Posts Tagged ‘nutrition’

Good diet trumps genetic risk of heart disease

October 20th, 2011

I posted last week about “epigenetics” — the idea that, while the genes you’re born with are unchangeable, environmental influences can dictate which of your genes are turned “on” or “off.” A few days later, I saw a mention of this PLoS Medicine study in Amby Burfoot’s Twitter feed. It’s not an epigenetic study, but it again reinforces the idea that the “destiny” imprinted in your genes is highly modifiable by how you live your life.

The study mines the data from two very large heart disease studies, analyzing 8,114 people in the INTERHEART study and 19,129 people in the FINRISK prospective trial. They looked at a particular set of DNA variations that increase your risk of heart attack by around 20%. Then they divided up the subjects based their diet, using a measure that essentially looked at either their raw vegetable consumption, or their fresh veg, fruit and berry consumption. Here’s what the key INTERHEART data looked like:

Breaking it down:

  • The squares on the right represent the “odds ratio,” where the farther you are to the right (i.e. greater than one), the more likely you are to have a heart attack.
  • The top three squares represent the people who ate the least vegetables, and the bottom three squares are those who ate the most vegetables.
  • Within each group of three, GG are the people with the “worst” gene variants for heart attack risk, AG are in the middle, and AA are the people with the least risk.

So if we look at the top group first, we see exactly what we’d expect: the people with the bad genes are about twice as likely to suffer a heart attack as the people with the good genes. But if you look at the middle group (i.e. eat more vegetables), the elevated risk from bad genes is down to about 30%. And in the group eating the most vegetables, there’s essentially no difference between the good and bad genes.

How does this work? The researchers don’t know — partly because no one’s even sure exactly how the bad gene variants cause higher risk. (There are some theories, e.g. that it affects the structure of your veins and arteries.) But the practical message is pretty clear: if you eat your veggies, you don’t have to worry about this particular aspect of your genetic “destiny.”


A few thoughts on the paleo diet

September 17th, 2011

I was asked in an interview a few days ago for my take on the “paleo diet,” and I figured I may as well share those thoughts here. I’ll start by saying that I’m not an expert in this area — these are just my impressions from the outside! For anyone who’s interested in the scientific rationale behind it, there’s a very comprehensive review paper that was published earlier this year and is freely available online. Anyway, a few scattered thoughts:

It’s not a diet, it’s a lifestyle. I’ve seen this sentiment expressed on a number of paleo-oriented blogs, and I think it’s a very important point. If you want to argue that humans are uniquely adapted to the paleolithic environment because that’s where we spent the most time, it’s meaningless to just consider one part of that environment. If you spend the day sitting on your couch watching TV, then picking up the phone and ordering an authentic ancestral meal from McPaleo’s isn’t going to make you healthy. The review paper focuses on the following key elements of the paleolithic environment:

  • regular sun exposure for vitamin D
  • plenty of sleep, in synch with light/dark cycles
  • lots of physical activity!
  • no exposure to pollution
  • fresh, unprocessed food
  • short bouts of acute stress (tiger!) rather than chronic stress

All of this stuff sounds great — I’m absolutely in favour of every element of this lifestyle.

Plants vs. animals. In the fantasies of some people, going paleo means you get to eat enormous Fred Flintstone-style chunks of meat — for every meal. Not quite: here’s a passage from a paper published in the British Journal of Nutrition last year:

[I]n contrast to common belief, hunting probably played a less dominant role from a nutritional point of view compared with gathering, and on average, it makes up 35% of the subsistence base for present-day worldwide hunter–gatherers, independent of latitude or environment.

This is a point picked up by David Katz in an article earlier this summer: you’re still going to eat, as Michael Pollan would say, “mostly plants.”

The evils of wheat and dairy, and the pace of evolution. Okay, this is where I believe we start to drift away from well-supported science and into the realm of unsupported hypotheses. The basic idea is that, since humans only started farming about 11,000 years ago, our genome hasn’t had time to adapt to these foods. Moreoever, grains like wheat actually contain “antinutrients” that hinder proper digestion and cause chronic inflammation — in everyone, not just those with celiac disease or gluten sensitivity. These results are not widely accepted — or at least, I personally don’t find the evidence convincing.

