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Aging & Longevity

Are Senescent Cells Turning Your Hair Gray? A New Aging Theory

The theory says our brain allocates resources to energy-consuming senescent cells at the body’s expense, accounting for gray hair, muscle shrinkage, and other signs of aging.

By Griffin Dean

Key Points: 

  • Below our conscious awareness, molecular damage accumulates within and across our cells, tissues, and organs. 
  • Molecular damage promotes the buildup of energetically expensive senescent cells, which signal the brain to redistribute energy expenditures. 
  • The redistribution of energy effectively destroys the body from within, leading to aging and age-related diseases. 

Our brain is the ultimate information integrator, attempting to predict environmental conditions to evoke a mind state that ensures our survival. Invisible to our conscious awareness, it communicates with the rest of our body, determining where to allocate finite energy. According to the brain-body energy conservation (BEC) theory of aging, precious energy is subverted to senescent cells, which are cells that accumulate in our body as we age. 

Aging Begins With an Imperfect Machine 

Behind the curtain, billions of trillions of biochemical reactions are allowing you to read this sentence. Such an unimaginable number of reactions, occurring each second over many years, leaves ample room for error. These errors lead to molecular damage, such as DNA damage, that triggers repair responses. Repair responses require energy, specifically cellular energy, known as ATP (adenosine triphosphate). 

Senescent Cells

Molecular damage also induces protective responses, such as senescent cells. In response to molecular damage, our cells enter a senescent state, taking the form of senescent cells. Because they are incapable of multiplying, senescent cells are thought to protect against cancerous cell growth. However, with age, studies show that our immune system fails to get rid of senescent cells, and they accumulate. 

Senescent cells are highly metabolically active — hypermetabolic — and secrete a host of energetically expensive proteins known as the SASP (senescence-associated secretory phenotype). The SASP includes pro-inflammatory signaling proteins that circulate through the body and contribute to chronic inflammation. Critically, the signaling proteins secreted by senescent (and other damage-ridden) cells alert the brain to where energy needs to be allocated.  

(Shaulson et al., 2025) Progression of Brain-Energy Conservation and Aging. 1) Molecular damage leads to the accumulation of senescent cells. 2) Senescent cells and the SASP contribute to age-related inflammation (inflammaging). 3) The brain senses the SASP factors and 4) responds by changing body-wide physiology to conserve energy, eventually 5) manifesting in aging.

The Brain Mediates the Aging of the Body 

One way the brain obtains information from the body is by receiving signaling proteins, such as SASP factors, which bind to specific receptors. It then integrates the input it receives from signaling proteins, along with information from other sources (including environmental and social cues), to determine an output. This output comes in the form of hormones and neural signals that can alter our physiology in ways that change our mood and behavior. 

According to the BEC theory of aging, signaling proteins such as SASP factors tell the brain that energetically expensive repair and protective mechanisms (e.g., senescent cells) are present in the body. In response, the brain suppresses energetically costly behaviors like physical activity, food seeking, reproduction, and socialization. It also triggers the breakdown (catabolism) of muscle, the biggest consumer of ATP in the body. Along those lines, the brain reduces the production of growth and sex hormones, as sexual reproduction and growth are energetically costly and unnecessary for survival. 

Ultimately, the redistribution of energy leads to age-related conditions like hair graying, reduced muscle mass and strength, stiff arteries, neurodegeneration, and a weak immune system. The saved energy is then allocated to senescent cells, protein signaling, chronic inflammation, and other hypermetabolic states induced by molecular damage.

(Shaulson et al., 2025) Consequences of Energy Recalibration. Via neural and hormonal outputs, the brain redistributes whole-body energy expenditure by shutting down energetically costly organs and altering behavior to reduce ATP-consuming activities, like reproduction, movement, and metabolism. This ultimately leads to chronic age-related diseases and frailty.

How to Speed Up or Slow Aging 

Based on the BEC theory of aging, there are several triggers of accelerated aging, along with interventions capable of slowing or preventing the aging process. Inducers of hypermetabolic states, such as psychosocial stress, toxins, and infections, can accelerate the aging process. On the other hand, the following interventions contribute to counteracting aspects of the hypermetabolic state: 

  • Senolytics: These are compounds that directly eliminate senescent cells, reducing chronic inflammation and protein signaling to the brain. Naturally occurring senolytics include fisetin and quercetin. 

  • Rapamycin: A repurposed drug that reduces protein synthesis, one of the largest consumers of ATP, by inhibiting the nutrient sensor mTOR. In doing so, it decreases the production of SASP factors and other signaling proteins. It also acts as a senolytic by reducing senescent cell accumulation. 

  • Caloric restriction: Eating fewer calories without malnourishment has similar effects to rapamycin, as it reduces protein synthesis, SASP factors, and senescent cells. Caloric restriction also activates energy-conservation responses, such as preserving muscle mass. 

  • Dilution: Diluting the blood through interventions such as plasma dilution reduces the concentration of signaling proteins that activate the brain’s reallocation of energy. 

  • Monoclonal antibodies: These are antibodies that can be synthesized to target and block specific SASP factors and signaling proteins before they can bind to brain cells. 

  • Exercise: According to the BEC theory of aging, exercise activates energy-conserving responses while increasing the capacity to utilize energy. For example, it promotes the generation of new mitochondria, the primary generators of ATP.

(Shaulson et al., 2025) Aging Accelerators and Geroscience Interventions. Aging accelerators are shown on top in red, while geroscience interventions are shown on the bottom in green.

Are Senescent Cells Turning Your Hair Gray?

According to the BEC theory of aging, the brain allocates energy to senescent cells at the expense of functions that are considered non-essential. Among these non-essential functions is melanin production in hair follicles. Thus, in the early stages of aging, the brain allocates energy in support of the hypermetabolic state of senescent cells, redirecting energy from the pigmentation of hair. 

However, when it comes to senescent cells and the BEC theory of aging, hair graying should be of little concern. As senescent cells continue to build up and higher concentrations of SASP factors reach the bloodstream, the brain is forced to allocate even more energy to senescent cells. With non-essential functions like hair pigmentation already turned off, energy must be gained by shrinking energetically expensive tissues, like muscle.

Eventually, this paradigm is said to lead to age-related conditions like cardiovascular disease, neurodegenerative disorders, and frailty, whereby the body becomes more vulnerable to adverse health outcomes. Some of these age-related conditions are the leading causes of death in the United States and worldwide. In other words, according to the BEC theory of aging, yes, senescent cells are turning your hair gray, and they are also causing you to age. 

Source

Shaulson, E. D., Cohen, A. A., & Picard, M. (2024). The brain–body energy conservation model of aging. Nature Aging, 4(10), 1354-1371. https://doi.org/10.1038/s43587-024-00716-x

References

Song, P., An, J., & Zou, H. (2020). Immune Clearance of Senescent Cells to Combat Ageing and Chronic Diseases. Cells, 9(3), 671. https://doi.org/10.3390/cells9030671

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