A previous video blog entry has the message that we are already evolving to live longer. But, does evolution set a limit on our lifespans, pre-ordain when we will die so to speak? Please see these videos for views of a few key longevity scientists. And then I will weigh in with my own opinions.
Most importantly, it appears that all these researchers and I agree on one central point – that there appears to be nothing about evolution that should prevent us from discovering means for extending our lifespans. As Aubrey de Grey colorfully puts it “aging can be combated more and more if you throw in more and more elaborate anti-aging machinery.”
Although my views appear to be close to those of Dr. Kenyon, I find myself on disagreement with the other video presenters on the role of evolution in determining lifespans. Instead of thinking that evolution has nothing to do with lifespans, I think it has everything to do with them. Being in the minority here, I will elaborate briefly.
The classical view of evolution is indeed that evolution works generally to keep people healthy through childbearing and child-rearing age and is thereafter indifferent to their wellbeing or longevity. This appears to be the expressed opinion of Dr’s de Grey, Kennedy – and of Austad in the prior video blog. Further, in the classical view evolution occurs through the processes of “random variation and natural selection” associated with mutations of genes and for humans takes a very very long time – hundreds of thousands or millions of years. Although over 200 years ago Lamarck had proposed that acquired characteristics could be inherited, this idea became rejected in part because of its seeming incompatibility with genetics.
A newer and increasingly popular view of evolution, the view I subscribe to, is that evolution takes place not just through genetic mutations but also via inheritable changes in the epigenome. Lararckism is back in a new sophisticated context! This kind of evolution can proceed vastly faster, in as little as a few generations, and still have major impacts. Further, I submit that the changes in the epigenome are driven by the external environment, both physical and social. As the physical environments of humans evolve – such as by providing cleaner disease-free water – so does our epigenome change and do we evolve biologically. As the social environment evolves – such as by requiring much more time for kids to become educated and get up to speed so they can participate effectively in an ever-more complex society – so does our epigenome change and do we evolve biologically. Dr Kenyon suggests this point in her presentation.
The classical theory of evolution cannot explain many observed phenomena which the newer view explains convincingly. One is why do human heights seem to vary so much by population circumstances and time frames? Canadians are now taller than Americans, who have suddenly plateaued — but all trail the towering Dutch. So what’s their secret?(ref)” No way these up-and-down trends in average heights could occur so fast through mutations in genes. Another example is given by the opossums talked about in the earlier blog. They too doubled their lifespans in response to a changed environment far too fast to be explained by plain genetics. But the important example for this discussion is that our average from-birth lifespans in Western and US countries are increasing by about two months for every year that goes by. Why?
(a) Our epigenomes are adopting to longer lifespans because of changed physical circumstances: freedom from predators, near-elimination of infectious diseases and better public health and diet. We are living longer not just because of better circumstances of the moment but mainly because of our epigemomes’ adoption to those circumstances. For example, relative freedom from predators means there is a lessened requirement for constant hyper vigilance implying much less chronic expression of cortisol, the “fight or flight” hormone that enhances responses to emergencies but suppresses the immune system and bone formation. So less chronic cortisol associated with freedom from predators can lead to evolution of stronger body defenses against disease, better bones, and consequently, longer lives.
b) Our epigenomes are adopting to longer lifespans because an increasingly complex society requires much more learning before people can effectively participate in it, and this demands longer lifespans. I laid out this viewpoint in the blog entries Social evolution and biological evolution – another dialog with Marios Kyriazis and Social ethics of longevity.
In the following video on Infection and Mortality, Dr. Kirkwood’s speaks powerfully supporting point (a) above.
So, evolution has had everything to do with lifespans. Evolution has always cared about how long we live. The good news is that as we find mechanisms to expand lifespans as Aubrey suggests, those mechanisms will become part of social evolution that drives biological evolution. We are not prisoners of an inexorable process of biological evolution. We can affect our evolution via research and applying knowledge. We have been doing that as long as we have been humans. Discovering how to start fires was an example, and applying the discoveries of Louis Pasteur was another of very very many. And I believe we can shape evolution so we live much longer lives. There will be more blog entries to come related to this point.
This video blog entry, like previous ones, is being brought to you in close collaboration with the filmmaker Robert Kane Papas. I expect we will generate more of these blog entries structured around short video segments on aspects of longevity science. Robert is the filmmaker who produced the recently-released film To Age or Not to Age. Robert captured hundreds of hours of interesting video in shooting the film over a 4-year period, including extensive interviews with a number of prominent aging-science researchers. It was possible to incorporate only a small fraction of that interesting material in the film itself. However, Robert will be identifying short but remarkable segments of materials both in the film and not in the film, and I will be remarking on them just as in this blog entry. I expect the videos and the remarks will appear on both this site and on the film site To Age or Not to Age.
Are you concerned at all about Benfotiamine?
I have been taking benfotiamine supplements for years now. It is included in the supplement regimen suggested in my treatise ANTI-AGING FIREWALLS – THE SCIENCE AND TECHNOLOGY OF LONGEVITY. At http://www.vincegiuliano.name/Antiagingfirewalls.htm
I mention benfotiamine several times and said “The other substance is a fat-soluble form of the vitamin B-1 known as benfotiamine. Benfotiamine inhibits the formation of AGEs. These firewall substances are particularly important for diabetics. They can mitigate or block the biochemical processes that lead to nerve, kidney, retinal and vascular damage associated with high blood sugar levels.”