Moreover, 11,000 years — or 366 human generations — is actually quite a long time. As a result, for example, it’s well understood that the gene allowing for humans to digest milk was selected through evolutionary pressure in populations that domesticated cows. The review paper I mentioned above notes this as a “key exception” to what they otherwise claim is the rule that humans haven’t had time to adapt to agriculture. I, on the other hand, would view it as “key evidence” that humans have had time to adapt to agriculture. Obviously, not all modern humans can digest milk — and those who can’t shouldn’t drink it! But I see no evidence that those who can drink milk should avoid it. Same goes for wheat: it’s certainly true that some people can’t process it adequately, but I’m not convinced that it’s full of antinutrients that are secretly poisoning the rest of us.

Overall, as Stephan Guyenet pointed out in his discussion of the review paper, the evidence seems to support the idea that “the main detrimental change was not the adoption of agriculture, but the more recent industrialization of the food system.” In other words, the diet we should be seeking to emulate is pre-1850, not pre-10,000 BC — which, not coincidentally, once again sounds a lot like Michael Pollan’s advice: don’t eat anything your grandparents wouldn’t recognize as food.

Post-exercise refuelling: all at once, or spread out?

August 29th, 2011

We’ve all heard about the post-exercise “window” for refuelling to maximize recovery and adaption: you need to take in carbs and protein with 0.5-2 hours. But does the timing really matter for building muscle? A new study from Stuart Phillips’ group at McMaster University compared two tactics for post-workout protein intake. Once group took 25 grams of whey protein immediately after a set of leg-extension exercises; the other group received the same 25 grams of whey protein in 10 2.5-gram doses every 20 minutes for 200 minutes. They measured “muscle protein synthesis” — basically a very accurate way of assessing how well you’re stimulating muscle growth after a single bout rather than having to run the experiment for several months to actually see muscle growth — and found that it was much higher in the group that took their protein all at once. After six hours, protein synthesis was elevated by 193% in the single-shot group and just 121% in the prolonged group.

The question this study was seeking to answer actually relates to the difference between whey protein (which is absorbed quickly) and casein (which is absorbed more slowly: the 2.5 grams of whey every 20 minutes was chosen to mimic the absorption pattern of casein). The problem is that if you compare two different proteins in a study, then you’re changing a bunch of different factors at once — the absorption timing, but also factors like the amount of leucine, a branched-chain amino acid thought to be key for muscle growth. Since both groups received 25 grams of whey (and thus identical amounts of leucine), this shows that absorption rate is key.

Practical takeaway: this was a muscle protein synthesis study, not a training study, so you have take the results cautiously. But it does suggest that if you’re trying to build muscle, taking in a big dose (i.e. 25 grams) of protein as soon as possible is preferable to snacking over the course of a few hours. It also confirms previous findings suggesting that whey (found in dairy products) has some advantages over other protein sources.


Fact-checking the backlash against recent salt studies

August 3rd, 2011

Look, I agree that the role of salt in food is complicated. It’s not that I think salt has no possible effect on health, and that people should just eat as much as they want. But I do think the reaction to recent studies questioning salt orthodoxy is ridiculous and closed-minded. I agree entirely with a recent statement from Yoni Freedhoff’s excellent Weighty Matters blog, in discussing a recent Scientific American article on salt:

So while I think healthy debate is in fact healthy, I would have thought that magazines like Scientific American, and many of the intelligent commentators on this and other blogs, would in fact do their due diligence to read and critically appraise studies, before getting on any particular bandwagon.

The thing is, I think SciAm did do its due diligence, and many of its critics didn’t. The most widely linked response to the recent salt studies comes from the Harvard School of Public Health, which posted a piece called “Flawed Science on Sodium from JAMA: Why you should take the latest sodium study with huge grain of salt.” It wastes no time in asserting that conclusions of the latest JAMA study (which I blogged about here) are “most certainly wrong.”

Why should we conclude that the JAMA study is wrong? Harvard doesn’t try to explain the results (which found that a measurement of sodium intake wasn’t linked to blood pressure, hypertension, heart disease in 3,681 healthy adults over a 7.9-year period). Instead, they offer some possible ways that random error could have crept into the results, such as:

  • the study was too small to support its conclusions, with just 3,681 subjects;
  • the study used 24-hour urine collection to assess sodium intake, which just provides a snapshot in time;
  • the study didn’t account for the fact that people who are tall and/or active eat more food (and thus salt) but have lower risk of heart disease.

