Kurt G. Harris MD

PāNu means paleonutrition. The "paleo" here signifies "old" and not necessarily paleolithic. The PāNu approach to nutrition is grounded on clinical medicine and basic sciences disciplined by knowledge of evolutionary biology and paleoanthropology. The best evidence from multiple disciplines supports eating a pastoral (animal-based) diet rather than a grain-based agricultural one, while avoiding what I call the neolithic agents of disease - wheat, excess fructose and excess linoleic acid.

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« I'm so bored with the Kitavans | Main | Intra-subject variability in Serum 25-D »

“Cardio” Causes Heart Disease.

I suppose that is not exactly what they had in mind when they first called chronic aerobic exercise “cardio” in the days of Disco.

I first saw this study by Brueckmann and Mohlenkamp last spring and I’m a bit surprised that the nutrition and fitness blogosphere hasn’t noticed it. I think you may have to be an acedemically-oriented cardiologist or radiologist to really understand the significance of the findings, as the MRI imaging science is a bit esoteric.

Also, it’s published in Radiology, which is not exactly Gina Kolata territory.

I’ll do my best to convince you of just how disturbing this study should be to those who believe that “aerobic” exercise will make you immortal.

The image is not the thing itself

As a radiologist, this is my coffee-mug aphorism for the epistemology of medical imaging. It reminds me that the picture or the test result is not the patient or even the disease.

Here is one of the heirarchies I use as a heuristic (a teaching device) when thinking about coronary disease. It’s a rough ordering from left to right of how far away you are from “the thing itself” when looking for evidence of a previous myocardial infarct.

From useless to definitive:

Framingham risk score - modern blood tests ( HDL , LDL-P, oxidized LDL, etc.)

calcium score (Heart scan for coronary calcium)

Intravascular Coronary Ultrasound

abnormal coronary angiogram

abnormal coronary CTA

EKG evidence of infarct

Stress SPECT Nuclear Medicine perfusion

cardiac perfusion MRI with dobutamine

Late Gadolinium enhancement cardiac MRI (LGE)

death with autopsy evidence of MI.


I have ordered these roughly according to how definitive they are in establishing myocardial injury - whether you have actually had a heart attack sometime in the past (not acutely, as that can often be shown with serum enzymes). I have not accounted for sensitivity, which for some of these tests is so poor as to make them useless.

Think of Lindeberg’s studies of the Kitavans. He used EKGs (electrocardiograms) to look for evidence of prior MI (myocardial infarct or heart attack). Comparing to the known prevalence of EKG abnormalities in western subjects, he concluded that there was no evidence of heart disease in Kitava.

The Kitavans are fascinating because they have high carb consumption and appear to be much healthier than those on the SAD. They also have some “paradoxical” lipid markers that (rightfully) call into question the very idea that the lipid markers that cardiologists love to measure mean anything outside the context of a particular diet. In my opinion, they help cast doubt on the very idea that either good or bad blood lipids “cause” anything. Rather, they are just markers for the diet - the diet effects the actual changes.

EKG is not that sensitive and can be false positive. 

Sidebar: Until we have CT angiograms or at least calcium scores on the Kitavans, I think we can conclude that heart attacks are pretty rare for them, but we cannot say they have no atherosclerosis - one reason I’ll stick to VLC, thank you.

What if we got a grant from Bill Gates? What if we wanted the most definitive evidence that we could get, short of sacrificing our poor subjects in the interest of science and having a pathologist look at their hearts.

How about flying all the Kitavans to the US or Europe to have invasive coronary angiograms? Unfortunately, a conventional angiogram only shows stenosis or narrowing of the coronary arteries and does not show a heart attack unless there is gross wall motion abnormality.

How about a nuclear medicine stress test? - this 20-year-old procedure is the most traditional non-invasive way to look for heart disease - unfortunately it also requires a fairly large infarcted area to reliably detect if there has ever been a heart attack. If looking just for physiologic evidence of stenosis, it requires a 75% or greater arterial narrowing to reliably detect disease. It is not very sensitive.

It would surprise even a lot of physicians to know that the most sensitive way to tell if there is any coronary atherosclerosis whatsoever is not nuclear medicine or an invasive coronary angiogram - it is CCTA or coronary CTA.

CCTA is not “calcium scoring” (I avoid calling calcium scoring a “heart scan” as at my center there are a half-dozen procedures that could be called that). CCTA is a CT scan done with a 64- slice multi-detector CT scanner that rotates fast enough to image the coronary arteries. Although the spatial resolution is not as high as conventional catheter angiography, CCTA can directly image early “soft” plaque that is totally invisible on conventional angiography or on simple calcium scoring. The only test that is better - the absolute gold standard for detection of coronary plaque in the living - is called intravascular ultrasound or IVUS. But IVUS requires invasive insertion of an ultrasound probe into the coronary arteries in a procedure similar to conventional angiography. It is mainly a research tool. Not so good for screening asymptomatic subjects.

So to detect any atherosclerosis whatsoever in a population, the best practical test would be CCTA.

But what if we wanted to know, with as great a degree of certainty as possible without waiting for the death of our subjects, whether they had ever had a heart attack or any damage to the heart muscle? After all, the important thing is if you have an actual heart attack or die - that is “the thing itself’

Then the choice would be cardiac MRI with late gadolinium enhancement or LGE.

Here is how LGE works. When heart muscle is damaged, there are pathologic changes in the tissue that we characterize, in our highly precise way as medical scientists, as “scar tissue”. This scar tissue will have a pattern of blood pooling or stasis, where, unlike normal heart muscle, blood leaks in slowly, and then does not wash out as fast with time.

LGE exploits this phenomenon. We give an agent intravenously that shows up bright on MRI images called gadolinium (It’s actually a chelate as free Gd is poisonous) We can first of all use this to look for ischemia or temporary insufficiency of blood flow with stress. Then we get delayed images. On these delayed images, normal heart muscle will return to its non- bright appearance, but the scar or damaged heart muscle will stay bright. The important thing to know is that we can detect such areas with much higher resolution than nuclear medicine techniques, and we can see non- transmural (less severe) infarcts and infarcts so small they have no effect on wall motion.

This LGE technique has been validated with animal and human pathologic studies. It truly is best way other than autopsy to tell if there has been permanent damage to the heart muscle.

Mainstream thinking still maintains that lots of aerobic exercise is good for cardiovascular health - to the point where everyone uses the word “cardio” as a synonym for long sessions of aerobic effort. Like the diet-heart and lipid hypotheses, this idea is actually only about 40 years old. In the first half of the 20th century, it would have been thought as absurd as the idea that butter clogs your arteries.

