Former president George W. Bush recently had surgery to open a blocked coronary artery.
As the NBC Nightly News reported (click link for video)
So George W. Bush, a famous fitness fanatic, had a blocked artery. Now, he was experiencing no symptoms, so “heart disease” may be a bit of a strong term. Indeed, it is disputed in the medical community if he even needed the stress test he underwent or the surgery he received. But, the larger point is inescapable: that someone in his physical condition could have this problem.
More telling was the advice that the NBC doctor chica gave when this story was reported. She was adamant that the problem here was that even vigorous and dutiful exercise could not make up for poor diet; “the cheesburgers of our life catch up to us,” she proclaimed. According to her, we all need to be on “a very low-fat diet”, need to perform aerobic exercise, and might even needed statins to keep our cholesterol levels down.
To borrow Tom Naughton’s actions: head. Bang. On. Desk.
How confident would Dr. Snyderman be in her recommendations if she ever saw this map?
This is a map of the mortality from cardiovascular disease (CVD) in Europe, as I’ve previously featured (especially here, where I showed that it corresponds to average minimum winter temperatures across Europe). While it’s not colored here, it continues to get worse as you go east.
I’m sure if only those poor Slavs would lay off the beef, they’d be fine… :
She recommends vigorous exercise. Unfortunately, as I’ve previously reported, when this was tested in a controlled clinical trial (on diabetics), it didn’t seem to work in warding off cardiovascular events:
The study randomly assigned 5,145 overweight or obese people with Type 2 diabetes to either a rigorous diet and exercise regimen or to sessions in which they got general health information. The diet involved 1,200 to 1,500 calories a day for those weighing less than 250 pounds and 1,500 to 1,800 calories a day for those weighing more. The exercise program was at least 175 minutes a week of moderate exercise.
But 11 years after the study began, researchers concluded it was futile to continue — the two groups had nearly identical rates of heart attacks, strokes and cardiovascular deaths.
But the outcome is clear, said Dr. David Nathan, a principal investigator and director of the Diabetes Center at Massachusetts General Hospital. “We have to have an adult conversation about this,” he said. “This was a negative result.”
Additionally, even if exercise did have any beneficial effect – which as we see here is questionable – is she sure it need be lengthy aerobic exercise? As reported by Steve Hsu, landmark research by James Timmons found that the asssumed markers of exercise’s beneficial effects, such as insulin response, and VO 2 max, can be obtained by 1-minute very high intensity workouts. Timmons found that individuals under these 1-minute programs overall improved their markers as well as people with traditional 20- to 30-minute aerobic workouts.
That is, people who benefit at all. As Timmons’s data show, a significant fraction of the people show little to no improvement. A sizable minority (~10%) are negatively impacted by exercise!
Timmon’s research found that this response is largely under genetic control (big surprise), and his work has spotted some of the genes that are activated within muscle tissue in response to exercise:
That original research, published in a landmark 2010 study, looked into the genetics of why some people respond to endurance exercise so robustly, while others do not. Some lucky men and women take up jogging, for example, and quickly become much more aerobically fit. Others complete the same program and develop little if any additional endurance, as measured by increases in their [VO 2] max, or their body’s ability to consume and distribute oxygen to laboring muscles.
For the 2010 study, Dr. Timmons and his colleagues genotyped muscle tissue from several groups of volunteers who had completed 6 to 20 weeks of endurance training. They found that about 30 variations in how genes were expressed had a significant effect on how fit people became. The new test looks for those genetic markers in people’s DNA.
OK, but we’re told exercise is good for mood and can help treat depression. That’s good reason to exercise, right? It turns out that too is bullshit.
Behavioral genetic studies – looking to tease out the causal relationship between exercise and mood – found that between identical twins, differences in exercise weren’t related to differences in the prevalence of depressive feelings. As one such study reports (emphasis mine):
If exercise causally influences symptoms of anxiety and depression, all genetic and environmental factors that influence variance in exercise behavior will, through the causal chain, also influence the variance in these symptoms. Translating this to the structural equation models used on twin family data, this means that, if A, C, and E contribute to both traits, the genetic (Rg) andenvironmental (Re, Rc) correlations between exercise and symptoms must both be significantly different from zero. Furthermore, this should apply to the cross-sectional cross-trait correlations as well as the longitudinal cross-trait correlations (De Moor et al., 2008). In spite of sufficient power, we found only the genetic correlation to be significant (ranging between 0.16 and 0.44 for different symptom scales and different time-lags). Environmental correlations, however, were essentially zero. This means that the environmental factors that cause a person to take up exercise do not cause lower anxiety or depressive symptoms in that person, currently or at any future time point. In contrast, the genetic factors that cause a person to take up exercise also cause lower anxiety or depressive symptoms in that person at the present and all future time points.
