The Unz Review • An Alternative Media Selection$
A Collection of Interesting, Important, and Controversial Perspectives Largely Excluded from the American Mainstream Media
 BlogviewJayMan Archive
Even George W. Bush Has Heart Disease
Email This Page to Someone

 Remember My Information


Bookmark Toggle AllToCAdd to LibraryRemove from Library • B
Show CommentNext New CommentNext New ReplyRead More
ReplyAgree/Disagree/Etc. More... This Commenter This Thread Hide Thread Display All Comments
These buttons register your public Agreement, Disagreement, Thanks, LOL, or Troll with the selected comment. They are ONLY available to recent, frequent commenters who have saved their Name+Email using the 'Remember My Information' checkbox, and may also ONLY be used three times during any eight hour period.
Ignore Commenter Follow Commenter
Search Text Case Sensitive  Exact Words  Include Comments
List of Bookmarks

Former president George W. Bush recently had surgery to open a blocked coronary artery.

As the NBC Nightly News reported (click link for video)

050705_bush_vmed_1p_lwa9s 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?

Europe Heart Death Men 2000

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!

Screen Shot 2013-05-06 at 1.09.52 PM

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.

As for statins, a 2012 meta-analysis found that they work in warding off CVD (sort of, there’s a great deal of individual variation), but not necessarily because they lower cholesterol.

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)…

Cardiovascular disease rates global

…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:

Cardiovascular Deaths vs Pharma Innovationm830a1f1

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. 😉

(Back to text)

(Republished from JayMan's Blog by permission of author or representative)
Hide 28 CommentsLeave a Comment
Commenters to FollowEndorsed Only
Trim Comments?
  1. elijahlarmstrong says: • Website

    Ooo! Tangerine Dream!

  2. Amos says: • Website

    Stunning post. I wonder if similar maps exist for other conditions, e.g., skin cancer. It’d be interesting to overlay that map with the map of average temperatures you provided in the original post you linked.

    It’s now verging on the border of gross incompetence to exclude genetic makeup from these studies. It’s only a matter of time, however, before there’s a paradigm shift (a-la Thomas Kuhn) towards taking race and genetics seriously in this area.

    I hope.

    • Replies: @Greying Wanderer
  3. I think it’s premature to rule out a strong dietary component in heart disease. Cardiologist William Davis has been blogging for years about interventions and their outcomes. One thing he’s doing right is using heart scan calcium scores as a measure of heart disease–it’s a far better measure than any kind of cholesterol or blood lipid, and you can more quickly detect the effects of interventions on calcium scores than on CVD death rates. He’s best known for his book bashing wheat for causing heart disease, but there’s other strong evidence for that hypothesis too, including Denise Minger’s reanalysis of the data from the China Study:

  4. JayMan says: • Website
    @Johnny Caustic

    @Johnny Caustic:

    One thing he’s doing right is using heart scan calcium scores as a measure of heart disease–it’s a far better measure than any kind of cholesterol or blood lipid, and you can more quickly detect the effects of interventions on calcium scores than on CVD death rates.

    No offense, but are you serious? You can always claim to develop a better marker, but that means nothing unless it actually marks something. Unless a strong association is established between the purported marker and an adverse health outcome, like heart attack, stroke, or death, it’s worthless, and I wouldn’t be too concerned about it.

    The only reliable interventions are ones that show that they reduce the incidence of such events, nothing less.

    He’s best known for his book bashing wheat for causing heart disease, but there’s other strong evidence for that hypothesis too, including Denise Minger’s reanalysis of the data from the China Study:

    That’s all correlational; that’s evidence of didly squat, my friend…

  5. Sisyphean says:
    @Johnny Caustic

    Yeah, the problem I have with nutrition is that everyone has their own theory with its own countless correlations drawn from gobs of pointless observational studies. What you end up with is people grouping together into foodie camps more by ideology than by evidence. You see militant hippy lefties on the veggie blogs, iconoclastic (and also often caustic) libertarians on the paleo blogs and regular folks making fun of the weirdos while populating the ‘lowfat run from death’ or ‘eat whatever, you’ll die either way’ camps.

