The topic of healthspan is increasingly being raised in the popular media, but what does it really mean? Simply put, healthspan means the period of your life in which you remain healthy and free from age-related diseases. The Roman poet Virgil once said “The greatest wealth is health”, so the concept of healthspan was something valued as far back in time as then.

Today, we are going to take a look at how we have been trying to increase human healthspan in the past and what science is doing now to take us to new frontiers of health through a new approach to medicine called rejuvenation biotechnology.

So, why is healthspan becoming such a popular saying, and why is it appearing frequently in articles and in other media now? Quite simply, the advances in our understanding of the aging processes and our ability to do something about them has reached the point at which taking measures to increase healthspan is now plausible.

All approaches to healthspan are not equal

People have been attempting to increase healthspan for decades. Fitness and nutrition are excellent ways to help slow the ravages of time, and they are currently the best methods we have personally available to us while more robust therapies are developed. While they are necessary, they are insufficient; aging eventually catches up and diseases develop, despite the best of efforts.







Supplements are another common approach to improving healthspan. Unfortunately, a lack of data for many supplements and questionable marketing makes supplement use of questionable value in the pursuit of healthspan. Supplements are effectively unregulated drugs, and they affect us in a similar way that controlled medicines do; some may, in fact, be useful in improving healthspan, but the data for humans is simply not good enough to be certain.

Even drugs like metformin, a diabetic drug, only partially maintain health. Some studies have shown that it might be useful if taken by non-diabetics to help control blood glucose levels; this may slightly slow down aging, increasing healthspan[1]. Unfortunately, this approach is incomplete; because metformin does not fully address any of the fundamental aging processes, it cannot possibly prevent the broad spectrum of age-related diseases to deliver robust healthspan.

Think of it like a car. If metformin was fuel and using it was like filling your tank with petrol, but at the same time you had a hole in the tank leaking fuel, and your brake fluid was also leaking, and your transmission and engine oil were running dry, metformin could do nothing whatsoever about these other problems.Supplements, metformin, and even diet and exercise do not fully maintain human health because they do not address all the things that go wrong during aging. At best approaches like this can only deliver modest healthspan.

To effectively maintain health and thereby increase healthspan, we must choose a better way.

There could be a better way







Fortunately, there is potentially a comprehensive way to allow people to enjoy good health for longer: rejuvenation biotechnology.

The objective of rejuvenation biotechnology is to help us to maintain our health by keeping our body functionally younger, and so remain free from the diseases of aging by periodically repairing the damage that the aging processes do. These aging processes, known as the hallmarks of aging, lead to damage; that damage gradually reaches pathological levels, and then the familiar diseases of aging develop[2]. The graphic below shows the main processes of aging and describes briefly what each is.

The strategy here is simple; by targeting these processes directly, science can prevent the development of age-related diseases before they appear, comprehensively maintaining health. The graphic below helps to visualize the concept; the aging processes are the natural and pathological series of events and form the foundation of age-related diseases. By attacking those processes, science seeks to prevent or even reverse those diseases.







An example of rejuvenation biotechnology that addresses one of the core aging processes is senolytics, a therapy that removes unwanted and toxic senescent cells from the body that accumulate with age. These excessive numbers of senescent cells cause inflammation, reduce our ability to heal wounds, impede tissue repair, and encourage age-related diseases to develop[3-5].

Thus, the most direct and logical approach is to remove them in order to improve healthspan. Indeed, this is the exact outcome observed in animal studies; removing these problem cells improved healthspan and tissue repair[6] while improving the aged cardiovascular system[7].

Now, you might be thinking that senolytics, like metformin, also does not address the entire range of aging processes, and you would be right. However, the key difference between metformin and senolytics is that the latter approach is part of a comprehensive panel of rejuvenation biotechnology therapies that treat all of the aging processes. Rejuvenation biotechnology has a proposed way to address each of the above hallmarks of aging and aims to deliver robust healthspan by deploying them together.

Conclusion

By attacking the root causes of aging through periodic repair, we can improve healthspan more thoroughly and completely than with incomplete, partial methods such as supplements and metformin. It is short-sighted to use lesser methods when we have the possibility of rejuvenation biotechnology on the table, which has the potential to completely maintain human health and thereby considerably extend healthspan.







Literature

[1] Bannister, C. 1., Holden, S. E., Jenkins‐Jones, S., Morgan, C. L., Halcox, J. P., Schernthaner, G., … & Currie, C. J. (2014). Can people with type 2 diabetes live longer than those without? A comparison of mortality in people initiated with metformin or sulphonylurea monotherapy and matched non‐diabetic controls. Diabetes, Obesity and Metabolism, 16(11), 1165-1173.

[2] López-Otín, C., Blasco, M. A., Partridge, L., Serrano, M., & Kroemer, G. (2013). The hallmarks of aging. Cell, 153(6), 1194-1217.

[3] Freund, A., Orjalo, A. V., Desprez, P. Y., & Campisi, J. (2010). Inflammatory networks during cellular senescence: causes and consequences. Trends in molecular medicine, 16(5), 238-246.

[4] Coppé, J. P., Desprez, P. Y., Krtolica, A., & Campisi, J. (2010). The senescence-associated secretory phenotype: the dark side of tumor suppression. Annual review of pathology, 5, 99.







[5] Childs, B. G., Baker, D. J., Wijshake, T., Conover, C. A., Campisi, J., & van Deursen, J. M. (2016). Senescent intimal foam cells are deleterious at all stages of atherosclerosis. Science, 354(6311), 472-477.

[6] Zhu, Y., Tchkonia, T., Pirtskhalava, T., Gower, A. C., Ding, H., Giorgadze, N., … & O’Hara, S. P. (2015). The Achilles’ heel of senescent cells: from transcriptome to senolytic drugs. Aging cell, 14(4), 644-658.

[7] Roos, C. M., Zhang, B., Palmer, A. K., Ogrodnik, M. B., Pirtskhalava, T., Thalji, N. M., … & Zhu, Y. (2016). Chronic senolytic treatment alleviates established vasomotor dysfunction in aged or atherosclerotic mice. Aging cell.