So let’s say you want to see just how protective “cardio” is against the number one killer of Americans -coronary heart disease. Instead of just looking for atherosclerosis, though, we want “the thing itself” of actual myocardial damage. Who knows, maybe runners get more plaque but have fewer plaque ruptures or a less thrombogenic blood profile?

So in the Breuckmann study, they recruited 102 active marathon runners. To be a marathon runner (and perhaps to maximize their power to show how healthy “cardio” is) required at least 5 marathons in the past 3 years. Many had run dozens or more in their lifetime. Anyone with a known history of heart disease or diabetes was excluded. The average age was 57 with age 50-72. The median number of marathons was 20. Weekly mileage was 35 (55km). Mean work was 4700 METs per week.

Yikes! 5 years ago, I ran 30 miles a week. Good thing I just did it for one summer.

There were 102 totally asymptomatic age-matched controls, also with no history of diabetes, who had no significant history of vigorous exercise.

All subjects had cardiac MRI with LGE imaging. Those with LGE abnormalities were called back to have perfusion imaging as well to help tell if they had evidence for ischemia.

Sidebar: Ischemia means temporary and reversible changes in oxygenation of tissue. Infarction means ischemia has occurred to the point that tissue has died and this is irreversible. LGE means irreversible loss of tissue or infarction.

What do you think they found? After all, these were a bunch of completely asymptomatic runners. Conventional wisdom will assure you that only eating copious fiber and making turds like a gorilla could make you healthier than being a serious runner.

Would you believe 12% of asymptomatic marathon runners had evidence of myocardial damage on LGE?

Would you believe that among the sedentary controls only 4% had abnormal LGE?

I am obliged to point out that by the conventional arbitrary criteria used in biomedical publishing, the difference was “not statistically significant”. To meet the standard definition, there would have to be a 95% chance the difference is real. Instead, the significance level was 8% by McNemar’s  test, so there is only a 92% probability that the difference is not due to chance.

That’s a relief.

Sidebar: Does anyone else think it’s strange that if your doctor said “you have a 92% chance you are disease free” you would find that reassuring, but we are supposed to dismiss a mere 92% probability that a study result is real? Stop doing what you are told and read the statistics without letting the authors or editors tell you what is “significant”. Yes, P = .00001 is better than .05. But decide for yourself, it is not written in stone.

Let’s take a closer look at the results.

Among runners with LGE, there were two patterns of abnormality. In the first pattern, found in 5, there was evidence on perfusion imaging and an anatomic pattern that confirmed these were typical ischemic infarcts. That is, they are evidence of heart attacks due to insufficient blood supply in the distribution of a particular diseased coronary artery. The kind of heart attacks we are all familiar with that kill 500,000 Americans a year. Two of the controls had these classic appearing infarcts.

Runners           5 classic heart attacks
Sedentary        2 classic heart attacks

The second pattern of abnormality, seen in 7 runners and 2 of the sedentary, was non-classic LGE. These areas of dead tissue were found in the middle or outer layers of the heart muscle, rather than the subendocardial layer. They also tended to be more patchy in disrtibution. This non-classical pattern can indicate scarring or fibrosis from non-ischemic injury to the heart muscle, including myocarditis. However, despite lack of evidence for ischemia on perfusion MRI, this pattern can also occur to due coronary microembolization, where a coronary artery is not narrow enough to cause ischemia, yet small bits of plaque break off or tiny blood clots form and plug the arterioles deep in the muscle - causing infarction and permanent scarring in an “atypical” pattern.

The authors speculate that this atypical infarction could be due to exaggerated shear stress related to marathon running and disturbance of prothrombotic and fibrinolytic systems contributing to microthrombotic emboli.

I think that is a reasonable speculation.

Runners        7 non-classic heart attacks
Sedentary     2 non-classic heart attacks

So whether we are looking at classic heart attacks or non-classic, the ratio is about 2.5 or 3 to 1 in favor of being relatively sedentary.

But, you might say, how do we know this LGE is significant?

First, there was evidence of ischemia in most of the classic cases even if you don’t buy my statement LGE by itself is definitive evidence of a heart attack.

Second, in only 21 months of followup, 1 of 90 runners without LGE had a significant coronary event and 3 of 17 runners with LGE had a significant event. Significant events included two cases of collapse and EKG abnormalities after a race. None died, but all were proved to have severe coronary disease by conventional angiography and were stented or had bypass surgery. This event-free survival was significant by log-rank at the .0001 level.

Third, the median CAC (coronary artery calcium score) in the runners with LGE was 192, and in the runners with no LGE it was 26. This is a big difference and shows that coronary atherosclerosis is tracking the LGE evidence of heart attacks. So it’s probably not just thrombogenicity or arrythmias on top of an invariant level of coronary disease.

Now I’ll be good and put on my Karl Popper hat for jusr a second. Maybe the runners all took up running a few years ago and had bad CAD to begin with? Maybe they had not yet run enough marathons to reverse their disease?

From another good paper by the same group on the same subjects:

1) The more marathons run, the higher the likelihood of heart disease. The number of marathons run was an independent and significant predictor of the likelihood of myocardial damage.

The runners had about the same prevalence of non-zero coronary calcium compared to age matched controls randomly assigned from a survey population. This was so despite the Framingham risk score being lower for the runners and there being more than 5 times as many smokers among the controls.

2) Compared to age-matched controls, the runners had 40% higher HDL -c (mean of 74 mg/dl) and 18% lower LDL (121) Again, these more favorable lipid risk factors did not show a benefit in calcium scores, which correlate well with atherosclerosis (not heart attack, but coronary heart disease).
Statin deficiency, I guess. How many torpedoes before the Bismarck of the Lipid Hypothesis finally sinks?

3) Compared to age and risk factor matched controls (a second set of controls with similar rates of smoking and other risk factors), 36% of runners had a calcium score or CAC above 100, versus 21% of age and risk factor matched controls. (High CAC means more coronary atherosclerosis) So if the “risk factors” like lipids and BMI and such really are helping you, running seems to be doing something to undo the effect.

There are many good references quoted by Brueckmann and Mohlenkamp.

Among them is This paper by Kwong and Chan from Circulation. They looked at the presence of LGE as a predictor of major cardiac events (heart attack) and the ultimate relevant end point for us all - death.

They said:

“LGE demonstrated the strongest unadjusted associations with MCE and cardiac mortality (hazard ratios of 8.29 and 10.9, respectively; both P 0.0001).
LGE remained the strongest predictor selected in the best overall models for MCE and cardiac mortality.”

A hazard ratio of 11 for future cardiac mortality is very, very very, high. 1100% more likely to die is gold standard hazard ratio, of the same magnitude as smoking and lung cancer. This makes it hard to doubt the significance of having LGE and would not be seen if there were benign explanations for it.

This makes sense. How could there be a better predictor of whether you will have a heart attack than evidence that you have already had a clinically silent one?