We have also addressed the association between exercise and well-being in a sample of 5140 Dutch adult twins and their non-twin siblings from 2831 families using self-rated health as an index of well-being (De Moor et al., 2007b). Bivariate genetic models tested the contribution of genetic and environmental factors to the observed correlation between exercise participation and self-rated health. We showed that the genetic factors influencing exercise participation and self-rated health partially overlap (Rg 0.36) and, importantly, this overlap fully explains their association.
Again this argues in favor of genetic pleiotropy and suggests that the well-being of genetically identical individuals shows a high resemblance, even if one is a fervent exerciser and the other is a couch potato.
Based on the work described above, we conclude that, in the population at large, exercise participation is associated with higher levels of perceived health, life satisfaction, and happiness, as well as lower levels of anxiety and depression, largely through genetic factors that influence both exercise behavior and psychological well-being.
So exercise is useless-to-perhaps only marginally useful for curbing heart disease risk or lifting mood, but what about weight loss? The whole “Let’s Move” campaign is predicated on the belief that Americans are fat because we don’t exercise enough. Well, sure enough, that turns out to be bullshit too.
As reported by Gary Taubes in his essay in New York Magazine (Does Exercise Really Make Us Thinner?), evidence for the effect of exercise in weight maintenance is lacking. As he puts it (emphasis mine):
If lean people are more physically active than fat people—one fact in the often-murky science of weight control that’s been established beyond reasonable doubt— does that mean that working out will make a fat person lean? Does it mean that sitting around will make a lean person fat? How about a mathematical variation on these questions: Let’s say we go to the gym and burn off 3,500 calories every week—that’s 700 calories a session, five times a week. Since a pound of fat is equivalent to 3,500 calories, does that mean we’ll be a pound slimmer for every week we exercise? And will we continue to slim down at this pace for as long as we continue to exercise?
For most of us, fear of flab is the reason we exercise, the motivation that drives us to the gym. It’s also why public-health authorities have taken to encouraging ever more exercise as part of a healthy lifestyle.
The report that these experts cite most often as grounds for their assessments was published in 2000 by two Finnish researchers who surveyed all the relevant research on exercise and weight of the previous twenty years. Yet the Finnish report, the most scientifically rigorous review of the evidence to date, can hardly be said to have cleared up the matter. When the Finnish investigators looked at the results of the dozen best-constructed experimental trials that addressed weight maintenance—that is, successful dieters who were trying to keep off the pounds they had shed—they found that everyone regains weight. And depending on the type of trial, exercise would either decrease the rate of that gain (by 3.2 ounces per month) or increase its rate (by 1.8 ounces). As the Finns themselves concluded, with characteristic understatement, the relationship between exercise and weight is “more complex” than they might otherwise have imagined.
Mayer’s hypothesis always had shortcomings, but they were ignored for the same reasons they still are—who wants to openly question the idea that physical activity is a panacea? The first issue is a logical one: That conclusion that the fatter we are, the more sedentary we’re likely to be is actually a correlation; it tells us nothing about what is cause and what is effect. “It is a common observation,” noted Rony in 1941, “that many obese persons are lazy, i.e., show decreased impulse to muscle activity. This may be, in part, an effect that excess weight would have on the activity impulse of any normal person.” Equally possible is that obesity and physical inactivity are both symptoms of the same underlying cause.
Ultimately, the relationship between physical activity and fatness comes down to the question of cause and effect. Is Lance Armstrong excessively lean because he burns off a few thousand calories a day cycling, or is he driven to expend that energy because his body is constitutionally set against storing calories as fat? If his fat tissue is resistant to accumulating calories, his body has little choice but to burn them as quickly as possible: what Rony and his contemporaries called the “activity impulse”—a physiological drive, not a conscious one. His body is telling him to get on his bike and ride, not his mind. Those of us who run to fat would have the opposite problem. Our fat tissue wants to store calories, leaving our muscles with a relative dearth of energy to burn. It’s not willpower we lack, but fuel.
This view is backed-up by several studies, including a 2005 meta-analysis of diet and exercise interventions that failed to find significant weight loss with exercise programs.
Of course, one has to wonder if the overall null finding seen in controlled trials was the result of a distinct pattern of individual variation within them, such as the type seen in the data discussed by Timmons. This is a possibility, so it remains likely that some of you will respond well to exercise; others, little-to-none; and yet others, you’ll respond adversely (and will likely give it up before it gets all that bad).
