There are over 20,000 articles about telomeres and at the current rate of production, I could blog about several a day and never present them all. Instead, I will summarize the literature for you. There are the WHO, the HOW, and the WHY.

The WHO – the vast majority of studies are what we call case-control or randomized studies. They take a group of affected individuals and unaffected individuals and compare leukocyte telomere lengths. The vast majority are case-control which attempt to look at people who are exposed to one variable, like eating olives or running marathons, and compare them with people who appear as similar as possibly by established arbitrary criteria, such as gender, age, ethnicity, weight, comorbid conditions etc.  Telomere tend to be shorter in those with the studied variable because that justifies the vast effort and expense to write the study.

The HOW – these are much more interesting works because they involve elucidating the mechanisms of telomere lengthening, shortening, and regulation and although the benefits of them are nearly inaccessible to the non-scientist, they are invaluable in eventually decoding the language of cells.

The WHY – this type of research is unfortunately, dead on arrival, for three main reasons. Firstly, because it would involve presuppositions with placeholders for theism (or evolution, the scientists’ new godhead)

“We know that evolution (or God) intended man to get old”

anthropomorphizing cells and molecules in a way that is abstruse

“We know the cells want to die and shut down gene expression”

and reverse logic (or teleological, no pun intended) such as working back from a phenomenon such as mitochondrial dysfunction or inflammation to an illusory set of conditions that don’t flow from your arbitrary premise (inferring the cause from the result).

“We know that oxidative damage at mitochondrial dysfunction occur in older cells therefore this must be the root cause of aging”

What we need is to imagine different types of questions that incorporate more meaningful queries; garbage in, garbage out, in other words. Time to ask better questions!

The questions we should be asking should be simpler, bigger, and more syncretic in nature. In my estimation (and I am probably alone in this regard), the cause of aging and most of disease has already been answered: it is telomere attrition in stem cells leading to mutation and depletion. I believe the reason for correlation in 20,000 articles is that telomere shortening is causal.

That is why I am saddened by the billions that continue to pour into discovering that all bad things correlate to telomere dysfunction. It is like publishing articles about how hammers can break glass, pottery, windows, toys, eyeglasses, picture frames – we get it….there is a strong correlation between bad telomeres in co-variable white cells and conversely healthier telomeres associated with “good” behaviors.  In truth, if scientists were doing their jobs better they would actually study telomeres in the organs of interest and not just blood cells, such as the liver in drinkers or the lungs in smokers, the relationship would be even stronger.

The accretive bench research establishing the HOW is important and should continue. Witness the recent article explaining how TZAP trims and regulates telomere length and how stem cells that dedifferentiate express pluropotency and relengthen telomeres like a pinball machine resetting to zero.

The WHY research that we desperately need on telomeres comes in the form of questions that haven’t been asked because they seem tangential to the field. What we really need is a better understanding of the ecology of cells with regard to how they interact. Think of telomeres as stamps in your passport. If you travel a lot, you get a lot of stamps (the telomeres shorten). Some secret agents get many passports and relengthen their telomeres so you can’t tell much about how many airline miles they have. But wouldn’t it be great to know how those agents are deployed? We need to crack the codes of how they get their orders, decide to perform their secret missions, and how to mimic those signals. Telomeres are not where the treasure is to be found any more than passport stamps are; the goal is to understand stem cell ecology and behavior.

Aging is slowed when we can enhance telomerase function – I beleive we already can do that using telomerase activators like TA-65 and is step one. Aging will be mitigated when we can store and replace young stem cells -that is technologically feasible now and is step 2. But aging will be cured when we can control the orderly destruction of damaged stem cells in the presence of plentiful healthy stem cells (steps 2 and 3).

See this blog for further explanation of my trimurti model of aging.