Is Aging a Disease?
The fact that aging is not a sickness is one reason against treating it. To some part, this viewpoint is based on the fact that the term "aging" can refer to a variety of things. The first is the sensation of time passing. Another advantage of living a long life is the opportunity to gain experience and wisdom. To distinguish these positive elements, biologists use the term "senescence" to describe the increasing frailty and danger of disease and death that accompany aging. To put it another way, the topic at hand is this: Is human aging a disease?
A comparison of a specific situation to good health has been used to define sickness. Seems to be a person's condition typical of a certain gender or age group? For example, having ovaries is beneficial to a woman but not to a guy. Similarly, muscle atrophy in a 20-year-old may suggest significant disease, but not in a 90-year-old. Given that everyone who lives long enough will ultimately experience senescence, I can understand why some people believe it is a natural and not abnormal condition. Still, as someone who studies the molecular causes of aging, it's difficult not to regard it as an illness.
Senescence is a molecular, cellular, and physiological process characterized by dysfunction and degeneration. Aging illnesses are caused by this endemic dysfunction. Even if one lives a long and healthy life, free of cancer and type 2 diabetes, one still dies, and one dies of something. Furthermore, aging appears to have no actual purpose in evolutionary terms, implying that it does not contribute to evolutionary fitness. So, why has aging progressed? J. B. S. Haldane and later Peter Medawar of University College London, as well as American scientist George C. Williams of the State University of New York, Stony Brook, formulated the primary theory in the 1930s.
It claims that aging reflects a decrease in the force of natural selection against late-life mutations that cause harm. An inherited mutation that causes severe pathology in childhood reduces the chances of reproduction, and hence the population will vanish. Another mutation with identical consequences that appears after a person's reproductive years, on the other hand, is more likely to persist. Natural selection may even favor mutations that improve fitness early in life but have a negative impact on health later in life. This is due to the fact that genes' effects on fitness are substantially stronger in early life. As a result, populations accrue mutations that have negative late-life consequences, and the aggregate of these consequences is aging. Here, evolutionary biology sends a somber warning about humanity: Aging is primarily a hereditary disease with multiple causes. Only in that we all inherit it does it differ from other hereditary disorders. This universality does not rule out the possibility of aging as a disease. Instead, it's a unique type of illness.
Another concern with reframing aging as an illness is that the elderly would be stigmatized. Perhaps, but the identification of late-onset Alzheimer's disease as a pathology generated an ethical necessity for research into the condition's causes and treatments. It's reasonable to assume that the same is true with aging. A redefinition like this would also assist to combat the scourge of so-called anti-aging medicine practitioners swindling the elderly. The Food and Drug Administration (FDA) ensures the safety and efficacy of medical treatments in the United States. Because aging is not considered a disease, orally taken medications promoted as anti-aging remedies (such as resveratrol) are subject to to the FDA's far laxer dietary supplement standards. Redefining aging as an illness would not only re-energize treatment research, but it would also put a stop to snake-oil salesmen.
The prospect of curing aging isn't just a pipe dream. One of the most astounding discoveries in biology in recent decades is that it is possible to halt aging in experimental animals. Surprisingly few people are aware of this. It is, in reality, simple. My own research focuses on the Caenorhabditis elegans nematode worm, which is commonly utilized in genetic studies. These critters age and perish in two to three weeks, even under ideal culture circumstances. In the early 1980s, American biologist Michael Klass discovered that slowing aging in C. elegans might be accomplished by modifying their DNA. As a result, the worms live significantly longer and remain more youthful and healthy. The current record for increasing C. elegans lifetime is an incredible tenfold increase, which was achieved by a team at the University of Arkansas. It has now been discovered that genes that affect worm aging also affect aging in mammals (in mice, to be precise). We can learn about the fundamental biology of aging by discovering genes that affect aging rates.
We can investigate how genes influence aging-related processes. A nutrient-sensitive signaling network that includes insulinlike growth factor 1 (IGF-1) and an intracellular protein called TOR is linked to many aging genes. Slowing growth, increasing stress tolerance, and increasing lifespan can all be achieved by dampening the signals that this network transmits. The goal of research in my group and others at University College London's Institute of Healthy Aging is to figure out how this network controls aging. To do so, you must first answer the basic question: What causes aging? It could be due to a buildup of molecular damage, according to one idea. Another factor is excessive biosynthesis; many genes and processes that affect aging are linked to biosynthesis and growth control. However, the truth remains a mystery.
Here is a short video about "should we stop aging?":