Okay, fair enough. Getting good epidemiological data on salt consumption and health outcomes is very difficult, and this study certainly would have been better if it had a million people in it and kept them in boxes for 20 years to prevent any confounding factors. Presumably that’s what the salt-is-bad studies did, right? It certainly sounds that way, according the Harvard article:

Furthermore, the study’s findings are inconsistent with a multitude of other studies conducted over the past 25 years that show a clear and direct relationship between high salt intakes and high blood pressure, and in turn, cardiovascular disease risk. (4-10)

Conveniently, the (4-10) refers to links to these studies — the strongest evidence Harvard could marshal to prove that salt is dangerous. So what happens if we actually bother to read and critically appraise these excellent studies — perhaps using the same standards they’re applying to the JAMA study?

Uh-oh. This Intersalt study uses 24-hour urine excretion (“unreliable,” according to Harvard). This BMJ study only had 3,126 subjects, smaller than the JAMA study. This AIM study used 24-hour urine and only had 2,974 subjects — and not only that, it found no significant relationship between sodium levels and heart disease. (They tried to salvage the “right” answer by saying there was a “nonsignificant trend” — imagine if the JAMA study had been so brazen!) This NEJM study only had 412 participants, and based its primary conclusion on a comparison of a regular, high-salt diet with a low-salt version of the DASH diet, which “emphasizes fruits, vegetables, and low-fat dairy products, includes whole grains, poultry, fish, and nuts, contains only small amounts of red meat, sweets, and sugar-containing beverages, and contains decreased amounts of total and saturated fat and cholesterol.” Sounds like a fair comparison to me!

Okay, seriously. There’s no doubt that salt has an effect on blood pressure. That’s just basic chemistry. But does it have a clinically significant effect? The DASH study I mentioned above found that cutting salt intake by about 55% (good luck with that in the real world, and feel free to donate your taste buds to science, since you won’t be needing them) reduced systolic and diastolic blood pressure by 6.7 and 3.5 mmHg respectively. For comparison, to go from stage 1 hypertension to normal, you’d have to reduce systolic pressure by a minimum of 20 mmHg. So if eliminating more than half the salt in your diet is able to (barely) move the needle on blood pressure, isn’t it reasonable to question whether dramatic society-wide efforts to reduce salt consumption even in healthy people are rational and useful? And given these small effects, isn’t it plausible that in a real-world epidemiological study of healthy (non-hypertensive) people (like the JAMA study), sodium intake might have no bearing on subsequent health outcomes? Why would such a finding be “most certainly wrong”?

The point is that applying double standards to evaluate studies doesn’t serve science, and it doesn’t serve the public interest. This latest JAMA study appears to me to be no better and no worse than the studies used to justify the “war on salt,” so promptly dismissing it because of its conclusions (rather than its methodology) is lazy at best, and dishonest at worst.

Final note: I still find it interesting that Walter Willett (the key voice in the Harvard School of Public Health article dissected above) himself published findings showing that salt intake in the U.S. essentially hasn’t changed over the last 50 years, while hypertension has risen dramatically. I’m still not sure how he explains this, if salt is such a key driver of blood pressure.

The Australian Paradox: less sugar, more obesity

July 13th, 2011

I’ve been debating whether to blog about this study since I received an e-mail about it from the Canadian Sugar Institute last week. In general, information from food marketing agencies is pretty suspect. For example, this press release from “Pistachio Health” that also went out last week about a new study:

[…] Additionally, pistachios – also known as the “Skinny Nut” – are shown to be a “mindful snack” in terms of taking longer to eat and requiring the snacker to slow down and be more conscious of what has been consumed. […]

Yeah, everybody calls them the “Skinny Nut.” Riiiight. Now I really believe that the information you’re sending me is impartial…

Anyway, I’ve decided to blog about this study — a look at sugar consumption and obesity rates in Australia, the U.S. and the U.K. between 1980 and 2003 — because the information is interesting. It’s by two very well-respected Australian researchers (one of whom, for the record — Jennie Brand-Miller — is a lecturer at the University of Sydney’s medical school, where my wife is studying). It’s in a peer-reviewed journal, Nutrients. And as far as I can tell from the disclosures in the paper, it wasn’t in any way funded by the sugar industry: it was a masters project supervised by the two authors. The only reason the sugar lobby is e-mailing it around is because — as you’ll see — they like the results.

