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

They say, statistics lie.

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

Which is why you should be a skeptic when someone is giving you the creeps about your food habits. For instance, by saying that "high sodium intake is associated with an increased risk of stroke", as the researchers of one recently published study do [1].
To be a skeptic isn't about habitually disbelieving. It is about asking the right questions. And there is a method behind this questioning. Unsurprisingly it is called statistics. The good news is, you don't need to be a statistician to become a methodical skeptic. You only need a little help on how to ask those questions and, more importantly, on how to find the answers for yourself. Which is what we are going to do.

On April 12 this year, Hannah Gardener and her colleagues published their findings about the associations between salt intake and risk of stroke in a community of people residing in northern Manhattan [1]. This appropriately named Northern Manhattan Study, or NOMAS, enrolled 2657 residents with a mean age of 69 years, roughly two thirds of whom were aged between 59 and 79 years. Participants completed a food frequency questionnaire with which the researchers attempted to assess the participants' dietary patterns over the one-year period, which preceded this investigation. I'm not going into discussing the potential pitfalls of using a 12-months recall to calculate how many grams of salt you consume every day. Let's just take those numbers as if they were accurate reflections of participants' salt intake. The researchers categorized participants into four groups according to how much sodium they had in their food:    

1.     1.5 grams/day or less

2.     > 1.5 grams - 2.3 grams per day

3.     > 2.3 grams - less than 4 grams per day

4.     4 - 10 grams per day

These categories didn't just occur to them from a close look at the tea leaves. The American Heart Association (AHA) recommends not to take more than 1.5 grams of sodium per day. Before 1.5 grams became the order of the day, it was 2.3 grams in the previous recommendation . Which is why the researchers used group number 1 as the reference, to which they compared the remaining 3 groups. By the way, only 12% of the study participants were in group 1.  

The researchers then checked how many stroke "events" occurred in each group over an average period of 10 years. And they also checked whether there was a significant difference when comparing the groups of higher salt intake with the reference group.

When you do this type of comparison, it pays to keep in mind that salt is not the only potential cause of stroke. Age is too, because the older you are the more likely it is that you'll suffer a stroke within the next ten years. So the researchers had to adjust for age. That's a statistician's way of asking "what would the rate of stroke events be if all participants were equal in age?". They did this adjustment thing not only for age but also for sex, ethnicity and education. Simply, because we know that these factors have an influence on stroke risk, too. This demographic adjustment was the researchers' first model of adjustment. They went a step further with a second and a third model, in which they additionally adjusted for behavioral and then, on top of that, for biological risk factors. In other words, they were very thorough in isolating the stroke risk that associates with eating salt, irrespectively of what else you do to your health. That's good statistics work. Now let's look at the results.

Only in the group of people with a daily sodium intake above 4 grams per day was the rate of stroke significantly higher than in the group of people who had reported to take no more than 1.5 grams. The take-home point in this case is, that consuming 4 grams or more of sodium per day was associated with a significantly increased risk of stroke in this population. Now here is the first question which you should ask:

What do you mean with "significant"?

To a statistician it does NOT mean what it probably means to you - "substantial". "Significant" is statistician speak for "probably not due to chance". In this case it means, there is some association between eating more than 4 grams of sodium per day and the risk of suffering a stroke within 10 years from now. Now you can shoot the second question:

How large is this "significant" difference in risk?

Let's take the AHA's demarcation line of 1.5 grams of sodium: Of those whose salt consumption was not more than that, 7.5% suffered a stroke. Whereas 9% of the sodium delinquents did. While this is not the correct way of comparison, it puts things into a clearer perspective. So, let's do it the correct way, and look at the risk in terms of event rates, that is in events per thousand person-years. There you have 7 strokes per thousand person-years in the group of low-sodium consumers vs. 8.9 strokes per 1000 person years in the rest. With these figures you can ask one very important question:

How many strokes could have been prevented among the sodium delinquents if they had gone easy on the salt?

