Atherosclerosis is a fearsome age-related condition, as it is quite possible to suffer the progressive build up of arterial plaque with few or no apparent symptoms all the way up until some of it suddenly ruptures to cause the catastrophic blockage of blood flow known as an infarction, and that either cripples you or kills you over the course of an exceedingly painful few minutes. If this affects your heart or your brain you will be lucky to survive, and luckier to recover.
The various contributing causes of atherosclerosis are numerous, each layer of cause and effect feeding into the one above. An incomplete list might include: the evolved reaction to disturbed blood flow in blood vessel walls; the details of fat metabolism; accumulation of lipofuscin constituents such as 7-KC in macrophages attracted to blood vessel damage; damaged cholesterol molecules created by the toxic output of cells overtaken by damaged mitochondria; and last but far from least the standard issue risk factors for all of the common age-relate diseases: becoming fat, being sedentary, and taking up smoking.
I'll point out the recent article on atherosclerosis quoted below as it caught my eye by virtue being interesting and balanced within its own lack of vision regarding the treatment of the condition. The author discusses diet, which is of little consequence in comparison to the outcome of medical research. Atherosclerosis is not a modern condition, and indeed the progress in health over the past few centuries has rendered us far better off at any given age than our distant ancestors. If we see more of atherosclerosis and its threat of sudden death today, it is because we have engineered longer lives, control of the lion's share of serious infectious disease, and the medical technologies need to pay closer attention to the progression of atherosclerosis as we age. Now more people survive or never even see the mortal threats that thinned the ranks of those who came before us:
Many different societies in human history have mummified their dead, using naturally occurring cold, hot, or dry conditions with or without embalming, and HORUS researchers took these ancient corpses, from different societies and times and continents, and put them through CT scanners. The deposits of atherosclerosis proved common. They were present in a third of the mummies, despite their average age at death being 36 (an age which does not fit neatly with the idea of a "natural" life being blissfully healthy). Atherosclerosis was as easily spotted in the dead gatherer-hunters as in the late pastoralists; as common in those who had lived on fish and seafood as in those who feasted on steak.
The HORUS study cannot tell us anything about the superiority of one diet over another, but it does reveal that when it comes to tackling atherosclerosis by altering diet and lifestyle, there may not be a magic preventive or cure. Far from being the peculiar side effect of modernity, problems with blood vessels narrowing and hardening occur routinely with age in all human societies. The foggy idea that modern life fosters atherogenesis - a notion that for too long was accepted without having been properly examined - evaporates under the sunlight.
Outside of the SENS vision of reversing and preventing age-related disease by fixing root causes, which include the lipofuscin and damaged mitochondria mentioned above, much of medical science operates at a higher level in the chain of consequences. Researchers aim to interfere much further along, in attempts to reduce the severity of the results without reducing the the severity of the underlying causes. This doesn't sound very sensible when put this way, and from a high level perspective it really isn't the best way forward. Medical science works this way because, constrained by regulation, research tends to run backwards from the end state of a defined, named disease, so the first new things discovered are the proximate causes. Thus when it comes time to try to create profitable therapies from these discoveries, the development community has to work on patches that make things somewhat better for late stage disease rather than working on methods of prevention and repair that can stop the disease from ever happening in the first place, and cure it for those who do suffer its effects already. This state of affairs will change, and it has to change if we are to see great improvements in the health of the elderly and the prospects for defeating age-related disease.
Here is an example of the sort of research that results from the working backwards approach, the identification of risk factors in metabolism that might be modified to reduce the accumulation of root causes. This is of course of limited utility to those already damaged, as it does nothing to remove existing damage:
Danish researchers [have] shown that people with variation in a gene that inhibits a specific protein in the blood - the so-called apolipoprotein C3 - have a significantly lower level of normal blood lipids than people without this gene variation [as] as well as a significantly reduced risk of cardiovascular disease. Furthermore, the same individuals also have a 41 per cent lower risk of arteriosclerosis. The research is highly relevant as at least one pharmaceutical company has a drug in the pipeline which inhibits precisely apolipoprotein C3.
The scientific results are based on two of the world's largest population studies, the Copenhagen City Heart Study and the Copenhagen General Population Study, with a total 75,725 participants who were followed for 34 years.