Showing posts with label stroke. Show all posts
Showing posts with label stroke. Show all posts

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.  



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

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.



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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

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?