The answer is: one in five. That is, 80% of the strokes that did occur in this group would have occurred even if they had consumed salt according to AHA recommendations. The picture is quite a bit different if you look only at the group of highest salt consumers, those who reported consuming more than 4 grams of sodium per day. In that group, "only" 60% of the strokes that did occur would have happened if they had lowered their salt consumption. Now, here comes your (almost) final question:

How relevant are these data to me?

Not at all if you are below the age of 40. That was the threshold for enrollment. Which obviously doesn't mean that you should go on a salt rampage until you hit 40 and then cut back to a daily dose of 1.5 grams of sodium per day. It simply means, the data from this study are not applicable to you, because your profile doesn't match the profile of the study participants.

Now let's assume, you are on the wrong side of 60, and let's also assume, that you measured your sodium intake to be more than 1.5 grams per day (and mind you, to get 1.5 grams of sodium you need to put 3.75 grams of salt on your food). Your next question would be:

What's MY stroke risk for the next 10 years?

About 9%. That is, of 11 guys who have exactly the same profile as you do, one will suffer a stroke over the next 10 years. Whereas, if you had found yourself to consume less than the 1.5 grams of sodium, that ratio would still be 1 out of 14.  That's a 20% reduction. And who says that cutting down on salt will get you this 20% risk reduction? Which amounts to your last question:

Does high salt consumption cause stroke?

Who knows? The study of Hannah Gardener and colleagues CANNOT answer this question. Their study design can only show you that there is an association. It CANNOT show causation. Which is why Dr. Gardener  and colleagues are not correct to conclude that "The new American Heart Association dietary sodium goals will help reduce stroke risk." That's an assumption of causality, which would require a different study design. For example, a study in which one group of participants is given sodium at the AHA recommended level and at least one other group is given sodium in excess of those 1.5 grams. For ten years, mind you. And without the participants or their physicians knowing who gets what. It's called a double blinded, randomized, controlled trial. It's the gold standard to prove causality. Try to do that with salt in a real life setting.

Naturally, Reuters blared out on 25th April "High salt intake linked to higher stroke risk". As usual, the media types gleefully dramatize studies like these. They feed you the bits and pieces which sell print.

But statistics are above the razzle-dazzle. Those who interpret them are obviously not. That's why it pays to be a skeptic and to take those statements literally with a pinch of salt.  

1.           Gardener, H., et al., Dietary sodium and risk of stroke in the northern Manhattan study. Stroke, 2012. 43(5): p. 1200-5.

Gardener, H., Rundek, T., Wright, C., Elkind, M., & Sacco, R. (2012). Dietary Sodium and Risk of Stroke in the Northern Manhattan Study Stroke, 43 (5), 1200-1205 DOI: 10.1161/STROKEAHA.111.641043

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...

you can fly from one place to another, and watch any place on this Earth without ever leaving your cave. You tell him you never have to run after your food, or fear that you run out of it. Your ancestor will have a hard time believing you. In his world only his gods can do all that.

Then you tell him how some of your friends think his way of life is preferable for health, which is why you are visiting him because you want to see for yourself. Before I get to your ancestor's most likely answer, let's get on the same page with those friends of ours first.

You have probably heard them talk about the past 10,000 years having done nothing to our genetic make-up. In other words, your ancestor's DNA blueprint was the same as yours. Today this blueprint collides  with a space age environment in which we don't expend any energy to get our food, and the food we acquire delivers far more energy and far less nutrients than what had been the case during 99.9% of human evolution. 

According to this view, today's epidemics of obesity, diabetes, cardiovascular diseases and cancer are simply the collateral damage of this collision. This explanation is so persuasive that it is being parroted by every media type and talking head who can spell the word  'genetics'. I'm afraid it is not that simple. Here is why:

Remember when the 3 billion letters, or base-pairs, of the human genome had first been decoded at the beginning of this century. This decryption had been delivered with the promise of revolutionizing medicine. Aside from new therapies, the hottest items were prognostic and diagnostic tools, which, we were made to believe, would lay in front of each individual his biomedical future. And with this ability to predict would come the ability to prevent, specifically all those diseases which result from an unfavorable interaction between genes and environment.

