are people dying early because they sit too long, or are they sitting so long because they'll die earlier? Stay skeptic! [tweet this]. 

1. Katzmarzyk PT, Lee IM: Sedentary behaviour and life expectancy in the USA: a cause-deleted life table analysis. BMJ Open 2012, 2(4).

2. Katzmarzyk PT, Church TS, Craig CL, Bouchard C: Sitting time and mortality from all causes, cardiovascular disease, and cancer. Med Sci Sports Exerc 2009, 41(5):998-1005.

3. Patel AV, Bernstein L, Deka A, Feigelson HS, Campbell PT, Gapstur SM, Colditz GA, Thun MJ: Leisure Time Spent Sitting in Relation to Total Mortality in a Prospective Cohort of US Adults. Am J Epidemiol 2010:kwq155.

4. Brown WJ, Trost SG, Bauman A, Mummery K, Owen N: Test-retest reliability of four physical activity measures used in population surveys. J Sci Med Sport 2004, 7(2):205-215.

Katzmarzyk PT, & Lee IM (2012). Sedentary behaviour and life expectancy in the USA: a cause-deleted life table analysis. BMJ open, 2 (4) PMID: 22777603

Katzmarzyk PT, Church TS, Craig CL, & Bouchard C (2009). Sitting time and mortality from all causes, cardiovascular disease, and cancer. Medicine and science in sports and exercise, 41 (5), 998-1005 PMID: 19346988

Patel AV, Bernstein L, Deka A, Feigelson HS, Campbell PT, Gapstur SM, Colditz GA, & Thun MJ (2010). Leisure time spent sitting in relation to total mortality in a prospective cohort of US adults. American journal of epidemiology, 172 (4), 419-29 PMID: 20650954

Brown WJ, Trost SG, Bauman A, Mummery K, & Owen N (2004). Test-retest reliability of four physical activity measures used in population surveys. Journal of science and medicine in sport / Sports Medicine Australia, 7 (2), 205-15 PMID: 15362316

Supplements: Nutrition Science Or Nutrition Crap?

Nutritionists claim they are doing science, consumers buy it, and the supplements industry makes a healthy living from it. Only you probably won't. Here is why: 

[tweet this].

One of the enduring diet questions is whether supplements are a good tool to (a) improve health, and (b) compensate for nutritional deficits of an enjoyable but less than healthy dietary habit.  

To most people, the answer seems to be a resounding "Yes". In the U.S. more than 65% of the population are regular supplement users. They spend north of 28 Billion US$ annually on their pills and potions. To put this into perspective:  28 Billion is more than the gross domestic product of Cyprus - the latest EU country in need of being bailed out. While Cyprus circles the drain, the supplement industry doesn't. In fact it is growing by 10% annually. A growth, which, in 2008, Dr. Daniel Fabricant, then vice president of the Natural Products Association (NPA), had correctly predicted. He knew the drivers of that growth: "...the products that grow are the ones with science behind them. When there’s good science like there is behind ... vitamin D and omega 3s, that’s really where the dollar is going to be spent.” So, let's have a look at how good that science really is.  

Remember the time when Vitamin E and beta Carotene - the thing in veggies and fruits, which your body turns into Vitamin A - were found to be associated with decreased risk of lung cancer. The year was 1981 and the knowledge of that time had been summarized in the journal Nature [1]. You must keep in mind: if it's in Nature, it's like God's gospel.  Also keep in mind, that those studies were observational by design, that is, they observed an association between increased beta-carotene intake and lower incidence of lung cancers. Such observations do not allow us to say that one causes the other, even though the media types are typically quick in doing just that.  So, the natural conclusion from these association studies was: give smokers, those people who have the highest risk of getting lung cancer, a Vitamin supplement to reduce their risk. 

Then, in 1985, a group of Finnish researchers (The Alpha-Tocopherol, Beta Carotene Cancer Prevention Group, ATBC) did the one and only thing, which can establish a cause-effect relationship: a study in which male smokers, the people at highest risk for lung cancer, were given the supplement and another group wasn't [2]. In fact, the 29,000 participants had been randomized into one of 4 equal-sized groups, with group A receiving Vitamin E, group B receiving Vitamin A , group C receiving both Vitamins and group D getting simply a placebo. In 1994 the results came out. Certainly not in favor of the supplement. The guys on beta-carotene had an 18% higher rate of developing lung cancer than their peers who did not get this Vitamin. Actually, this rate was seen accelerating over time.

Another large trial, the beta-carotene and retinol efficacy trial (CARET) did essentially the same thing. It investigated the effect of beta-carotene on lung cancer risk in more than 18,000 participants at elevated risk due to their being smokers or having been exposed to asbestos. CARET was done in the U.S., and it delivered more sobering results: A 28% increase in lung cancer risk among those who had been randomized to receive the beta-carotene supplement [3]. The trial was halted, and follow-up observations showed a gradual reversal of elevated risk. That's a clear indication that the increased risk of lung cancer was attributable to the supplementation with beta-carotene and vitamin E. 