    I decided to take an experimental approach and try everything and see what worked best. Turns out that for me taking wheat out was an unmitigated good, even though I’m not celiac, I used to have asthma but when the wheat went away so did the asthma (and it comes back when I have some). I’m not going to generalize and suggest everyone must lose wheat, just my own experience. I eat a modified paleo-ish diet and can now maintain a trim, muscular physique in my late 30’s with minor weekly effort. I am currently working on fine tuning my muscles, which even though I have a solid build I never did as a younger man, and it’s going quite well actually. There is heart disease in my family but it’s nearly all late in life, 60’s plus with one outlier who died (ironically due to heart attack on a treadmill) in his late 40’s. I don’t lift so I can live until 80, I do it to look good, be strong, and so I can go and do anything I want. There’s no guarantee that any of us will live to see our 50’s or 60’s, that’s life, enjoy it while you can.


    • Replies: @JayMan
  6. JayMan says: • Website


    Great comment, sounds like you’re right on the money, and have the right attitude.

  7. n/a says:

    This may be yet another diversion, but take a look at an article which Mr. Mangan linked to recently:
    “Correlation between oxysterol consumption and heart disease”

  8. Anthony says:

    Why the high CVD mortality in Afghanistan? High-velocity lead poisoning?

  9. Outstanding post.

    • Replies: @JayMan
  10. Well put. Have to agree with you, although wouldn’t necessarily have agreed a few months back. Until I read that up to one third of ancient mummies from Egypt and the Americas show signs of probable or definite atherosclerosis, according to CT scans:-

    Atherosclerosis across 4000 years of human history: the Horus study of four ancient populations


    “Atherosclerosis was common in four preindustrial populations including preagricultural hunter-gatherers. Although commonly assumed to be a modern disease, the presence of atherosclerosis in premodern human beings raises the possibility of a more basic predisposition to the disease.”

    In any case:-

    Human MHC region harbors both susceptibility and protective haplotypes for coronary artery disease.

    “[…..]In conclusion, human MHC region harbors genes that protect from and predispose to CAD.”

    • Replies: @Hindu Observer
    , @Sisyphean
  11. @Amos

    “It’s now verging on the border of gross incompetence to exclude genetic makeup from these studies.”

    Yes, and more that not taking it into account is possibly a major cause of death in itself.

  12. @Johnny Caustic

    @Johnny Caustic
    “He’s best known for his book bashing wheat for causing heart disease”

    If population genetics is a significant factor then it seems to me the causes may vary with population genetics also i.e. there might be cause 1 for heart disease across all populations plus cause 2 for some populations and cause 3 for other populations. This might make it difficult to pin down the causes if the different populations were studied on the assumption they were the same.


    “Yeah, the problem I have with nutrition is that everyone has their own theory…What you end up with is people grouping together into foodie camps more by ideology than by evidence.”

    I think there’s a lot of truth in that but i think there is also another possibility which is that a lot of different theories may all be partially true i.e. they’re true for people descended from one particular population but not true generally hence masses of contradictory evidence.

  13. This is not very likely but is there any evidence that the populations in the orange and red zones had *less* heart disease before the industrial revolution?

  14. @chrisdavies09

    Makes sense as Egyptians were huge wheat eaters, and the other cultures consumed it too.

    If you research the history of wheat and how it has “evolved” since its first cultivation, its quite interesting.

    Sissyphean, I just eat the least processed foods that I can. I grow some of my own food and supplement that with store bought organic fruits, veggies, seeds and nuts and have never felt healthier. Fermenting, soaking and sprouting are key.

    Fermented coconut water, coconut vinegar, homemade saurkraut and homemade rejuvelac – all good for the gut.