Brueckmann and Mohlenkamp are German, but get points for an English level of understatement:

“...It seems safe to state that marathon runners most likely did not have a lower rate of LGE than did the healthy control subjects, who did not regularly exercise.”

Do you think that might be why this paper was in Radiology instead of JAMA or NEJM? Is that why there was no press conference before the paper came out?

Do you think maybe Kolata or Jane Brody might have told you about this study in the New York Times if the numbers had been reversed?

It’s time for some Kuhnian iconoclasm. Let’s take the hammer to some “normal science”.

I think that atherosclerosis is not caused by lack of sustained high-level aerobic (“cardio”) exercise.

Just like I don’t think lack of “cardio” is the cause of the obesity epidemic.

I think premature atherosclerois is caused by diet. Our susceptibility to a bad diet is contributed to by genetics.

I think that not only does sustained “cardio” not protect you from atherosclerosis, I think it is quite likely that through repetitive shear stress with endothelial damage and promotion of an inflammatory state, that it promotes atherosclerosis.

Further, I think that “cardio” can precipitate the thromboembolic and acute inflammatory events like plaque rupture - acute heart attacks, even if it does not directly contribute to atherosclerosis, which I think it does.

Could “cardio” promote atherosclerosis and myocardial damage by being confounded by diet? That is, could the wheat, carbohydrate and linoleic acid found in low fat “healthy” diets be more prevalent in marathon runners by virtue of their greater caloric intake of this noxious garbage?

That’s a possibility. I think it may apply to cyclists, most of whom seem to eat horribly and who seem to be prone to osteoporosis.

Even if these findings are all confounded by a noxious athletic diet, I still find no grounds at all to believe that “cardio” protects your heart or makes you live longer.

I think a modicum of repetitive physical activity can improve your mood. I like to a run a 5 k every now and then. It feels good and cross-country seems good for your coordination with all the varied terrain. A little cross-country and some sprinting sure seems to make me more functional.

I am not under the delusion that it will improve my overall health or my longevity, though.

Same goes for eating vegetables, fiber, antioxidants, and most supplements. No magic foods.

The good kind of exercise, resistance training, makes you more functional and stronger. That is the only sensible definition of fitness if we follow the hippocratic oath with our selves.

Primum Non Nocere

I think if you eat the SAD that adding a little exercise may mitigate some damage in a compensatory fashion by improving your glucoregulatory function and sucking up some of that excess glucose.

I don’t eat the SAD, though.

I vote we keep the terminology. We should keep calling marathons, centuries on the bicycle and  hours on those ridiculous stairmasters and treadmills “cardio” to remind us which organ we are likely to be putting at risk.

Running a marathon is looking about as smart as boxing or playing football.

So maybe you should stick to crossfit and weightlifting for your exercise. Or TV watching.


Myocardial late gadolinium enhancement: prevalence, pattern, and prognostic relevance in marathon runners.

Running: the risk of coronary events

Impact of Unrecognized Myocardial Scar Detected by Cardiac Magnetic Resonance Imaging on Event-Free Survival in Patients Presenting With Signs or Symptoms of Coronary Artery Disease


Alberto Salazar image by Olivia Bucks of the Oregonian.
The only difference between Salazar and Jim Fixx, is that when Salazar experienced sudden cardiac death due to myocardial infarct from an 80% stenosis of his right coronary artery at age 48, someone showed up with a defibrillator to get his heart re-started. Salazar was a world class marathoner who trained about 30 miles a week at an easy 7:30 pace.


Reader Comments (39)

Great, Dr. Harris.

My additional thoughts:

Running long-distances at the same rate--jogging, cycling--also paces our heart beats into sinusoidal, simplistic rhythms that resemble the heart beat patterns of Congestive Heart Failure patients. Healthy heart beat patterns are multifractal, information rich, and reflective of power-law neuronal signaling patterns--these hearts are robust to sudden cardiac death. Moving about at very low-intensity levels for long durations (hiking, walking) and then mixing in high-intensity, low-duration exertion spikes (lift heavy, sprint, etc.) produces an anabolic, multifractal energy expenditure and nerve-firing physiological landscape that enhances and maintains multifractal complexity in our heart rhythms. Music does this as well; music is fractal, the math of mother nature. Jogging reduces the information content in our heart rate rhythms, increasing our risk to sudden cardiac death: a 'cardio'-trained, metronomic heart is a heart ready to fail.

Ancestral mimicry in how we expend energy can help on this signaling mathematics front.

Start with diet, but when you decide to move, move ancestrally.



November 1, 2009 | Unregistered Commenterepistemocrat

What's not to say that marathon running might not just be too much of a good thing? I can easily see the chronic cardio crowd spinning it this way.

November 1, 2009 | Unregistered CommenterAtticus Acton

Hi Kurt,
still I´m wondering why the Tarahumara Indians live healthy up till 80 years and run their whole lives about 30 Miles or even more a day. They eat a high carb diet (a lot of corn), drink a lot of corn beer etc.

November 2, 2009 | Unregistered CommenterGeorge


I was wondering who would be first to bring up the fabled Tarahumara.

You win!

We have no clue how long either the Tarahumara or the Kitavans would live on low carb diets, or how much healthier they would be if so, do we?

My grandfather lived to be 93 and was 100 lbs overweight for that last 50 years of his life. No stroke, no CAD, just a touch of hypertension. (Oh, and he smoked about 50 pack years)

Should I smoke and gain 100 lbs so I can live to 93 or should I assume these were things my grandfather tolerated by virtue of lucky genetics?

You say they run their whole lives 30 miles a day every day? I am sorry but that sounds like pure crap. Would you like to revise that claim?

I just don't get the whole "but these people eat a lot of carbs so maybe carbs aren't so bad" thing with a handful of primitive agriculturists or HGs who seem to be the exception to the rule.

Does anyone seriously think they are eating corn because it is healthier than animal products? Isn't that the only interesting question ultimately? I grant it is interesting that carbs can be tolerated at a higher fraction than we might expect outside the SAD, but that proves what?

Show me the Tarahumara have no silent ischemia and I'll start drinking beer again and run more.

November 2, 2009 | Registered CommenterKurt G. Harris MD

I wonder why this isn't being more widely reported? If a particular food or drug raised the risk of cardiovascular disease this much I think the media would be all over it.

