Circle Dance
Irradiated by LabRat
One of today’s headlines at Science Daily is the interesting finding that patients who recieve a pneumococcal vaccination cut their risk of heart attacks in half. The Science Daily article is brief and merely mentions that pneumonia is “associated” with cardiac events, but gives no explanation as to why that is. One is left with the vague impression that you can cough yourself into shorting your ticker and that’s why. While it is true that more pulmonary stress leads to more cardiac stress, there’s a little more going on here than just that.
Paul Ewald is an evolutionary biologist studying the evolution of infectious diseases and in particular of virulence who has a number of radical ideas- chief among them that most of the big diseases we think of as “lifestyle diseases” or lightning-strokes from God are actually chiefly caused by pathogens. He points to the relatively-recent discoveries that Helicobacter pylori is responsible for the vast majority of ulcers, and that human papillomavirus is probably responsible for most cervical cancers, and makes the evolutionary argument that simple fitness calculations say that most “genetic diseases” should disappear within a few thousand years. (Ewald even goes so far as to argue for a pathogenic explanation for homosexuality. Not ENTIRELY out of the realm of possibility, but I don’t think so.)
Ewald definitely suffers from a case of hammer/nail syndrome- he doesn’t seem to take much into account the likelihood that genes that cause genetic diseases may also confer some advantage that, in long stretches of human history, balanced the cost and kept the alleles in the population. We already know for sure that the allele for sickle cell anemia is definitely a huge advantage in not contracting malaria, and theories abound that several genetic lung ailments- like cystic fibrosis- might be great for resisting tuberculosis. (Then again, it circles right back around to his point that here are pathogens, driving human diseases and human evolutionary fate- just not in the way he’s usually arguing.) However, even if he’s a bit overenthused with his theory, his point is sound; we usually don’t look for a microbe when we’re dealing with something that seems like a simple body breakdown, like heart attacks or cancer or dementia, and that is to our detriment. Not all pathogens have sudden and dramatic effects.
One of Ewald’s hobbyhorses to whip was the high association of a pneumonia-causing species of Chlamydia that is frequently found in arterial plaques Roto-rootered out of atherosclerotic blood vessels. As the original study that the Science Daily article is reporting on points out, antibiotic treatment for chronic infections of that particular bug hasn’t had any particularly convincing effects on rate of subsequent cardiac episodes. The thrust of the article is the idea that ACUTE infection might cause changes in major plaques through suddenly increased inflammation- after all, the heart and the lungs have some rather major shared blood supplies. Pneumococcus was a logical suspect for the majority of these more acute infections, and given the results of the study, they were on the button.
However, merely because antibiotic treatment for the relevant Chlamydia bug were not effective in reducing cardiac episodes in patients with known heart disease, it does not necessarily follow that the Chlamydia is an innocent bystander, a commensal bug just hanging out in the blood vessels.
The authors of the Pneumococcus article hit another thing right on the button- inflammation. The scientific assumption for the last several decades has been that heart disease is caused by high cholesterol caused by too much saturated fat in the diet; this has become known as the lipid hypothesis. The lipid hypothesis, once recieved wisdom, is challenged with increasing intensity- especially as new studies that remove some of the assumptions of the old ones (or control their variables better) are starting to show that cholesterol and heart diease are not as associated as once thought, and more particularly that consumption of “saturated fats” (not all created equal) aren’t nearly as tightly linked to either as once thought. Opponents of the fat->cholesterol->atherosclerosis model argue that, as cholesterol has a critical role in repairing damaged cells, if we see choesterol plaques on chronically inflamed (and over time, damaged) vessels and conclude that cholesterol did the damage, that’s like concluding that butterfly bandages cause lacerations.
The most common opponents of the lipid hypothesis are advocates for either a low-carb diet or a “paleo” diet- which, to be fair to the paleo diet folks, seems to work pretty darn well*. They see the inflammation link, but they chalk it up to two major factors- the body trying to keep up with eating way more strange sugars, fats, and starches (and yet stranger things) than it was ever designed to deal with, and the stress of life in general and the kind of long endurance exercise that has been touted as superior, which they argue the human body was ALSO never designed for. And they have a point- stress hormones, whether caused by a dickhead of a boss or by running six miles every day, do cause chronic inflammation. Do note, by the way, that the statins that have shown good results in reducing rates or further development of heart disease are also anti-inflammatory.