    The so called “paleos” have basically hacked the raw vegan movement and added cooked foods and animal products. Yet its hilarious how they think they re “cutting edge” and “something new” (have you seen that movie Jayman?). And the never give credit to the raw foodists who came before them (probaby because they are vegan). But also because they are such newbs that they don’t even know about the decades old raw began movement.

    From what I gather paleos are your typical mainstream Americans, into having mainstream American jobs and consuming mainstream American culture, but think they are somehow unique for eating grass fed beef.

    Come on!

    Somebody needs to kick their butts and it just may be me who will do that.

  15. If it is correct that testosterone has protective effect effects on the heart, then the advice given to eat a low fat diet may be wrong, given that testosterone is made from cholesterol.

    J Endocrinol. 2013 May 7;217(3):R47-71. doi: 10.1530/JOE-12-0582. Print 2013 Jun.
    Testosterone: a vascular hormone in health and disease.

    Kelly DM, Jones TH.

    Department of Human Metabolism, Medical School, The University of Sheffield, Sheffield S10 2RX, UK.

    “Coronary heart disease is a leading cause of premature death in men. Epidemiological studies have shown a high prevalence of low serum testosterone levels in men with cardiovascular disease (CVD). Furthermore, a low testosterone level is associated in some but not in all observational studies with an increase in cardiovascular events and mortality. Testosterone has beneficial effects on several cardiovascular risk factors, which include cholesterol, endothelial dysfunction and inflammation: key mediators of atherosclerosis. A bidirectional relationship between low endogenous testosterone levels and concurrent illness complicates attempts to validate causality in this association and potential mechanistic actions are complex. Testosterone is a vasoactive hormone that predominantly has vasodilatory actions on several vascular beds, although some studies have reported conflicting effects. In clinical studies, acute and chronic testosterone administration increases coronary artery diameter and flow, improves cardiac ischaemia and symptoms in men with chronic stable angina and reduces peripheral vascular resistance in chronic heart failure. Although the mechanism of the action of testosterone on vascular tone in vivo is not understood, laboratory research has found that testosterone is an L-calcium channel blocker and induces potassium channel activation in vascular smooth muscle cells. Animal studies have consistently demonstrated that testosterone is atheroprotective, whereas testosterone deficiency promotes the early stages of atherogenesis. The translational effects of testosterone between in vitro animal and human studies, some of which have conflicting effects, will be discussed in this review. We review the evidence for a role of testosterone in vascular health, its therapeutic potential and safety in hypogonadal men with CVD, and some of the possible underlying mechanisms.”

    Atherosclerosis, Inflammation, Testosterone, Vasoreactivity

    • Replies: @JayMan
  16. JayMan says: • Website


    “Observational studies” was your clue. This is correlational, so you have to take it for what it’s worth (i.e., not a whole lot).

  17. Sisyphean says:


    Incidentally, before becoming pretty much paleo (I say pretty much because I still occasionally eat good cheese) I was a raw vegan for over a year and was absolutely the sickest I’ve ever been in my life. My allergies and asthma went through the roof, the doctors had to put me on inhaled steroids, it was a living hell.

    The funny thing about the Vegans vs the Paleos arguments is how each sees a world where their own diet is the gold standard and all others only get results by virtue of their proximity to perfection. Paleos think Vegans ought to add grass fed meat and natural saturated fat and the Vegans would be on the right road while the Vegans believe the exact opposite about the Paleos. It would be hilarious if it were not so pathetic. Jayman, I ask you: where did western civilization get all these overbearing full of themselves assholes and is there a return policy? (Yes, I know this is the puritan impulse, and I know Europe would give us the finger, but one can dream!)


  18. Anonymous • Disclaimer says:

    It’s genetic. Slavs and nords have higher blood pressure than people who have r1b y-dna, on average. That corresponds perfectly to your map. r1b people have lower blood pressure than EVERYONE on average. Especially basques and irish.