OK, so what about diet, which according to Snyderman, needs to be “very low-fat?” Well, Tom Naughton made a movie and has a website devoted to questioning that notion. An older essay by Gary Taubes questioned the wisdom of low-fat diets in warding off heart disease. Stephan Guyenet also discussed a meta-analysis of correlational studies that failed to find a link between saturated fat consumption and heart disease. I will leave it to these men and others to hash out what the optimal diet is, for now.
So if diet and exercise don’t ward of heart disease, what does? Well, unfortunately, the answer to that question isn’t clear, and may in fact be “not much”. As the above map of the distribution of mortality of CVD in Europe (and this map of CVD mortality globally)…
…make clear, there is a strong genetic component to heart disease. Heart disease incidence is heritable even on the individual level, with one study finding the heritability of heart disease being about 65%.
This is sadly illustrated by the story of Rick Del Sontro and his family:
Early heart disease ran in Rick Del Sontro’s family, and every time he went for a run, he was scared his heart would betray him. So he did all he could to improve his odds. He kept himself lean, stayed away from red meat, spurned cigarettes and exercised intensely, even completing an Ironman Triathlon.
Rick Del Sontro keeps himself lean and watches his diet, but despite his efforts, he has heart disease like many in his family.
“I had bought the dream: if you just do the right things and eat the right things, you will be O.K.,” said Mr. Del Sontro, whose cholesterol and blood pressure are reassuringly low.
But after his sister, just 47 years old, found out she had advanced heart disease, Mr. Del Sontro, then 43, and the president of Zippy Shell, a self-storage company, went to a cardiologist.
An X-ray of his arteries revealed the truth. Like his grandfather, his mother, his four brothers and two sisters, he had heart disease. (One brother, Michael, has not received a diagnosis of the disease.)
DNA is clearly the culprit in this family’s case, as it is with all of us.
Contrary to what we’ve been led to believe, it is possible – and indeed quite likely – that heart disease is an inevitable consequence of living. In other words, lifestyle, including what you eat, drink, where you work, how much you work out, etc, may have little to nothing to do with your chances of developing heart disease.
This is hinted by the Scherrer et al study mentioned above. They found that common genetic pathways are in good part responsible for the link between depression and heart disease. There was some non-genetic spillover, indicating that “environmental” factors could influence each (which could just mean non-additive genetic effects). (To be fair, smoking does appear to be one “lifestyle” factor that influences heart disease risk.)
The incidence of CVD mortality has changed significantly over time:
But as Taubes noted, this pattern may mask several underlying secular trends. Apparently, while mortality from cardiovascular disease has declined sharply over time, the incidence of these diseases has remained flat. Better medical treatment has served to reduce deaths from CVD.
As well, Taubes notes that the apparent post-War rise may be due both to changes in ways cause of death was attributed and to the fact that medicine became so much better at preventing people from dying from other causes. As deaths from these other maladies and accidents declined, more people lived longer to die from CVD.
While the issue of weight didn’t come up with Bush, it is a related matter of faith that obesity is “bad for you”. Well, as I’ve previously reported, the situation is not what is commonly assumed:
The suspicion dawned on me that the connection between mortality and obesity could be mostly, if not entirely, a result of IQ.
And sure enough, I found something that strongly suggested this. It turns out that the venerable Satoshi Kanazawa did a study that found, in a White British sample, IQ measured in childhood predicts obesity at age 51. I discussed this in a post, that is currently experiencing decent readership thanks to the Geoffrey Miller fiasco: Obesity and IQ
The next logical step was to ask the question of how well IQ correlates to shortened lifespan. And I did that with my 99th post, IQ and Death. Looking at a meta-analysis of several studies of IQ and mortality, it was found that IQ is associated with longer lifespan. Indeed, at least one study in the meta-analysis did look at other possible attenuating factors. It found that IQ was by far the strongest predictor of death. Indeed, “marital status, alcohol consumption, systolic and diastolic blood pressure, pulse rate, blood glucose, body mass index, psychiatric and somatic illness at medical examination) was negligible (10% attenuation in risk)!”
The association between obesity and shortened life, and perhaps most health problems, is mostly, and perhaps entirely, a result of obesity’s association with IQ. As I have noted, and as I have been embroiled in a little controversy over, the “conventional wisdom” on diet, exercise, obesity, health, and death is pretty much bullshit.