The full text of the study is actually available online, so I’m not going to dissect every detail. But the key result is very simple: unlike in the U.S., where sugar consumption has been climbing, per capita consumption of refined and added sugars actually declined by 16% in Australia between 1980 and 2003. During the same period, rates of obesity tripled. Here’s the sugar data:

Now, population data like this always raises lots of questions. The paper discusses the various ways of estimating sugar consumption, along with their pros and cons, and also breaks down sub-categories like sweetened beverages and so on. Without getting bogged down in all that, I think the important point is — as we should all know by now — putting two graphs side-by-side and saying “Hey, they have the same shape! Graph A must have caused Graph B!” is not good science. The recent debate about Robert Lustig’s “sugar is toxic” crusade has involved a lot of this sort of analysis: added sugar intake has increased in the U.S. and so has obesity, ergo A caused B. But if the trend really is the opposite in Australia (and if anyone can suggest reasons why the data above shouldn’t be trusted, please chime in below!), then those arguments are considerably weakened.

Does fat matter?

May 23rd, 2011

Just a decade ago, our concept of “healthy eating” was so simple and straightforward: fat is bad. These days, not so much. Amby Burfoot’s most recent Peak Performance blog post summarizes the key points from “The Great Fat Debate” held among four highly respected nutrition experts (Walter Willett, Alice Lichtenstein, Lewis Kuller, and Darius Mozaffarian) in the current issue of the Journal of the American Dietetic Association.

There was plenty of disagreement, but some common ground. For example, total fat is less important than the type of fat: saturated fats (e.g. dairy and meat) are less desirable than unsaturated fats (e.g. olive oil). But replacing fats with processed carbs isn’t the answer, and will probably make things worse — which brings up the fundamental problem with this kind of debate. As Harvard’s Mozaffarian puts it:

Dietary recommendations that focus on selected nutrients, such as total fat or saturated fat, are often confusing for the public, result in illogical dietary decisions, and increase the potential for manipulation of nutrient targets by the food industry… If we’re eating an otherwise healthful diet including plenty of vegetable oils, fruits, vegetables, fish, and nuts, it will be much less important what the saturated fat level is.

Or as Lichtenstein (of Tufts) puts it, more simply:

I think we have to stop talking about individual dietary components because when one goes up another goes down.

Given the continuing disagreement about fundamental questions (is cholesterol bad?), it seems pretty clear to me that we don’t have enough understanding of the complex relationship between diet and health to successfully micromanage the ratios of specific nutrients. On the other hand, we have pretty unambiguous evidence about the benefits of certain patterns of eating — like getting lots of vegetables and fruit. Until the research is a little less murky, that’s the approach I’m sticking with.

Training in a carb-depleted state: pros and cons

May 16th, 2011

This week’s Jockology column in the Globe and Mail takes a look at some of the benefits and risks of working out in a carbohydrate-depleted state:

For decades, sports nutritionists have been devising ever more sophisticated ways to ensure your body is perfectly fuelled before, during and after every workout. With gels, bars and belt-mounted drink bottles, you can have calories within reach no matter where you are.

But what if quaffing fewer carbs and calories – or even none – resulted in a better workout?

At a recent sports nutrition conference at the Australian Institute of Sport in Canberra, researchers and coaches were buzzing about an emerging practice they refer to as “train low, compete high.” The idea is to do some of your workouts in a carbohydrate-depleted state – the nutritional equivalent of training while wearing a weighted vest – then race with a full tank of carbohydrates.

With initial research showing the technique boosts fat-burning, as well as other metabolic responses to exercise, elite athletes aren’t the only ones taking note. It remains a controversial approach – but it’s relatively easy to give it a try… [READ ON]

For more on this topic, including the idea that low-carb training might be suitable during base training but not other times of year, check out this blog entry from last month.

Salt, sugar, and the search for the root of all evil

May 6th, 2011

Two interesting articles appeared in the New York Times earlier this week, one on salt and the other on sugar. In both cases, it’s the responses rather than the research itself that are most interesting, because they nicely illustrate the confusion and contradictions that result from our endless quest to identify a single Nutritional Villain while ignoring the broader dietary and lifestyle contexts.