    Also, unfortunately, red meat does seem to cause problems, but it’s the actual carnitine in the meat being digested by your gut. So if you eat red meat every day it can be an issue, but if you take occasional breaks it will help because the gut bacteria that digests the stuff in a way that causes an unpleasant side effect will die out.

    • Replies: @JayMan
  19. JayMan says: • Website


    While interesting, I’m not sure the Y-chromosome haplogroups play any direct role in what we see for heart disease. (Indeed, if so, what’s up with Scotland?) Rather, I think particulars about the evolutionary history of these peoples is what does the trick.

    As well, I don’t think there’s any solid evidence red meat consumption in and of itself is dangerous.

  20. Anonymous • Disclaimer says: • Website

    The risks for heart disease increase with age and they are greater if a family member developed heart disease at an early age. Fortunately, there are lifestyle changes that one can make to reduce the risks of developing heart disease. You can easily reduce the risk of heart diseases naturally.
    The idea being live a healthier, more physiologically-sound lifestyle and drop your risk of not only heart disease but other chronic diseases. So eat to live healthy and always fit.

    • Replies: @JayMan
  21. JayMan says: • Website

    @Tips to Beat Heart Diseases Naturally:

    The risks for heart disease increase with age

    Since it’s something that generally occurs is late life for whatever reason, yes.

    and they are greater if a family member developed heart disease at an early age.

    Because there’s a heritable component, so this is as we’d expect.

    You can easily reduce the risk of heart diseases naturally.

    That appears to be not so clear.

    The idea being live a healthier, more physiologically-sound lifestyle and drop your risk of not only heart disease but other chronic diseases. So eat to live healthy and always fit.

    The point of this point is that it’s not so easy to do so. Do you have evidence otherwise?

  22. Barbara says:

    What a fascinating conversation. I am studying arts in medicine. We look at happiness, relaxation response, and how doing art positively influences the immune system. I wonder if one could study heart disease and those who sing? heart disease in those who consider themselves happy? Perhaps these studies are being or have been done. I’ll look. Otherwise, I agree that there is much more to learn about most things.

    • Replies: @JayMan
  23. JayMan says: • Website


    We look at happiness, relaxation response, and how doing art positively influences the immune system.

    Well, that would be an awfully hard thing to study, because you’d have to perform a very long randomized controlled trial…

    I wonder if one could study heart disease and those who sing?

    Sure, but it would be simply an academic inquiry. It wouldn’t be able to help anyone since the ability to sing is something you have or don’t have…

  24. peter says:

    Just pray to God, trust God, have faith.

  25. Latias says:

    I briefly read some of your posts about cardiovascular disease and death, and you noted the IQ is the strongest predictor of health and more importantly conventional wisdom dietary and lifestyle interventions do not alter mortality rates. If so, this should predict that conscientiousness has no link between mortality rates (as conscientious individuals are more likely to implement the recommended “common sense” interventions). Of course, this supposes that IQ and conscientiousness are not linked. I remember one study showing a negative correlation between IQ and conscientiousness, but it was probably in an academic setting. Perhaps, outside of an academic environment, the correlation may be positive between them,

    Asides from avoiding tobacco consumption, since you do not think behavioral interventions affect health, how can conscientiousness mediate health outcomes?

    But I am lazy. I have not done much research to even challenge your conclusions, and I took the conventional wisdom for granted: while I do believe genetics significantly affected health outcomes, I thought moderate lifestyle interventions could exert a significant modest effect.

Current Commenter

Leave a Reply - Comments on articles more than two weeks old will be judged much more strictly on quality and tone

 Remember My InformationWhy?
 Email Replies to my Comment
Submitted comments have been licensed to The Unz Review and may be republished elsewhere at the sole discretion of the latter
Commenting Disabled While in Translation Mode
Subscribe to This Comment Thread via RSS Subscribe to All JayMan Comments via RSS