Almost ten years later we are nowhere near this goal. OK, we have identified some associations between some genetic variants and the propensity to become obese or get a heart attack or diabetes. But these associations are far from strong and they hardly help us to improve risk prediction. Just this year, Vaarhorst and colleagues had investigated the ability of a genetic risk score to improve the risk prediction of conventional risk scores which are based on biomarkers, such as the ones used in the Framingham score. Less than 3% of the study participants would have been reclassified based on the genetic risk score [1].

In a study which was released just yesterday, genetic markers for the development of diabetes in asymptomatic people at high risk, did not improve conventional biomarker risk scoring at all [2]. 

Obviously we are not simply our genes. This is because genes do not make us sick or healthy. Genes make proteins. And on the way from gene to protein a lot of things happen on which genes do not have any influence. To express a gene, as biologists call it, that gene must first be transcribed on RNA and then translated from RNA into the final protein. Whether a gene is transcribed in the first place depends on whether it is being made accessible for this transcription process. Today we know at least two processes which can "silence" the expression of a gene, even though it is present in your DNA. These processes are called DNA methylation and histone modification. Simply imagine them as Mother Nature's way of keeping a gene under wraps.

That's a good thing if the protein product of the silenced gene would be detrimental to your health. It could well be the other way round, too. Anyway, these happenings have been called epigenetics. Epigenetic mechanisms enable cells to quickly match their protein production with changing environmental conditions. No need to wait for modifications of the genetic blueprint which takes many generations and a fair element of chance to materialize. The most astonishing discovery is that these epigenetic changes may become heritable, too. Which means, there is really no need to change the genetic code. 

I believe you get the picture now. While it is true that your ancestor's genetic code is indistinguishable from yours 10,000 years later, the way your body expresses this code in the form of proteins and hormones can differ in many ways. Which is why researchers are now as much excited about epigenetics as they used to be about genetics 10 years ago.

I don't want to be the party pooper, but whenever I see such excitement I'm reminded of how it has often evaporated after some further discoveries. Here I'm skeptical because of the picture, which we are beginning to see. Insulin, for example, is known to regulate the expression of many genes. At least in rats it has been shown that insulin's suppressive effect on gene expression in the liver, can be altered by short term fasting [3]. That means, relatively minor behavioral changes may affect the way our organism expresses its genetic code.   

Observations like these support the idea that we are not our genes, but what we make of them. In plain words: let's not hide behind the "it's-our-stone-age-genes" excuse, to explain why we are fat and lazy and ultimately chronically sick.

Now, back to your ancestor and his response to your friends' suggestions that his way of life is preferable for health. When you also tell him you live a lot longer than the 40 years he has on average, he'll tell you: You have got some nutcase friends over there. Let me live like a god first and then I'll worry about health later.

Maybe, we are not so different from our stone age ancestors after all. 

1.           Lu, Y., et al., Exploring genetic determinants of plasma total cholesterol levels and their predictive value in a longitudinal study. Atherosclerosis, 2010. 213(1): p. 200-205.

2.           Schmid, R., et al., Current Genetic Data Do Not Improve the Prediction of Type 2 Diabetes Mellitus: The CoLaus Study.Journal of Clinical Endocrinology and Metabolism, 2012.

3.           Zhang, Y., et al., Insulin-Regulated Srebp-1c and Pck1 mRNA Expression in Primary Hepatocytes from Zucker Fatty but Not Lean Rats Is Affected by Feeding Conditions. PLoS ONE, 2011. 6(6): p. e21342.

