Is Aging Natural or a Disease That We Can Treat?

By Steve Hill 

Aging is something that we all share, rich or poor; it is something that happens to us all, and we are taught from a young age that it is inevitable. However, some scientists believe that aging is amenable to medical intervention and that such interventions could be the solution to preventing or reversing age-related diseases.

Academics are currently debating whether aging is natural or a pathological disease that we can treat.

In fact, there is now pressure from many academics to classify aging itself as a disease; indeed, doing so could potentially improve funding for aging research and help to speed up progress in finding solutions to age-related diseases.[1] The debate continues, but does it really matter if aging is classified as a disease, or is it largely a matter of semantics?

Fighting a losing battle

Current medical practice sees us trying to treat age-related diseases in the same way we do other diseases; this is the “infectious disease model”, and when it comes to treating age-related diseases, it is a losing battle.

The current approach works like this: as soon as a disease appears, the doctor attacks the disease using everything in the medical armory, and the patient can then continue with life until the next disease happens; this process is repeated until failure. This is an excellent way to deal with infectious diseases, and it has helped to increase life expectancy greatly in the last century; however, there are signs are that this approach is starting to run out of steam.[2-4]

Unfortunately, this “whack-a-mole” approach is a poor choice when it comes to treating the chronic diseases of old age. This is because the damage that the aging processes cause still continues to take its toll; therefore, treating the symptoms will ultimately achieve very little and certainly not cure the disease.


So, given that the aging processes lead to the diseases of aging, it is understandable that scientists are starting to consider aging itself to be a disease. While we do not yet fully understand all the intricacies of aging, we already know a great deal about the individual processes.[5] Certainly, we now know enough about aging to begin developing and testing interventions that directly target the underlying processes in order to prevent or treat pathology.

Treating the underlying processes and repairing their damage, which leads to the familiar diseases of old age, is the basis for the medical approach known as rejuvenation biotechnology, a multidisciplinary field that aims to prevent and treat age-related diseases by targeting the aging processes directly.

Aging is the foundation of age-related diseases

Even if aging is not a disease itself, the individual processes do lead to pathology and age-related diseases, such as cancer, heart disease, Parkinson’s, and Alzheimer’s. So, knowing that these processes create the conditions for diseases to develop, it makes sense to target the processes themselves in order to potentially prevent or treat a slew of age-related diseases at once.

The changes that aging brings vary from one person to another, but the common processes of aging are at work in all of us, albeit with some small variances between individuals. For example, we all suffer wear and tear in our joints due to the loss of cartilage, and we all experience the loss of skin elasticity due to the degradation of elastin and the failure of connective tissues. We all encounter other age-related changes, such as the accumulation of non-dividing senescent cells that cause chronic inflammation and disrupt tissue repair, and we also suffer from the accumulation of metabolic waste products that collect in our bodies over time.

As these changes progress, they eventually lead to the familiar diseases of aging. For example, lipids are critical for the function of our metabolism and are essential as part of our diet; however, over time, these processed lipids begin to accumulate in the blood vessel walls. Macrophages arrive to clear the toxic fatty waste away, but they become immobilized and die. This causes inflammation, attracting more macrophages and continuing the cycle. Ultimately, this debris forms plaques that harden the blood vessels and cause them to narrow; this causes blood pressure to rise and can eventually result in a heart attack or stroke.

This demonstrates that the normal metabolic processes that keep us alive ultimately lead to disease. Importantly, in this case, the early age-related changes that set the scene for disease progression, such as high cholesterol, have no symptoms. Nevertheless, such changes are the precursors of deadly diseases and are considered suitable targets for treatment. The same can be said for the other, more subtle, changes and damages that the aging processes cause.


Age-related conditions, such as arthritis, diabetes, osteoporosis, Alzheimer’s, Parkinson’s and many cancers, all follow this dynamic. Simply put, given the sufficient passage of time, the aging processes will cause us to suffer from multiple diseases. Therefore, we should consider these diseases to be the clinical manifestation of these age-related changes. In fact, medicine has been fighting against age-related changes for a long time, even if it was not obvious. For example, a doctor recommending that his patient should reduce his fat and carbohydrate intake to delay heart disease is already fighting those age-related changes. The diabetic who modifies her diet to better manage blood sugar levels is also doing the same thing.

Some people might contest this point of view, stating that the aging process is “natural” and therefore cannot be a disease. The argument that natural things are always good, the appeal to nature, is a logical fallacy. Such people may see natural and pathological as being mutually exclusive. Thus, what is natural must always be good, and what is pathological is bad, and so it cannot also be natural. This is, of course, false when you consider the meaning of each word. Natural simply means something that follows the normal, established course of events, and pathological means something that is harmful.


So, is aging natural or pathological? Well, by the dictionary definitions, aging can be described as both natural and pathological without contradiction.

