The vast majority of research on aging aims to understand what happens as we age, to see the damage, to identify the origins of the changes; usually in order to better understand them or to develop treatments. Research into the prevention of aging has launched not so long ago. The reason is simple: until recently, in the early 2000s, aging was viewed as a build-up of wear and tear, mainly caused by oxidation. We were discussing then about:

  • The importance of telomere length,
  • Aging caused by cellular senescence,
  • DNA damage,
  • The dysfunction of mitochondria,
  • Epigenetic remodeling,
  • Protein damage,
  • Depletion of stem cells,
  • Problems detecting energy intake, or
  • Communication problems between cells.

These indicators were considered at the time to cause, at least in part, aging. In my first book (Live Young, Longer 2016), I explained that there were over 300 theories that attempted to explain biological aging. Even after observing that oxidation levels were not directly correlated with the rate of aging or longevity, it took more than 10 years for a new theory to be defended by scientists in the field in 2013, giving reason to a researcher who put forward this hypothesis in 1957 (George C. Williams, 1926 – 2010: antagonistic pleiotropy, 1957). It was later renamed by a great American researcher (Mikhail V. Blagosklonny): the theory of hyperfunction. We will come back to this in a future article. Let’s talk about research instead.


It goes without saying that one of the first research strategies was to consider genetics with the aim of discovering possibilities of intervention. The first important discoveries that gave great hope in genetics were made from microscopic worms. In the 1980s: a single mutation, the Age-1 gene of C. elegans, increased longevity by 40 to 65%. This was the first demonstration with a whole organism that genetics regulate, at least in part, longevity.

Another important discovery was made twenty years later in 2007. This time, a single mutation increased the lifespan of C. elegans by 10 times.

Genetically related aging was then seen as something encoded that we could understand and modify. Maybe we could act on a few genes and live ten times longer? For these microscopic worms, which only have about 1000 cells (the human body has about 100,000 billion), we now know that there are 550 genes that modulate longevity and that possibly half of the 20,000 genes are also involved. Also, the more complex the organism studied, the smaller the impact of genetic modification. For example, work on mice has not reproduced 10 times the longevity, but rather, only about one time. The reason for this phenomenon is that the more complex the organism, the more regulatory mechanisms exist for the same process, which reduces the impact of specific genetic modification.

Another example of this phenomenon is the action of calorie restriction. Calorie restriction remains the best documented approach to increasing longevity in all living organisms. The impact in yeast (eukaryotic single-celled organisms; cells similar to ours) is 150-200% longer life. In the nematode, this is a 50-150% impact. For the fly, and the mouse, respectively 100% and 30 to 50%. For primates, such as humans, the impact would be around 15-23%. Therefore, the more complex the organism, the more the effect decreases. In addition, it is important to remember that calorie restriction acts on a multitude of genes. An approach targeting a specific gene therefore has very little chance of yielding significant results.

The last ten years of research have shown us that genetics only account for 15 to 25% of human longevity. The remaining 75 to 85% is based on our lifestyle. Epigenetics are of course linked to the expression of genes that have positive or negative effects on our chances of disease.

Correction of dysfunction

As we age, a large number of cellular dysfunctions interfere with the functioning of tissues, and thus cause diseases associated with aging. Several research approaches have focused on correcting these dysfunctions, hoping to either restore a younger state, or stop the aging process, or even find ways to cure pathologies. These approaches are rather risky since it is often discovered that what we consider to be dysfunctions also have precise biological roles.

Take the case of telomeres; those repeating sequences that protect the ends of our chromosomes. They get smaller with each cellular division and cause the cell to die when they are too short. We thought we discovered the fountain of youth with telomeres by believing that if we continuously lengthened them, the cells would be eternal. It is true that it is possible to lengthen them in order to prolong the life of the cells.

Telomeres are indicators of the useful life of cells depending on a person’s state of health. A healthier person has longer telomeres because their cells are healthier and can be used for longer. If you intentionally extend the telomeres of an unhealthy person, these cells may be used longer than they can handle. Cells that are too old and not replaced in time could become dysfunctional and cause cancer. Thus, an approach aimed at increasing the lifespan of cells could increase the risk of cancer.

On the other hand, recent discoveries (2016) have focused on the removal of obsolete cells, the so-called senescent cells. One of the problems with aging is the buildup of outdated, dysfunctional cells that should have been replaced, but are now locked into a lifelong dysfunctional state called cellular senescence. Removing these senescent cells helped keep organs younger, longer, and extended longevity by 30% in mice. These mice stayed healthier, longer.

An American research group, based in California, is promoting a research program aimed at correcting 7 specific dysfunctions related to aging in order to slow/stop the process. This group led by Aubrey de Gray is called SENS for “Strategies for Engineered Negligible Senescence”. Personally, I don’t believe it, due to a fundamental reason: it will be more productive to act on the basic mechanisms of aging (prevention) than to try to erase problems once they are implanted. These dysfunctions have metabolic causes and we now know that it is possible to act on the mechanisms of aging to prevent the appearance of these dysfunctions and to improve healthy aging. It is therefore possible to act upstream in regards to aging, instead of aiming to correct its consequences.

Treat what is not a disease

One of the obstacles to the development of preventive approaches to aging is the structure of our health systems. We sell “treatments”, which are applicable when the “diagnosis” has established that it is necessary to treat. The Food and Drug Administration in the United States has already ruled that aging is not a disease and therefore there can be no diagnosis nor treatment. There is still a lot of research going on that is funded by very wealthy people who want to age well, or even stop aging. Hundreds of millions are currently being invested in aging research by various billionaires such as the founders of Google, who invested in Calico.

Another important obstacle will be the realization of clinical studies. The use of markers of aging will be questionable and a study of human longevity may need to last at least 25 years to be meaningful. However, a research team recently ruled that this type of study is feasible and that the markers to be used are sufficiently well documented to be valid.

The vast majority of scientists in geroscience agree that research on aging will focus diseases associated with aging for a shorter period at the end of life. This will extend the active, healthy period during which we maintain the independence and abilities necessary to enjoy life. Therefore, there is no question of being “old and sick longer”.

To be old and sick longer?

The modulators of primary aging, the gerosuppressive agents, which we are now discovering, should increase our chances of aging like centenarian people. You should know that the period of chronic disease in centenarians is about 6 to 10% of their life expectancy against about 19% for the North American population. Therefore centenarians, in addition to living longer, experience a much shorter period during which they are affected by diseases associated with aging. A recent study of 3000 people confirms this and in some cases the period of illness is limited to a few months or a few weeks in centenarians.

We look forward to helping you live young longer.


Originally published in the journal Vitalité QC:




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