As for resistance training versus "cardio", Nautilus inventor Arthur Jones was trying to get this across as far back as the 1970's, and during a TV appearance in the early 80's said,

“…the lifting of weights is so much superior for the purpose of improving the cardiovascular condition of a human being that whatever is in second place is not even in the running, no pun intended. That is to say, running is a very poor, a very dangerous, a very slow, a very inefficient, a very nonproductive method for eventually producing a very limited, low order of cardiovascular benefit. Any, ANY, result that can be produced by any amount of running can be duplicated and surpassed by the proper use of weight lifting for cardiovascular benefits. Now I realize that there are hundreds of thousands, perhaps millions of people in this country who don’t understand that, who don’t believe that, who will not admit that. Now these people are simply uninformed. Certainly, it’s possible to run with no benefit, it’s possible to lift weights with no benefit. I’m talking about the proper use of weight lifting; and properly applied, weight lifting will improve your cardiovascular benefit to a degree that is impossible to attain with any amount of running.”

It would be interesting to see a comparison of cardiovascular health between people who run and people who strength train or do only brief, high intensity interval-type training.

November 2, 2009 | Unregistered CommenterDrew Baye

We have no clue how long either the Tarahumara or the Kitavans would live on low carb diets, or how much healthier they would be if so, do we?

First off, I'm a big fan of LC and VLC eating. But, I don't think that it is the only way to eat and still be healthy. It's important to eat biologically appropriately be it with high fat or high carbs. And I think that's why this study seems to me to be comparing rotten apples to merely overripe oranges.

The problem with most runners is the carbo loading dogma they follow blindly. It's insane! My dad even feels the need to carbo load prior to a 5K race. It's over before his body even knows what's going on. What if instead of HC, they took the time to shift their body to be primarily fat burning? Yeah, for carbo junkies used to high miles, that's going to hurt like hell and they'll have to cut miles to start. But once shifted, how would they perform? Instead of GU and energy bars, try some pemmican... that's some high density energy right there.

What I would like to see is a study of HC versus VLC/LC marathoners that have similar training and pacing goals. I think that'd give a better apples to apples comparison.

November 2, 2009 | Unregistered CommenterDan

Hello Dan

"It's important to eat biologically appropriately be it with high fat or high carbs."

That sound suspiciously like metabolic typing. It is one thing to say that adjusting all the parameters but one, the fraction of carbs, makes you able to subsist on them with less ill effect. I do believe that. However, I do not believe there is anyone who is healthier substituting corn for animal flesh in any fraction of their diet. That is what I am saying. we can't just be fascinated by people not being sick, we need to say what is special about corn or sweet potatoes if we think that, ceteris paribus, it is a neutral choice between these glucose sources and meat.

"The problem with most runners is the carbo loading dogma they follow blindly."

That is why I said this in the essay:

Could “cardio” promote atherosclerosis and myocardial damage by being confounded by diet? That is, could the wheat, carbohydrate and linoleic acid found in low fat “healthy” diets be more prevalent in marathon runners by virtue of their greater caloric intake of this noxious garbage?

"My dad even feels the need to carbo load prior to a 5K race. It's over before his body even knows what's going on. What if instead of HC, they took the time to shift their body to be primarily fat burning?"

Read this.


I have friends who are endurance athletes. At an hour or so, their performance suffers with no added carbs during the event, even though they are mainly VLC with training. I have neo idea if these friends are promoting heart disease by running, but I am confident it is not the running that is preventing it.

"What I would like to see is a study of HC versus VLC/LC marathoners that have similar training and pacing goals. I think that'd give a better apples to apples comparison."

I still think there would be no benefit to the cardio vs sedentary VLC. You would only be testing diet.. assuming you are talking about the heart attack incidence.

November 2, 2009 | Unregistered CommenterKurt G Harris MD


I''ll be deconstructing more of the exercise literature. You can count on it.

November 2, 2009 | Unregistered CommenterKurt G Harris MD

My dad is a bike fanatic. He loves long, fast rides. I completed two centuries (100+ mile rides) with him last summer. One of them, the Blue Ridge Extreme, featured a finale of 7-8 miles up 14% average grade. It was hard. Finishing was a triumph of will and a testament to human endurance and all that good stuff.

He has, of course, taken an interest in my diet and one of his main criticisms is "you'd never get up Wintergreen (that final hill) eating fat!". This is an interesting point to me, for two reasons:

1) Bike culture is carb culture. The carb is worshipped to the point of godhood. I shudder to think of all the glucose gel and clif bars I ate trying to keep up. However, bike culture is also competitive. Competition is a maximizing algorithm - over time, behaviors converge on the best way to win given the technology at hand. Right now, if you were to suggest to a bike racer that they should go VLC, they would laugh in your face. The evidence for carb loading is extremely difficult to challenge; after all, Lance was eating gel and power bars, not pemmican.

2) If carb loading is necessary for that type of performance, how did the Inuit survive? I find it difficult to believe that they piddled around like sloths, trying desperately to avoid anaerobic activity. Similarly, the NA Plains Indians had a culture of ultra-marathoning that lasted into modern times. How did they manage to run 100+ miles without carb loading, etc? Massively long runs appear to be, if not routine, at least not remarkable. Even the Marathon run was supposedly 150+ miles each way, not just the storied last 26. Where did that endurance come from if they weren't slamming glucose gel every fifteen minutes?

Add these together to get the burning question: what happens if I train up to a century and ride it on zero-carb, eating pemmican the whole way? You could ask the same thing about a marathon. My dad's prediction is bonking followed by death, which is possible. It would be nice to tap into some magical store of endurance caused by fat, but I don't really see that happening. Realistically, I expect to be able to plod along and finish, albeit slowly.

My goal is to ride a century next year, if only because I can't find any contemporary VLC/ZC eater who has done a very long endurance event. It seems that a sane attitude towards exercise is a side-effect of the diet. I want to see what happens and try to put some of the debate to rest, although I know that's not going to happen. People will find what they want in it. Assuming I even finish, of course.

November 2, 2009 | Unregistered Commenterpfw

Kick ass post

November 2, 2009 | Unregistered CommenterAnthony

Hi Kurt,

I really enjoyed this post! It reminds me so much of being half way up Ben Lomond with a hard working CVS and modest oxygen debt. I remember thinking "This is NOT good for me, but look at the view!". In fact, looking at the view while my heart rate dropped is probably the best aspect!


November 2, 2009 | Unregistered CommenterPeter

I'm personally comfortable with an confidence interval greater than 90%. The way I look at it is this: Give me a P-value, I'll decide what's significant for me.

Great post Kurt. I look forward to you continuing to dig in to the exercise literature.

November 2, 2009 | Unregistered CommenterJM

I don't think you can look at marathon runners and draw the conclusion that cardio is damaging in all forms. Extended steady-state runs on flat pavement being bad seems a little closer to the truth, and Art DeVany has been beating that drum for a while now. As Brent similarly pointed out in his comment, I think it's the steady-state pattern here that's of concern, not so much the energy pathway. It would be interesting to analyze data from people who engage in other activities like swimming, cycling, hiking, hill running or ultramarathoning.

Somebody brought up the Tarahumara. They run long distances, but their energy output while running is as varied as the canyon terrain they inhabit.

