Ageing is a biological process characterized by a progressive decline in physiological function. This natural series of changes is distinct from disease, though the risk for certain health conditions increases as the body ages. It represents the cumulative effect of various molecular and cellular changes that impact tissues and organs. The rate of ageing differs among individuals, reflecting the combination of genetic and environmental factors.
The Biological Mechanisms of Ageing
Several interconnected processes drive the functional decline associated with ageing. One involves telomeres, the protective caps at the ends of our chromosomes, similar to the plastic tips on shoelaces. With each cell division, these telomeres become progressively shorter. This shortening eventually signals cells to stop dividing, a state that contributes to the ageing of tissues.
This cessation of cell division leads to cellular senescence. Senescent cells are not dead but enter a state of irreversible growth arrest. While they no longer replicate, they remain metabolically active and can release inflammatory proteins. This secretion, known as the senescence-associated secretory phenotype (SASP), can affect neighboring cells and contribute to low-grade, chronic inflammation.
Another mechanism is mitochondrial dysfunction. Mitochondria are organelles that generate most of the cell’s chemical energy. With age, mitochondrial efficiency can decline, leading to reduced energy production and an increase in reactive oxygen species (ROS), or free radicals. This imbalance contributes to oxidative stress, which damages cellular components like DNA, proteins, and lipids.
The accumulation of this cellular damage impairs the ability of tissues to regenerate and function. A decline in mitochondrial quality control mechanisms, which are responsible for removing damaged mitochondria, further exacerbates this cycle of dysfunction.
Physical and Cognitive Transformations
The microscopic changes in our cells manifest as observable physical and cognitive transformations. In the integumentary system, including skin and hair, these changes are often the most visible. The skin’s outer layer, the epidermis, thins, and the production of collagen and elastin in the dermis decreases, leading to reduced elasticity and wrinkles. Pigment-producing cells called melanocytes also decline, causing hair to lose its color and turn grey or white.
The musculoskeletal system experiences a gradual decline in muscle mass and bone density. The age-related loss of muscle tissue, known as sarcopenia, often begins after age 50, with an estimated loss of 0.5-1% of muscle mass per year. Bone mineral density can also decrease, a condition called osteopenia, which can precede more serious bone loss. These conditions often occur together, increasing the risk of falls and fractures.
Metabolic changes also accompany ageing. The basal metabolic rate, the number of calories burned at rest, tends to slow down. This is partly due to the decrease in muscle mass, as muscle is more metabolically active than fat. The body’s ability to regulate temperature can also be affected by reduced sweat gland production.
Cognitive function also undergoes age-related transformations, which are distinct from dementia. Normal cognitive ageing involves a modest decline in “fluid” abilities like processing speed, problem-solving, and working memory. In contrast, “crystallized” abilities, such as vocabulary and accumulated knowledge, often remain stable or even improve with age.
Theories Explaining Why We Age
Scientists have proposed several theories to explain why ageing occurs. These theories fall into two main categories: programmed theories and damage-based theories. Each offers a different perspective on whether ageing is a predetermined process or an unavoidable consequence of life.
Programmed theories suggest that ageing is a genetically determined process. One idea is that ageing follows a biological timetable, much like growth and development in early life, regulated by specific genes switching on and off. Another concept, antagonistic pleiotropy, hypothesizes that certain genes beneficial for reproduction in youth have negative effects that manifest later in life.
In contrast, damage or error theories posit that ageing is the result of accumulated damage that overwhelms the body’s repair systems over time. The free radical theory, for example, suggests that the accumulation of damage from reactive oxygen species produced during normal metabolism is a primary driver of ageing. Similarly, the DNA damage theory proposes that the lifelong accumulation of unrepaired genetic alterations leads to a gradual decline in cellular function.
Factors Influencing the Rate of Ageing
The rate at which an individual ages is influenced by a combination of genetic and external factors. A person’s genetic makeup helps determine lifespan and susceptibility to age-related conditions. Studies estimate that genetics account for 10-25% of the variability in human lifespan, influencing cellular repair mechanisms and disease predisposition.
Environmental exposures throughout life also have an impact. Chronic exposure to ultraviolet (UV) radiation from the sun is a main factor in the visible ageing of skin, damaging its connective tissues. Other environmental pollutants can contribute to oxidative stress and inflammation, which are linked to accelerated ageing and increased risk for age-related diseases.
Lifestyle choices are modifiable factors that influence the ageing process. A balanced diet, regular physical activity, adequate sleep, and stress management can all affect the rate of biological ageing. For instance, regular exercise is associated with slower epigenetic ageing, while smoking is linked to an acceleration of this process. These lifestyle factors can influence molecular processes, including DNA methylation, which can alter how genes are expressed without changing the DNA sequence itself.