But infection also causes inflammation, and infection does the job a lot more thoroughly than stress or sugar. The thing about the Chlamydia bugs is that the Chlamydia genus of bacteria consists entirely of professional parasites; there are no free-living Chlamydians, and they have outsourced a lot of their biochemical “work” to the host cells they infect. They are good at surviving as parasites- well-adapted parasites don’t kill or even too much inconvenience their hosts unless they have a REALLY fast and efficient way to spread- which means they cause quiet, low-level infections. The species of Chlamydia we’re all most familiar with- the one that causes a sexually-transmitted disease- can be so quiet and subtle it can live for years in a woman, slowly destroying her uterus and rendering her infertile without ever having noticed a thing wrong. Men tend to be more symptomatic, but even half of male infectees never have cause to suspect something amiss.
If patients with known heart disease don’t respond to antibiotic treatment for the pneumonia Chlamydia with an obligingly reduced rate of cardiac events, it may well be because the bug in question did the damage that caused the heart disease over YEARS of quiet residency, and the antibiotic treatment is a simple case of too little, too late- evicting the squatters after they’ve almost entirely torn down the building. The way it’s been studied so far is nowhere near sufficient to rule out the idea. There is no vaccine for this bug that I know of, though a vaccine for its venereal cousin seems to be doing well in animal trials.
Of course, even if the Chlamydia or the Pneumococcus really ARE playing a big role, that’s not exactly an argument that exonerates one from a cheeseburger-and-fries-intensive diet; being obese puts more strain on the heart, which is the same general size as it ever was (and you really don’t want it to get bigger), and has the same network of blood vessels that it always did, and thus has to do more and more work with less and less the more obese you are. For that matter, the paleo people are right too- stress also causes inflammation, and so does a crappy, sugary, hyper-processed diet. Even Helicobacter is not the sole king of ulcers- bad enough stress and bad enough diet and you can grow your very own bacteria-free ulcer.
The Ancel Keyes (father of the fat-is-bad in America), Robert Atkins, geneticists, and Paul Ewalds of the world are all right, and all wrong. You don’t need one agent to lead the dance of disease when they’re all feeding each other- though finding who stomps the hardest is a good place to start.
*The diet in that particular study was vegetarian, which isn’t necessarily a logical assumption with hominids, which probably DID eat more and more meat the further they got out of the tropics. Other aboriginal “hunter-gatherer” diets in frigid regions, like the Inuit’s traditional diet, seem to leave the consumer- provided he avoids modern processed foods- remarkably free of heart disease. There’s not much starch or sugar in either version, though.
October 11th, 2008 at 3:35 pm
And they have a point- stress hormones, whether caused by a dickhead of a boss or by running six miles every day, do cause chronic inflammation.
Except I’ve heard that humans evolved as cursorial hunters: evolved for running prey down over extremely long distances at a moderate pace. It’s why a human in good shape can outrun a horse in a long distance race.
Of course, we may be talking about different levels of exercise type exertion.
October 11th, 2008 at 3:57 pm
It was a popular theory in anthropology for awhile, but the problem is that very few hunter-gatherer cultures actually hunt like that, and those few that do don’t do it nearly as often as they use other tactics- mostly tracking over long distances (at a walking pace) and then using a combination of sprinting and medium-range weapons.
Chasing down prey over miles at a jog is not only energy-inefficient by comparison, but metabolically speaking, it requires massive amounts of carbohydrates to sustain- which a pre-agricultural hunter-gatherer could never expect to lay his hands on in large amounts. It works for four-legged animals just fine- they’re designed much better for energy-efficient running- but not so much for bipeds.
We still might have different levels of exertion in mind, but I’m thinking “fast walk” or hike that ends in a sprint, not jogging.