Anyway, thanks for a provacative and fascinating article.

November 2, 2009 | Unregistered CommenterJonathan

As someone who is utterly bewildered by the all the people on the hamster wheels at the gym, I do appreciate this post, however, I would still like more definitive direction on what a proper minimal fitness regimen would be --or does there even need to be one? I have no desire to do cardio or be more muscular than necessary for health and function. But nor do I want to be weak and frail as I age or unable to keep up while playing a sport or going for a nice hike. Thanks, S.

November 2, 2009 | Unregistered CommenterS.

I read the Book "Born to Run", maybe you should read that book too , in that book the Tarahumara are described there in a serious way, and that isn´t about just one person, but about many people with a long healthy and long history and my point wasn´t actually that they eat a lot of carbs, my point was especially that they run long distances every day. And yes, they don´t do that in a linear way, but in fractals. But also other people of this earth ran long distances, like the plane Indians. You say that these stories are fabled, how do you know these stories are not true? Look, I also believe that running marathons and all the training is not healthy, actually I do agree, that´s why I even wonder more why it is possible that those Tarahumara run that much without getting heart attacks etc.

November 2, 2009 | Unregistered CommenterGeorge

Great post, thanks for bringing forth this study.

marathon/chronic cardio is only a subset of cardio. However, it would be great if people realized running a marathon or running 5 miles every day does not make them healthy and it may do the opposite.

Glad to see you are taking up the challenge to review this hypothesis more. It will also be interesting to see what evidence you can come up with w/respect to the Kitavans and the Tarahumara.

November 2, 2009 | Unregistered CommenterGreg

Fantastic post!!

I have long been a fan of resistance exercising and feel that these long cardio sessions can't possibly be good!! As noted....sprints and some long runs are fine....but I just don't get the idea that there is a benefit to so many spending so much time on treadmills, stair masters, etc!!

Several years ago I worked in a cardiac monitoring center and part of the job was enrolling clients for different studies (we used even monitors, strips transmitted via telephone). We also had many clients that were known cardiac patients (many with AICDs and pacers). It was very common to find people making recording because of symptoms during exercise. SVT, heart blocks, short and prolonged runs of VT, etc. Of course we also had many making recordings of events during rest....but most of these tended to show NSR. It really seemed to us that the majority of the "real" events.....events that actually showed an EKG change were related to intense activity. I would love to see if there is any study that links the cardiac abnormalities to exercise, especially intense cardio.

I am also a big believer in VLC and paleo diets! More meat the better!!

November 2, 2009 | Unregistered CommenterAlcinda Moore

Great post, Kurt. I've seen other studies in which marathon runners had more atherosclerosis. I still think a couple of 3 mile jogs per week beats watching TV-- but the "more is better" crowd really lost out on this one. I know a number of type As that run marathons. Interestingly, one of them gained weight during training and lost it afterward.

As an aside, I don't know why they would have undertaken a study like this if it wasn't powered to detect significance at a 2.5-fold relative risk level. Maybe they detected fewer silent MIs than they were expecting.

Have you seen any data on the association between other types of exercise and silent MI or atherosclerosis?

November 2, 2009 | Unregistered CommenterStephan

The Tarahumara like the Kitavans do not eat that much sugar or processed vegetable oils compared to the SAD. The Tarahumsra don't eat any processed vegetable oils and likely use lard or schmaltz in the tortillas so it is a high saturated fat diet. Saturated fat is seen to be prophylactic against heart disease. Like Taubes pointed out the magic point where chronic disease emerges is around 70lbs/year of sugar and is worsened with increased vegetable oils and decreased saturated fat.

November 2, 2009 | Unregistered CommenterMarnee

Hey Stephan

Thank You.

I prefer a couple of 3 mile runs a week to TV, too. Even a few hours at the computer makes me feel like a caged animal.

Power calculations are woefully infrequent in the imaging literature. To be fair, this study is just one of a series they did on this set of marathoners. I don't think they expected to find a difference at all, actually. They say in the paper they were surprised. So, It's just the opposite, they found this big a difference by accident and decided to publish it!

As far as other data, more "nerd safaris" to come. I have a few papers on cyclists to review soon.

If you have any links to good refs I'd love to see them - you can PM me as you have my private email.


Send me a copy of the book and I'll send you a hardcover copy of Good Calories, Bad Calories.

Alcinda and Greg

Thank you

November 2, 2009 | Unregistered CommenterKurt G. Harris MD


I also should have mentioned it was not a trial, the runners were recruited so really they were sampling the universe of asymptomatic runners in germany. They were shocked when in the course of looking at a variety of cardiac parameters in the marathoners, they found 12% with LGE (compared to the literature for those of this age this is quite high) so then they took age-matched controls from a population of over 4000. These controls had a much lower rate of LGE, confirming that the LGE rate among the runners was high.

They did not a priori hypothesize that the runners would have more myocardial damage. They found it by accident. That is what makes it so convincing, in my view.

November 2, 2009 | Unregistered CommenterKurt G. Harris MD

Kurt wrote:
"We have no clue how long either the Tarahumara or the Kitavans would live on low carb diets, or how much healthier they would be if so, do we?"

Is there evidence that low carb diets will produce longer and healthier lives?

Taubes wrote a great book, but he presents only the evidence supporting his side of the story. In the epilogue, he mentions that "Nutrition and Physical Degeneration" was his inspiration for writing GCBC, but he never mentions any of Price's work anywhere in the book! It just didn't jive with his hypothesis. Same with TL Cleave, he is often used to promote low carb eating, but his main argument was that refined sugar were bad, not carbs in general.

There are more than just the Tarahumara and Kitavans who lived well on high carb diets. Most groups (other than the Inuit) who Price observed were healthy when eating a diet high in carbs. If your insulin is messed up, avoiding carbs might be important. But for someone with a healthy insulin metabolism, the evidence would seem to indicate that a high carb diet is fine.

November 2, 2009 | Unregistered CommenterDexter



November 2, 2009 | Unregistered CommenterKurt G Harris MD

Interesting post, though I'm not ready to accept your conclusion and title as proven. It seems that biases affect what we want to see- so it is important to try to be objective. That said, I'm glad someone is really looking into the mechanisms for the premise that exercise is beneficial for preventing CVD. This could be a very good sign for developing real understanding someday.

I read the second paper you referenced and don't see where you come up with your conclusion that "1) The more marathons run, the higher the likelihood of heart disease. The number of marathons run was an independent and significant predictor of the likelihood of myocardial damage." The paper specifically avoids saying anything like that.