First, the salt. I blogged last fall about a study that found that salt intakes in Western diets haven’t changed over the past half-century, despite claims that salt is responsible for the epidemic rise in hypertension. Now a new JAMA study measured sodium levels in the urine of 3,681 healthy people over a 24-hour period (the most reliable way to determine salt intake), and then followed them for an average of 7.9 years. They found little effect on blood pressure, no effect on the risk of hypertension, and — surprisingly — those who ate less salt were more likely to die. Here’s the data showing the risk of death and non-fatal cardiovascular disease, divided into low, medium and high salt consumers:

salt intake and mortality from JAMA paper

Interesting stuff. But even more interesting is the how eager everyone in the Times article seems to be to discredit the findings. Now, criticism of studies is certainly fair game. But instead of checking for flaws in the methodology to decide whether the findings are legit, the approach here seems to start with looking at the findings and then (since they run counter to orthodoxy) deciding that the methodology must have been flawed. The only really substantive criticism aimed at the data is the following:

But among the study’s other problems, Dr. Briss said, its subjects who seemed to consume the smallest amount of sodium also provided less urine than those consuming more, an indication that they might not have collected all of their urine in an 24-hour period.

Okay, so I can see two possible hypotheses to explain this apparent anomaly:

  1. Among the apparently healthy volunteers, those who had a premonition that they would die prematurely several years later were also disproportionately more likely to withhold some of their urine from the study in order to artificially reduce the amount of salt they were apparently consuming. Perhaps some underlying confounder explains it: the same character flaw that led them to hide their urine also led to the poor health decisions that eventually killed them.
  2. People who eat lots of salt get more thirsty, drink more, and thus provide more urine.

I’m not saying the study is definitive or without flaws. It’s relatively small, and its subjects were young and healthy — the authors are careful to note that it doesn’t mean that reducing salt intake isn’t useful to reduce blood pressure for patients who already have high blood pressure. But the point is that the establishment response to an interesting new study isn’t “How do we explain this new data?”, it’s “How do we dismiss it?” And that’s a problem.

The sugar article, by Gretchen Reynolds, is essentially aimed as a corrective in the ongoing debate about “toxic fructose,” stirred most recently by Gary Taubes’s Times magazine article. Reynolds sums up some of the recent research on how fructose can help endurance athletes both during and after exercise. In other words, fructose is actually quite useful in some contexts. The responses below the article are quite interesting; e.g.:

While interesting, how is this article RELEVANT to the general audience that reads the NYT? The study referenced in the article relates how sugar affected “highly trained” athletes, a group that measures less than 1% of the population…

But it is relevant. Because it suggests what we really mean is not “Sugar is toxic,” but rather “Excessive sugar in the context of a sedentary lifestyle is toxic.” The first statement is a more attractive one, because it means we have a simple, well-defined enemy to attack, so all we have to do is engineer a bunch of Lo-Sugar snack foods and we’ll all be healthy again. Unfortunately, I think that’s a false promise. You can’t ignore the overall dietary and lifestyle context.

Gary Taubes on “toxic” sugar

April 14th, 2011

A friend just forwarded the new Gary Taubes NYT Magazine article on Robert Lustig’s claims that sugar is “toxic.” It’s an interesting article, worth a read, and Taubes is reasonably circumspect in acknowledging the uncertainties in the current evidence. He starts with this acknowledgment:

The viral success of [Lustig’s] lecture, though, has little to do with Lustig’s impressive credentials and far more with the persuasive case he makes that sugar is a “toxin” or a “poison,” terms he uses together 13 times through the course of the lecture, in addition to the five references to sugar as merely “evil.”[…]

His critics argue that what makes him compelling is his practice of taking suggestive evidence and insisting that it’s incontrovertible. Lustig certainly doesn’t dabble in shades of gray.

Indeed, that’s precisely what’s at issue with Lustig’s lecture: not whether sugar is a problem, but whether it’s the problem. And to make that case, Taubes stacks the deck with statements like this:

The conventional wisdom has long been that the worst that can be said about sugars of any kind is that they cause tooth decay and represent “empty calories” that we eat in excess because they taste so good.