While these results certainly put a damper on the enthusiasm for vitamin A & E, the truly interesting finding is often overlooked and underreported: For the placebo guys in the ATCB study, there was a clear inverse relationship between intake of FOODS high in Vitamin E & A and the risk of lung cancer. The group with the lowest intake of those veggies and fruits, which deliver Vitamin E & A, had a 50% higher risk of developing lung cancer compared to those guys with the highest intake of fruits and veggies. 

These observation have been confirmed in the EPIC study which investigated the effects of diet on cancer. Also here, a high intake of fruit and vegetables, not supplements, was found to reduce smokers' risk of lung cancer considerably [4]. 

With these facts about nutrition science, and how the supplement industry uses it, I simply wanted to set the mood. Now, let's look at how this science is doing in the vitamin D and omega-3 department as emphasized by Dr. Fabricant.

Vitamin D supplements are believed to improve or maintain bone health in older adults, particularly in women. Indeed, what comes out of science labs seems to support this notion. Dr. Bischoff-Ferrari and her colleagues evaluated 11 randomized controlled trials to answer the question whether vitamin D supplementation reduces fracture risk in women aged 65 and older. It does. But only in those with the highest daily intake, more than 800IU. Good news for the supplement industry? You bet. But is it good news for you, too? Maybe not. Vitamin D needs to be taken with calcium to be effective. But high calcium intake by way of supplements appears to increase the risk for heart attacks, whereas dietary calcium intake, say from milk and cheese, does not [5]. 

In view of all this evidence the United States Preventive Services Task Force (USPSTF) recently issued its draft recommendation, which says that there is insufficient evidence to "...to assess the balance of the benefits and harms of combined vitamin D and calcium supplementation...". But rest assured, the supplement industry has all the evidence and science, which the USPSTF has not. Or so they want you to believe. 

Let's move over to the famous fish oils and their Omega-3s.

The Omega-3 fatty acids are often praised as the constituents of fish oil, which protect against heart disease. At least that's what the supplement industry says. Science says something else. A double-blind prospective study of 2500 men and women aged 45 to 80, who had experienced a heart attack or stroke, investigated whether omega3- supplementation would prevent further cardiovascular events [6]. It didn't. 

You might ask, why this study looked only at people who had already cardiovascular disease. Maybe they are so far down the drain, that fish oil can't do its trick any more. Wouldn't it be nice to know whether omega-3 is protective in people who do not have cardiovascular disease? Yeah, it would. It would also be nice for you to tell me how to run such a study. Realistically. You would have to enroll thousands of healthy people, randomize them into those who MUST NOT EVER get their hands on omega-3 supplements and those who MUST take it every day for many years. Go find those people. Then, after many years, you would have to compare the outcome between the two groups. And you also would have to rule out those outcomes to be affected by such factors as physical activity and all the different food habits those thousands of people have. Of course, you would need funding for this type of research. Only, who will give you the funds? Certainly not the pharmaceutical industry. It pumps billions into research, yes, but only for proprietary chemicals. There is nothing proprietary about a vitamin, which every Tom, Dick and Harry can put into a pill. Which is why even the supplements industry won't give you a single dollar for your research. Now you know why such studies are not being performed. And why nutrition science is so fickle with its results. 

What's the taking home point: When it comes to nutrient-health interactions, it is obviously not as simple as boiling down the effects of food to an individual vitamin or other nutrient. Neither is it as simple as stuffing this nutrient into a pill and shoving it down your throat. In the words of Einstein: "Make things as simple as possible, but not simpler." Reducing the effects of food to individual vitamins or other nutrients is obviously an oversimplification. When, as a result of oversimplification, nutrition science makes you jump from one supplement to the next, what does the supplement industry do? They are laughing their way to the bank. And, as we have seen, Mr Fabricant knows why. He is no more with the NPA, though. He has switched sides to work now for the FDA as director of its Dietary Supplement Programs division. Let's hope the FDA's view on nutrition science remains as skeptical as it ought to be. In the interest of your health. [tweet this].

1. Peto R, Doll R, Buckley JD, Sporn MB: Can dietary beta-carotene materially reduce human cancer rates? Nature 1981, 290(5803):201-208.

2. The effect of vitamin E and beta carotene on the incidence of lung cancer and other cancers in male smokers. The Alpha-Tocopherol, Beta Carotene Cancer Prevention Study Group. N Engl J Med 1994, 330(15):1029-1035.

3. Goodman GE, Thornquist MD, Balmes J, Cullen MR, Meyskens FL, Jr., Omenn GS, Valanis B, Williams JH, Jr.: The Beta-Carotene and Retinol Efficacy Trial: incidence of lung cancer and cardiovascular disease mortality during 6-year follow-up after stopping beta-carotene and retinol supplements. J Natl Cancer Inst 2004, 96(23):1743-1750.

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