They said instead that "We found NO age-adjusted Spearman correlation between weekly METs and CAC in marathon runners (R2 ¼ 0.02, P ¼ 0.13) or in age-matched controls (R2 ¼ 0.001, P ¼ 0.36). In marathon runners, CAC was also NOT associated with years of running (R2 ¼ 0.024, P ¼ 0.12), with the number of marathon races completed (R2 ¼ 0.007, P ¼ 0.39), or with training mileage (R2 ¼ 0.014, P ¼ 0.23). Regression analyses revealed NO hints for curve-linearity in any of these relations, and the respective 95% confidence intervals (CIs) of estimated slopes all included zero." (My emphasis with the capitalized "NO"s and "NOT".)

If a certain type of exercise is associated with CVD development and progression, there should be a dose response relationship- here they did not find one.

I do think you are right in suggesting that diet plays a role, especially since the running community is still vehemently high carb, and is more likely to be "health conscious" and avoid eating meats, butter and other sources of saturated fats, and substitute vegetable oils and margarines and sugars instead. I'm so tired of vegetarian runners who think that is the way to be healthy. I would like to see a study of sedentary vs exercising eating the same diet. As you say, that would be more relevant.

I also don't see why running is being bashed here as opposed to weight lifting, or any other type of exercise. After my run today, I tried to incorporate a little weight lifting (just some squats and step ups with weights) and was easily able to get my heart rate right back up to where it was while running, and this was only using light weights. I haven't researched this matter or done much of my own investigation (need a proper weight room), but I suspect that someone doing a full round of weights with multiple sets and addressing multiple muscle groups could easily keep their heart rate high for 30 min to an hour. The higher intensity the exercise (weights or sprints or higher VO2 training of any sort) also results in greater adrenaline release and glycogen mobilization and raised metabolic rate (with increased heart rate) for longer periods of time as well. These factors are all relevant too, and they don't necessarily differ between resistance exercise and endurance exercise.

You might find this article by Linda K Curtiss in J Lipid Research interesting. The first sentence is a pretty good start "Atherosclerosis was once thought to be a simple lipid storage disease that caused pathology by arterial obstruction."

It talks specifically about inflammatory signals in endothelial cells mediated by Toll-like receptors in response to infection, oxidized LDL etc. Basically, atherosclerosis does not progress unless inflammation is triggered, even in hypercholesterolemic animal models.

Here is a portion:

"Notably, the factors that promote atherosclerosis do not do so uniformly throughout the arterial tree. Site-specific plaque development is the result of disturbed hydrodynamic blood flow (10). Regions of the arterial tree exposed to laminar flow are protected from endothelial activation and atherosclerosis. This antinflammatory activity is mediated by mitogen-activated protein (MAP) kinase phosphatase (MKP-1), a negative regulator of p38 and JNK (11). Lesion susceptible sites are vessel bifurcations and the lesser curvature of the aortic arch. These sites display an inflamed phenotype even in the absence of any additional exacerbating disease factors (12-14). The biochemical mechanisms that enable endothelial cells to detect flow patterns are beginning to be understood (15-17). Arterial endothelial cells possess a single cilium able to detect the mechanical forces of blood flow (18-20) that distinguish disturbed flow from laminar flow. This in turn dictates endothelial cell phenotype. Cells at plaque susceptible sites have a proinflammatory phenotype, which is both permissive and causative of plaque development. For example, the proinflammatory endothelial phenotype is permissive in that it allows expression of proinflammatory receptors such as Toll-like receptors (TLR) and causative in that it permits expression of cell surface adhesion molecules (such as VCAM-1), which foster inflammatory leukocyte accumulation into the intima (21-23). No specific disease risk has been identified that would promote a pro-inflammatory phenotype only at arterial bifurcations and the lesser curvature of the aortic arch. TLRs expressed by endothelial cells may provide a clue to this conundrum. "

So, oxidized LDL is implicated as a major pro-inflammatory signal, inducing the endothelial cells to produce plaques. This could easily be a factor in people with a lot of small dense LDL (those eating lots of carbs) polyunsaturated lipids and producing relatively more free radicals.

Thanks again for addressing the issue.

November 3, 2009 | Unregistered CommenterCynthia

"Taubes wrote a great book, but he presents only the evidence supporting his side of the story. In the epilogue, he mentions that "Nutrition and Physical Degeneration" was his inspiration for writing GCBC, but he never mentions any of Price's work anywhere in the book!"

Taubes said in an interview that the Price stuff was cut due to space concerns in the editing process. He also doesn't say that Price's work was "his inspiration", at least not singularly; he was motivated, as he had been throughout his whole career, to examine science that he found to be wanting and reveal the ways in which it fell short.

November 3, 2009 | Unregistered Commenterpfw


You are correct. Also, contra Dexter's earlier assertion, Taubes also points the finger primarily at processed carbs and sugar.


"I read the second paper you referenced and don't see where you come up with your conclusion that "1) The more marathons run, the higher the likelihood of heart disease. The number of marathons run was an independent and significant predictor of the likelihood of myocardial damage." The paper specifically avoids saying anything like that."

Try reading the paper(s) again more carefully. You are quoting a section irrelevant to your claim. They most certainly do specifically say that and they say it again in the main paper!

CAC is just coronary calcium. LGE is the actual evidence of heart attack.

Number of marathons predicted the likelihood of LGE

From page 1906:

"In univariate analysis, the CAC score, CAC percentile values, and the number of marathons but not the FRS were associated with LGE "

Univariate analysis
Absolute CAC score [log2(CAC + 1)] Two-fold 1.36 1.08–1.71 0.009
CAC percentile value 5 units 1.17 1.03–1.34 0.02
Number of marathons completed (log-transformed) Two-fold 1.62 1.07–2.46 0.02
Framingham risk score 5% 1.55 0.79–3.01 0.2

Doubling the number of marathons completed increased the risk of having LGE evidence of heart attack by 60%.

"If a certain type of exercise is associated with CVD development and progression, there should be a dose response relationship- here they did not find one."

If you count having a heart attack, they did.

"I also don't see why running is being bashed here as opposed to weight lifting, or any other type of exercise."

Well, if you find a similar study of weight lifters or cross-fitters, or whatever, email it to me and I'll "bash" them too.

Thank you for the link - in future no need to post the whole abstract.

November 3, 2009 | Registered CommenterKurt G. Harris MD

This is an interesting study for me as a hockey player, too. Although hockey is an intermittent high-intensity sport (skate your ass off for a minute, go sit down), many of us in my local league may end up playing 2-3 games in a row, sometimes short-handed pond-hockey style with much longer shifts on the ice, which obviously becomes a somewhat different metabolic activity from the sport in its "pure" state. My gut feeling from personal experience is that trying to maintain intensity for 3+ hours at a time is probably not a healthy idea regardless of method.