Additionally, as it is currently classified, aging could be considered a syndrome, specifically a co-morbid syndrome. This really does describe aging perfectly; it is a group of symptoms that consistently occur together and a condition characterized by a set of associated symptoms. Ultimately, aging is an umbrella term describing a range of pathological changes; it may struggle to be accepted as a disease, but it already qualifies as a syndrome.

However, the question of aging being a disease or not is essentially semantic in nature. What rejuvenation biotechnology seeks to achieve is nothing more than preventing age-related diseases by treating the early stages of pathology, which are considered a natural process. While these early age-related changes have not been given a disease name, they are instrumental in the development of diseases, and surely, when it comes to medical treatment, that is all that matters.


[1] Bulterijs, S., Hull, R. S., Björk, V. C., & Roy, A. G. (2015). It is time to classify biological aging as a disease. Frontiers in genetics, 6.

[2] Crimmins, E. M. (2015). Lifespan and healthspan: Past, present, and promise. The Gerontologist, 55(6), 901-911.

[3] Olshansky, S. J., Passaro, D. J., Hershow, R. C., Layden, J., Carnes, B. A., Brody, J., … & Ludwig, D. S. (2005). A potential decline in life expectancy in the United States in the 21st century. New England Journal of Medicine, 352(11), 1138-1145.

[4] Reither, E. N., Olshansky, S. J., & Yang, Y. (2011). New forecasting methodology indicates more disease and earlier mortality ahead for today’s younger Americans. Health Affairs, 10-1377.

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

Starving Cancer Cells to Death

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Bile Acids Turn Cells from Fat-storing to Fat-burning

Obesity arises from an imbalance between energy intake and energy expenditure. As a result, current treatments try to decrease calorie intake and/or increase energy expenditure.

The problem is maintaining long-term effects. Non-invasive treatments, like diets and drugs that reduce intestinal ingestion are widely unpopular among patients, while bariatric surgery seems to be the only reliable treatment for obese people, despite being both expensive and invasive.

But now a new study led by the lab Kristina Schoonjans at EPFL, suggests that a specific group of bile acids could directly burn away the lipids in our fat depots, effectively making it a new therapy against obesity.

Bile acids are important constituents of bile, a yellow-green fluid produced in the liver that is stored in the gallbladder and secreted into the intestines during a meal. Bile emulsifies dietary fat into tiny globules that can be broken down by digestive enzymes to be absorbed by the intestine.

The EPFL scientists discovered that bile acids can turn fat-storing cells into fat-burning ones. This process is called thermogenesis (literally, “heat production”) and it helps maintain body temperature in cold environments.

There are three different types of fat cells: white fat cells, which store energy; brown fat cells, which expend energy; and the so-called “beige” fat cells, which are functionally related to brown cells while being located in typically white-fat depots.

Beige cells have recently attracted a lot of attention, especially because adults have very low numbers of active brown adipocytes that burn energy. But what can turn a white cell into a beige one – a process called “beiging” – and shift the balance from fat-storing to fat-burning?

The work of Schoonjans’ team suggests that this process can be coordinated by secondary bile acids, metabolites that are generated by our liver and gut bacteria.

The study shows that activating the bile acid receptor TGR5 with molecules that mimic the action of bile acids (so called “mimetics”) induces a remodeling of white fat cells into beige fat cells. The bile acids accumulate in the blood and interact with the TGR5 receptor on white fat cells to change their metabolic function.

This is more than a mere change of color, as the researchers also found that these bile acids increase the number of mitochondria in the new fat cells. This indicates higher energy consumption in the new, beige fat cells.

The bile-acid mimetics also triggered lipolysis, the first step in fat degradation, allowing the fat cells to use fatty acids as their main fuel source.

The study provides a direct connection between bile acids and fat loss and envisions novel therapeutic intervention in obese people. “We showed that bile acids are much more than a soap for digestion,” says Kristina Schoonjans. “When their concentration in the blood reaches a certain level, it can turn up the thermostat and increase fat burning for energy and heat production”.

“What is exciting about our discovery is that low concentrations of TGR5-selective molecules are sufficient to promote the beiging of white fat-storing cells, thereby bypassing the need to increase the total bile acid pool,” says Laura Velazquez, first-author of the paper.

“Moreover, this study highlights mitochondrial fission —or the splitting of mitochondria— as a pivotal mechanism by which bile acids turn white fat into beige fat,” adds Alessia Perino, co-first author. “It will be interesting to explore if mitochondrial fission is a universal mechanism for beiging in response to other stimuli”.

This article has been republished from materials provided by EPFL. Note: material may have been edited for length and content. For further information, please contact the cited source.


Velazquez-Villegas, L. A., Perino, A., Lemos, V., Zietak, M., Nomura, M., Pols, T. W., & Schoonjans, K. (2018). TGR5 signalling promotes mitochondrial fission and beige remodelling of white adipose tissue. Nature Communications, 9(1). doi:10.1038/s41467-017-02068-0

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