Despite this reality, studies continue to come out talking about the detrimental effect of obesity, including one that went out with the headline “Obesity’s death toll could be higher than believed.” Within, it made the usual sensational claim “that 18.2% of premature deaths in the U.S. are associated with excessive body mass,” (italics mine). First of all, as we see, the idea of “premature” death is questionable. But secondly, we also see that it’s the same old story again: they found a correlation between two variables, and assumed that they necessarily existed in a causal relationship. Almost all the conventional health wisdom is based on such studies.
How did we end up here with this shitty health advice? Fundamentally, the problem is in assuming that correlation necessitates causation. As Gary Taubes explains (quoted in my post Gary Taubes on Obesity and Bad Science – emphasis mine):
Another problem endemic to obesity and nutrition research since the second world war has been the assumption that poorly controlled experiments and observational studies are sufficient basis on which to form beliefs and promulgate public health guidelines. This is rationalised by the fact that it’s exceedingly difficult (and inordinately expensive) to do better science when dealing with humans and long term chronic diseases. This may be true, but it doesn’t negate the fact the evidence generated from this research is inherently incapable of establishing reliable knowledge.
The shortcomings of observational studies are obvious and should not be controversial. These studies, regardless of their size or number, only indicate associations—providing hypothesis generating data—not causal relations. These hypotheses then have to be rigorously tested. This is the core of the scientific process. Without rigorous experimental tests, we know nothing meaningful about the cause of the disease states we’re studying or about the therapies that might work to ameliorate them. All we have are speculations.
The medical establishment will loathe to admit it, but knowledge of proper health advice is currently in a very sorry state, primarily for the above reason. Hopefully, with properly designed studies, genomic evidence, and by taking human biodiversity – both between individuals and between groups – into account, the state of knowledge on this matter can improved. Perhaps we are living at the beginning of a new golden age in health advice.
Of course, returning to the former president’s condition, calling his apparently asymptomatic blocked coronary artery “heart disease” may be a stretch. As Tom Naughton discussed, blocked arteries are quite common, and don’t necessary indicate a disease state (or more accurately, an impending heart attack). It is possible Bush may have lived with his blocked artery just fine, and continue on for decades more without intervention (unfortunately now, we’ll never know).
Nevertheless, where does that leave the poor average schmo who is trying to slog his way through life – who may not be svelte or able to run a 10K marathon – and is trying to navigate a conflicting maze of health advice. Ironically, the best advice – for now – might just be to eat, drink and be merry. If you actually enjoy working out and eating “right”, by all means keep doing it. If you don’t, it might be better for you to go ahead and quit.
One thing we do know: of all the variables examined, IQ appears to be far and away the single best predictor of health, both in terms of quality of life and its length. Why this is so may be as Satoshi Kanazawa…
One alternative explanation for the significantly negative association between childhood intelligence and obesity is the ‘‘general fitness factor’’ approach (26), which suggests that both higher intelligence and health (including the ability to stay within the normal weight range) reflect underlying genetic quality
and Kevin Mitchell noted:
Various researchers have suggested that g may be simply an index of a general fitness factor – an indirect measure of the mutational load of an organism. The idea is that, while we all carry hundreds of deleterious mutations, some of us carry more than others, or ones with more severe effects. These effects in combination can degrade the biological systems of development and physiology in a general way, rendering them less robust and less able to generate our Platonic, ideal phenotype. In this model, it is not the idea that specific mutations have specific effects on specific traits that matters so much – it is that the overall load cumulatively reduces fitness through effects at the systems level.
Supporting the idea that lifestyle has minimal effect on chronic disease incidence is the fact that IQ is in fact unrelated to cancer incidence, despite the fact that both are known to be highly heritable.
Medicine may have gotten better at treating the ailments that burden man – even eliminating some that have known external agents (for example, infectious diseases such as polio or smallpox) – but we have largely run up against a wall where it comes to cardiovascular disease. Despite our best efforts, we can’t seem to get it below a certain level. This may be because this may be a feature, and not a bug of the system. Or at least, this is an inevitable mode of failure for which selection has only been weakly able to act against. But the Puritan will to perfect man and society causes us to fight against this – even blaming ourselves for not living “well” enough – despite the fact that we may be fighting a (for now) hopeless war. A serenity moment if there ever was one.
I’m going leave off with a song that I first encountered many, many years ago (in MIDI form, if that tells you anything) from the old Lies, Damn Lies & ICQ Messages page. Since then, I’ve regarded this track as a general bullshit-debunking theme, and will likely use it again quite a few times. 😉