Lu, Y., Feskens, E., Boer, J., Imholz, S., Verschuren, W., Wijmenga, C., Vaarhorst, A., Slagboom, E., Müller, M., & Dollé, M. (2010). Exploring genetic determinants of plasma total cholesterol levels and their predictive value in a longitudinal study Atherosclerosis, 213 (1), 200-205 DOI: 10.1016/j.atherosclerosis.2010.08.053 

Zhang Y, Chen W, Li R, Li Y, Ge Y, & Chen G (2011). Insulin-regulated Srebp-1c and Pck1 mRNA expression in primary hepatocytes from zucker fatty but not lean rats is affected by feeding conditions. PloS one, 6 (6) PMID: 21731709

To hell with exercise

Who says that exercise is medicine? For one, the American College of Sports Medicine (ACSM) of which I'm a professional member. Then, how can I say it isn't?

Let's look first at the conventional view of the benefits of exercise. There is a large and increasing amount of evidence which clearly tells us that exercise prevents today's number 1 killer: cardiovascular disease. That is, heart attack, stroke and peripheral vascular disease. Mind you, what is common knowledge today emerged only some 50 years ago when Morris and colleagues discovered that UK bus conductors, the guys climbing up and down the double-decker London buses, had better fitness and fewer heart attacks than their all-day-seated driver colleagues [1].

In the years since then our knowledge about the effects of physical activity on cardiovascular, metabolic and mental health has virtually exploded. From this evidence the U.S. Dept. of Health and Human Services (HHS) concluded in 2008 that the most active people of the population have a 35% reduced risk of dying from cardiovascular disease compared to the least active people [2]. The WHO lists insufficient physical activity (PA) as the 4th leading cause of death world wide after high blood pressure, tobacco use and high blood glucose. What's wrong with this picture? High blood pressure and high blood glucose are known consequences of a sedentary lifestyle. So is obesity, which ranks 5th place on the WHO killer list. Which is why physical inactivity deserves top spot on that list.

What most people don't know is the way lack of physical activity causes all those diseases, from insulin resistance and diabetes to arterial dysfunction and atherosclerosis, and from there to heart attack, stroke, kidney failure. The mechanisms are extremely complex, and, while we have untangled quite some of them, there are probably a lot more to discover. I'll try to make this the subject of one of the next blog posts. 

Now you are probably asking yourself, how the hell, with all this evidence, will I ever be able to make my point that physical activity is not a medicine. Ok, here it comes: it's a matter of viewpoint. The one I'm taking is the one of evolutionary biology. Let me play its advocate and present as evidence a couple of insights.

First, our human ancestors, who had roamed this Earth as hunter/gatherers for the most part of human existence, had, by necessity, a much more physically active lifestyle. A lifestyle which required at least 1.7 to 2 times the normal resting energy expenditure [3]. [To get an idea about resting energy expenditure and physical activity levels and how they are calculated, simply follow the links to the videos.] Those ancestors' genes are what we have inherited. And these genes are exposed to a lifestyle which is vastly different from the ones under which these genes evolved. Specifically with a view to physical activity, which brings me to evidence no 2:

What we typically observe today are physical activity levels with factors of somewhere between 1.2 and 1.4 of our resting energy expenditure. That's true for most people.

Even if you were to follow the ACSM's recommendation of 30 minutes of moderate to vigorous exercise on at least 5 days per week, would you NOT reach the level of 1.7 if you are working in a typical office job or doing house work. Which means, the physical activity levels which we recommend today, do not add a behavioral type of medicine into our lives, they merely reduce the extent of a "poisonous" behavior called sedentism. It's like cutting down from 2 packs of cigarettes per day to 1 pack. Would you call this a "medicine"? Would the ACSM call that a medicine? With respect to exercise they do.

So, OK, if you had been attracted to this post in the hope of finding some excuse for not doing exercise, or some argument to get those exercise evangelists, like myself, off your back, I'm sorry to have disappointed you. No, actually, I'm not sorry. And neither will you be, if you get your physical activity level above those 1.7. Then you may just start calling exercise a medicine. Until then, chances are you will still go to hell with exercise, because you get too little of it. Certainly too little to stay out of that hell of heart disease, stroke, diabetes and many cancers.

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

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

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

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

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.

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.