Journal of Internal Medicine, Special Issue on Aging

The latest issue of the Journal of Internal Medicine focuses on aging. Some interesting material in there, and you'll note that the publisher is allowing free access to the full text of some papers. For example:

Mitochondrial dysfunction as a cause of ageing

Increasing age in mammals correlates with accumulation of somatic mitochondrial DNA (mtDNA) mutations and decline in respiratory chain function. The age-associated respiratory chain deficiency is typically unevenly distributed and affects only a subset of cells in various human tissues, such as heart, skeletal muscle, colonic crypts and neurons. Studies of mtDNA mutator mice has shown that increased levels of somatic mtDNA mutations directly can cause a variety of ageing phenotypes, such as osteoporosis, hair loss, greying of the hair, weight reduction and decreased fertility. Respiratory-chain-deficient cells are apoptosis prone and increased cell loss is therefore likely an important consequence of age-associated mitochondrial dysfunction.


Mitochondrial dysfunction is clearly involved in the human ageing process, but its relative importance for mammalian ageing remains to be established.

Understanding ageing from an evolutionary perspective

A belief that ageing and longevity are governed by genetic factors has led to growing excitement that research on the human genome will soon uncover the genes for ageing and perhaps open new paths to longer life and health spans. Even if direct gene modification is remote, a clearer understanding of the pathways regulated by such genes may point the way to nongenetic interventions that exploit this knowledge. But what is the evidence that genes do control ageing and how realistic is it to expect that the 'new genetics' can secure for us a modern-day elixir of youth? And how can we accommodate the genes responsible for ageing within the framework of natural selection, when surely the decline in vitality that results from the ageing process would appear to run counter to the principle of maximizing Darwinian fitness?


Although the evolutionary theory of ageing is by now well established, there has continued to be a tendency to seek explanation of ageing in terms of some kind of adaptive genetic programme. The attractions of this concept are easily understood. First, ageing is phylogenetically a very widely distributed trait and in species where senescence occurs, it affects every individual that lives long enough to experience its adverse impacts on fertility and vitality. Secondly, there are clear genetic effects on longevity and this leads naturally to supposing that the relevant genes specify some kind of 'ageing clock'. In spite of these attractions, the programme theory, as a general explanation for ageing, is both logically and empirically unsound.

About the most profound thing I've read in the past few months on the nature of aging research - and I forget the source, so apologies to whomever I'm lifting this from - is that most gerontologists believe that the only viable way to extend healthy life span is to slow aging by re-engineering the complexities of metabolism and genetics. This is generally agreed to be very hard; it's a long, long road and we stand at the very beginning, barely assembling the necessary knowledge to build a roadmap. Thus most gerontologists think that major changes to human life span within our lifetime are extremely unlikely, even in the scenario of muliple, large-scale, coordinated research and development initiatives

Fortunately, engineering a better human is not the only way to greatly extend the healthy human life span. It's not even plausibly the fastest, most efficient way to do it. Instead of engineering new biochemistry, we can focus on repairing the biochemistry we have today. Don't slow aging, but rather reverse it by fixing the damage that is aging as it occurs. Significant near-term progress in this endeavor is more plausible than significant near term progress in metabolic re-engineering, and it will also benefit those people who are already damaged by aging.

We don't need to walk the long road to better, engineered humans, and see all of us alive today die along the way. We can walk the much shorter road to medical technology to repair the aged, learning to better maintain the biology we have today.


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