Tohtori Kurt Harris pieksää lipidihypoteesiä ja "kroonista cardiota" oikein Isän kädestä:
[list:2b4dqi7a][size=150:2b4dqi7a]“Cardio” Causes Heart Disease.[/size:2b4dqi7a] ( )
[size=85:2b4dqi7a]- -the choice would be cardiac MRI with late gadolinium enhancement or LGE. 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.
[size=130]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?[/size:2b4dqi7a]
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.
[size=85:2b4dqi7a]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.[/size:2b4dqi7a]
[size=85:2b4dqi7a]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.
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.[/size:2b4dqi7a]
http://www.paleonu.com/panu-weblog/2009 ... sease.html[/list:u:2b4dqi7a]
Juokseminen ja erityisesti "krooninen kardio" & maratonien juokseminen näyttää johtavan huomattavaan sydänkohtausriskiin !
Ihan sama miltä kolesteroliarvot näyttävät.
PS: Ehkä juoksijoilla oli/on todennäköisemmin geneettisesti korkea Lp(a), joka on suurina pitoisuuksina erittäin voimakas riskitekijä ? Monet hyvin urheilulliset kaverit omaavat kovaa sukurasitetta sydänsairauksille ja liporoteiini a on ainoa toistaiseksi tunnettu veriarvoihin liittyvä selittäjä tälle ilmiölle - se auttaa immuniteettia ja voi myös ohjata rajujen urheilulajien pariin koska saattaa auttaa urheilussa ?
Pretending to be certain about propositions for which no evidence is even conceivable—is both an intellectual and a moral failing. —Sam Harris