And I do think that the sustained intensity of the competitive (even if competitive against only herself) marathon trainee is part of the problem here. IIRC cortisol levels go up during long hard runs, and blood glucose levels are also likely to be higher than ideal throughout due to the Cori cycle/gluconeogensis/constant Gatorade intake...these are just the first two culprits off the top of my mostly-uninformed head. I'm sure there are plenty of traditional cultures where people traveled marathon or near-marathon distances on foot as a matter of necessity, but I highly doubt any of them were thinking about setting a PR while they did it. Jogging or trotting at an intermittent, comfortable pace is a different animal metabolically than riding the edge of the anaerobic threshold for a couple of hours straight.

Incidentally, I'm not anti-running any more than I'm anti-hockey. We exchange risks for fun, regardless of which activities we choose. The more information available about the specific risks being chosen, the better, IMO.

Oh and on the dietary tip: Research (and incidentally personal experience) shows that performance in ice hockey goes down with a dietary intake of less than 55% CHO...which makes sense for an activity where anaerobic glycolysis is the name of the game. VLC/ZC *will* get you through your first few shifts (the body does maintain glycogen stores to some level even without carbohydrate intake), but after that point you will be noticeably slower and possibly uncomfortable. For runners and cyclists who are riding the edge of the anaerobic threshold I would expect something similar: if they can go the distance in the short time before glycogen stores are depleted they should be OK, otherwise they'll probably slow down and feel crappy before long. If the VLC/ZC athlete chooses a pace that's less dependent on anaerobic glycolysis I would expect her to feel just fine throughout and finish strong.

November 3, 2009 | Unregistered CommenterKim

Thanks for pointing out page 1906. The section I was reading (pg 1905) said there was no association with CAC scores. Apparently with LGE there was association with # of marathons, but presumably not with training mileage or years of running, since they looked for those associations with CAC but made no comment about them with respect to LGE.

I looked at a few other papers re LGE to try to understand what it is about. There seems to be some distinction between ischaemic and non-ischaemic patterns, but maybe you can elaborate on how that is relevant to this study. For example, the Abstract of http://www.ncbi.nlm.nih.gov/pubmed/17401755?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_SingleItemSupl.Pubmed_Discovery_RA&linkpos=4&log$=relatedreviews&logdbfrom=pubmed

states: "Typical patterns of [LGE] hyperenhancement exist in ischemic heart disease but also in dilated cardiomyopathy, hypertrophic cardiomyopathy and other inflammatory or infiltrative myocardial disease and are described in this article." (No full text though )

It is well known that endurance athletes (as well as 400m sprinters and soccer players) can develop left ventricular hypertrophy as a means of increasing stroke volume and cardiac output (at least in men, it's not very prevalent in women). Maybe the LGE is picking up on changes that result in this hypertrophy, which is not generally regarded as pathological.

Non-ischaemic damage to muscle and changes in electrical conductivity can be a problem too of course, if that's what is happening, but it's not necessarily related to atherosclerosis, or is that what they are trying to say- that LGE picks up subclinical signs of ischaemic damage? It wasn't clear to me what they were trying to say about the distinction between ischaemic and nonischaemic patterns.

Weight lifters can develop left ventricular hypertrophy too (in response to pressure overload as opposed to volume overload in endurance training). So I don't think bashing cardio is exactly the point. Perhaps the take home message should be that overdoing it is not a good idea, because you can cause heart damage doing any number of activities, especially when we get competitive and go all out. Maybe that is why there was association of LGE with # marathons- because during competition, people might push themselves harder than they would otherwise. It seems that frequent all out efforts might be more neolithic than paleolithic (as per Mark Sissons), because exhaustion and injury leaves you more vulnerable.

November 4, 2009 | Unregistered CommenterCynthia


"states: "Typical patterns of [LGE] hyperenhancement exist in ischemic heart disease but also in dilated cardiomyopathy, hypertrophic cardiomyopathy and other inflammatory or infiltrative myocardial disease and are described in this article." (No full text though )"

The atypical enhancement that was described was thought most likely due to microemboli, but if it were due to cardiomyopathy (often autoimmune) that would be even more disturbing. The marathon runners with the typical pattern all had coronary disease in the relevant vascular distributions - it was not, according to these cardiologists -hypertrophic or dilated - for one thing, those are easy diagnoses on MRI and would not confuse me or them. You have to appreciate how detailed and visual the information on cardiac MRI is. It is not crude and indirect like an EKG.

"It is well known that endurance athletes (as well as 400m sprinters and soccer players) can develop left ventricular hypertrophy as a means of increasing stroke volume and cardiac output (at least in men, it's not very prevalent in women). Maybe the LGE is picking up on changes that result in this hypertrophy, which is not generally regarded as pathological."

No for the reasons stated above. LGE is a scar - it is not more heart muscle - it is missing heart muscle.

"Non-ischaemic damage to muscle and changes in electrical conductivity can be a problem too of course, if that's what is happening, but it's not necessarily related to atherosclerosis, or is that what they are trying to say- that LGE picks up subclinical signs of ischaemic damage? It wasn't clear to me what they were trying to say about the distinction between ischaemic and nonischaemic patterns."

They were saying that there were obvious heart attacks with permanent myocardial scar in coronary artery territories (classical) and there were also areas of such scar that were most likely due to microemboli ( infarcts due to occlusion of smaller vessels) or what might be worse, cardiomyopathy Subclinical only means at the time of the scans they had not had chest pain - the heart attacks were as all real.

BTW, the way heart attacks kill you is usually that the dead heart muscle causes electrical changes - ventricular fibrillation that makes your heart just quiver and not pump blood any more - that is what happened to Salazar (who was save) and probably Fixx (who wasn't)

LGE = heart attack. The equation is almost as definitive as having the heart tissue under a microscope.

"Weight lifters can develop left ventricular hypertrophy too (in response to pressure overload as opposed to volume overload in endurance training).

Give me a good reference for that if you don't mind. Also, LVH has nothing to do with atherosclerosis (in the sense of causing it) so there is no applicability of these findings at all to resistance training.

" So I don't think bashing cardio is exactly the point. Perhaps the take home message should be that overdoing it is not a good idea, because you can cause heart damage doing any number of activities,"

That is not the take home poiint if you read the study - it is quite specific to marathoners.

November 4, 2009 | Registered CommenterKurt G. Harris MD

Here is an interesting review article that discusses cardiac remodeling in endurance and power sports:

It has been well-known for as long as I've been reading about strength training -- which is admittedly only maybe 4-5 years -- that some thickening of the left ventricle is a benign adaptation to weight training. I thought I'd first read about it in "Starting Strength", but now that I go back to it I don't see the reference. This is the first I've heard of similar adaptations to endurance activity but it's pretty neat. Either way, it seems pretty clear that this is not "damage".

November 4, 2009 | Unregistered CommenterKim

Thanks for the explanation.