Who the heck claims this? (In journalistic jargon, phrases like “The conventional wisdom has long been…” are known as “weasel words,” because they allow you to make statements that help your argument without finding anyone stupid enough to actually say them.) It’s a convenient distortion, because it lends some misplaced novelty to the “Men Land on the Moon!” discussion that follows, about the links between sugar and metabolic syndrome. Come on, we’ve been talking about “glycemic index,” in which glucose is assigned the nominal maximum value, since the early 1980s. This is an important topic, and perhaps one that not everyone fully appreciates, but it’s tangential to Lustig’s central claim that sugar (and fructose in particular) is a “toxin.”

The central question here is really about dose. Is sugar “unsafe at any dose,” as Ralph Nader might put it? Or is it only unsafe when consumed to excess? And if the latter, what constitutes “excess”? To his credit, Taubes makes this point, though he weakens it by putting it in the mouth of someone he identifies as a lobbyist for the corn refining industry:

[S]ugar and high-fructose corn syrup might be toxic, as Lustig argues, but so might any substance if it’s consumed in ways or in quantities that are unnatural for humans. The question is always at what dose does a substance go from being harmless to harmful? How much do we have to consume before this happens?

Much of the rest of Taubes’s article explores how much sugar we’re now eating, how much it has increased, and how diseases like diabetes and cancer have increased in parallel. It makes a strong case for eating less added sugar — pretty much exactly the same case that Taubes made in his 2007 book Good Calories, Bad Calories, as far as I can tell. Heck, I was convinced in 2007, and I’ve been very conscious of my sugar intake — along with other highly refined carbohydrates — ever since then. What I don’t see here is any reason to be more scared of sugar than I was before on the basis of Lustig’s “sugar is a toxin” argument.

Taubes describes the mechanism of fructose’s action as follows:

In animals, or at least in laboratory rats and mice, it’s clear that if the fructose hits the liver in sufficient quantity and with sufficient speed, the liver will convert much of it to fat. This apparently induces a condition known as insulin resistance…

Again, scary stuff. But how is this different from, say, glucose, or even refined carbs from white bread, which are thought to stimulate insulin resistance if they enter the body “in sufficient quantity and with sufficient speed”? If we’re concluding that fructose is “toxic,” shouldn’t we also conclude that glucose and white bread and all other refined carbs are too? Oh wait, that’s what Gary Taubes proposed in 2007. So what has Lustig added? Fructose causes the same problems as other foods, but through a different biochemical pathway.

What would get my attention is evidence that cumulative exposure to fructose — independent of the rate of intake — accumulates over time to produce problems. In other words, does eating 50 pounds of sugar spread out over 30 years ultimately produce essentially the same bad effects as eating 50 pounds of sugar in a single year? Or is it only a problem when the dose comes “in sufficient quantity and with sufficient speed”?

To be clear, I have no doubt whatsoever that Lustig is right that we eat too much sugar and it’s causing health problems. I just wonder if there’s actually anyone in the country who didn’t already think that.

Protein during exercise: good for strength not endurance training

March 5th, 2011

Does adding a bit of protein to a carb-heavy sports drink improve performance? That’s the claim of drinks like Accelerade, which boast a 4:1 ratio of carbohydrate to protein. But the research showing any performance advantage has been controversial. There’s a new study in the American Journal of Physiology: Endocrinology and Metabolism that put this to the test once again (hat tip to Amby Burfoot for pointing it out).

The study is quite complex, but basically it involved putting 12 cyclists through a two-hour cycling test at 55% maximum power while ingesting either a carbohydrate drink (at a rate of 1 gram per kilogram of body weight per hour) or a 4:1 carb-protein drink. They did a whole bunch of tests, including repeated muscle biopsies, to evaluate whether the protein boosted rates of muscle protein synthesis during exercise. The result: it didn’t.

An interesting wrinkle: the same group (from Maastricht University in the Netherlands) did an similar study on resistance training. In that case, adding protein did boost protein synthesis rates. The researchers speculate that muscle protein synthesis is blocked during actual exercise, but can take place in the short rests between sets of a strength training routine. Thus, the protein only helps for intermittent exercise.

Two final notes. First, this wasn’t a performance study, so it certainly doesn’t prove anything either way — that debate will continue, though my sense is that dominant current opinion is that protein during exercise doesn’t help endurance. Second, we’re only talking about drinks ingested during exercise; it’s clear that protein is very important after exercise.