This reference "Cardiac remodelling: concentric versus eccentric hypertrophy in strength and endurance athletes" was pretty good. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2300466/?tool=pubmed

I am interested in the findings of the LGE paper you've summarized, but reluctant to draw the same conclusion you do as yet. I didn't stop eating red meat because one study showed a bad association with red meat and health. That said, it wouldn't surprise me to find small localized damage in the heart muscle, and perhaps some damage is inevitable, and possibly ubiquitous. It's possible that LGE is detecting nonpathological changes as well however, and that could confuse the issues. For example, would it pick up increased collagen deposition? I will certainly keep an open mind and make it a point to read these papers as they come out, and am glad that people are looking into it finally.

I am more concerned about the CAC scores being higher relative to the FRS scores. This is a finding that could help turn the tide away from overcarbing and the SAD if the higher CAC score is due to bad diet, but would be meaningless and encourage sedentary lifestyles if it is due to heart stress per se. Of course it might be more related to omega-6 and clotting disturbances rather than carbs. Since the running community thnks they are pursuing a healthy lifestyle, they might be amenable to changing diet if there was good reason to. Most of them eat horribly and think they can get away with it because they can just "run off" extra calories. I met one woman who even admitted to eating mostly candy. Because they are thin and generally insulin sensitive, have lower blood pressure, LDL, etc, they believe they are doing the right thing and can eat whatever they want. I would be curious what difference it would make to their health if they ate more paleo/low carb.

And I disagree with those who suggest you must have carbs to do aerobic (or anaerobic) exercise. My husband and I run quite a lot but eat only a small amount of carbs usually (<100g per day) and he has even run races (50K) without eating any carbs before or during.

November 5, 2009 | Unregistered CommenterCynthia

Some great posts! About 8 yrs ago I switched my exercise regimen from 3 or 4 slow jogs sessions (at age 45)per week to 3 heavy resistance training sessions per week. At a height of 5'11, I went from 165 lbs to 215 lbs (I'm now age 53). I went from looking 10 yrs older than my age to at least 5 years younger than my age. I went from being a bag of bones to having a quite solid musculature. Oh, by the way, the 50 lbs increase in weight increased my waist size by only about an inch or so-but looks thinner than when I was 165 lbs 'cause my shoulders are so much wider.
The bottom line for me is this- cardio is a destructive process whereas resistance training is constructive-would you rather DESTROY or CONSTRUCT?

November 9, 2009 | Unregistered CommenterPaul

Lift weights instead. If you Deadlift and Squat a lot, the next time you compare your endurance to the chronic treadmill runners, say, on a skiing/hiking trip, you'll both be surprised when they're huffing and puffing and you're not. Granted, Deadlifts make my heart rate scary high, but only for a minute or so.


When I run as fast as I possibly can - sprints or 5K, my heart rate rarely is over 170. When I do snatches as quickly as I can with good form (like, 8 of them) my HR can be 182! My restign HR is 48-52.

November 10, 2009 | Unregistered Commenterzach

You hit a home run with this one. Talk about knocking it out of the park. What a great piece of writing on a subject that has dogged many of us our entire lives: How much "cardio" should we be doing for our health? And how many of us have felt guilty - guilty! - for years for believing we "don't do enough."

Excellent piece. Bookmarked. :)

November 16, 2009 | Unregistered CommenterMolly

Thank you for this interesting post.

The idea that people are by nature long distance runners seems in vogue, but I think the idea has to be that no one in their right mind would willingly run 26 miles without stopping to rest. Or run 26 miles repeatedly. As I recall, the original marathon runner is said to have died from it, which could be taken as a lesson.

In terms of practicality, in Paleo terms. perhaps, one would run for a while and see if the critter you were chasing was tired or not and if you could get close enough to kill it. If not, you collect yourself and run more. And only as fast as was necessary. And what were you eating while all this was going on?

I am 65 now, and still moving well. I used to run and play tennis, and before that I was on the gymnastics team at Michigan. I never really liked running more than 3 miles. Now I lift weights and play tennis. Most people talk about lifting weights, do more talking than lifting, and when they lift do so with no intensity whatsoever. I believe that after 45 minutes of lifting weights you ought to be exhausted, and 45 minutes of that is enough. Free weights are preferable.

My brother-in-law was a fanatic bicyclist, fell gently one day, and broke his leg due to osteoporosis. His whole skeleton was a mess. At about age 50.

What you did not address in your article was the personality issue of marathon runners: I know we no longer talk of type A and Type B personalities in heart attack relationships, but what kind of person trains so frantically and then undertakes these activities? Talk about a bizarre motivation, and being driven. I could understand it in a young professional athlete, but as a sport for the aged? Perhaps these people felt the pain in their chest and continued on anyway?

Maybe they needed to eat more cheese, which they were probably avoiding due to fat content.


I did hove one stress test, a few years ago, and one angiogram, and both times they found no plaque or, as they put it, clean as a whistle. I don't know if that's a medical term.

November 29, 2009 | Unregistered CommenterRichard


I have a friend with high cholesterol but a good heart scan score. I told him not to worry but he asked whether there are kinds of plaque that don't have calcium and would therefore not appear on a heart scan. True? If so, are there any other non-invasive tests you would recommend to put his mind at ease, other than NMR profile? Thanks for your time.


Age sex and score?

December 8, 2009 | Unregistered CommenterTodd Hargrove


Thanks for the response. He's 44. Says his TC is 250, doesn't even know the breakdown. He doesn't want to get educated on cholesterol, just wants to know if the good heart scan means that cholesterol numbers are irrelevant.


You said the heart scan score was good -- do you mean zero? What was the numerical score?

December 8, 2009 | Unregistered CommenterTodd Hargrove


He can only remember that the score was that of a 22 year old.

December 9, 2009 | Unregistered CommenterTodd Hargrove

Cardiologist William Davies has proposed that jogging does not *cause* CVD - rather it may be the lipoprotein (a) aka Lp(a) that may be the causal factor:



I read that and do not agree. For one thing he presents no evidence that cases of sudden death in runners are due to Lp(a)- as i read it he speculates that it might be. Lp (a) is the latest brick in the crumbling edifice of the lipid hypothesis. The epidemiology effect size of LP (a) is not that big in the first place, and if you eat a high fat diet without PUFAs I think it is irrelevant.

I am probably biased as my own Lp (a) is 85 and my CAC is zero and my CIMT is like a 30-year-olds at age 48. If Lp (a) is supposed to be some kind of inherited death sentence how come my parents are heart attack free at ages 75 and 71 and they have CAC at the 25th %tile and 0 (Dad and Mom respectively) after a lifetime of eating the SAD?

Chronic cardio provides zero protection against CAD or is actually promoting of inflammation, in my opinion.

January 2, 2010 | Unregistered CommenterJohnny Bourdeaux PhD
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