NUTRITION AND AGEING

Many animal studies have shown that life expectancy can be extended by restricting food intake. It is, however, not known whether the ageing process in humans can be altered by nutrition.

The ageing process

The process of ageing is not well understood. While wear and tear may play a role, it is an insufficient explanation for the causation of ageing. The 'programmed' theories depend on inbuilt biological clocks that regulate lifespan, and involve genes that are responsible for controlling signals that influence various body systems. The 'error' theories involve environmental stressors that induce damage (e.g. mitochondrial DNA damage or cross-linking).

The search for a single cause of ageing, e.g. a single gene defect, has been replaced by the view that ageing is a complex multifactorial process that involves an interaction between genetic, environmental, and stochastic (random damage to essential molecules) causes. The following theories have been suggested:

Molecular theories

Gene regulation - ageing, for example, results from changes in expression of genes that regulate both development and ageing. An insulin-like signalling pathway has been linked to the lifespan of worms, flies and mice (activation of a transcription factor in response to reduced insulin-like signalling prolongs lifespan).
Codon restriction - inadequate mRNA translation resulting from inadequate decoding of codons in mRNA.
Error catastrophe - errors in gene expression result in abnormal proteins.
Somatic mutation - cumulative molecular damage mainly to genetic material.
Dysdifferentiation - cumulative random molecular damage detrimentally affects gene expression.

Cellular theories

Cellular senescence-telomere - an increase in senescent cells occurs from:
(a) Loss of telomeres, which is known to occur with ageing (with each cell division a small amount of DNA is necessarily lost at each end of the chromosome). Activation of the telomerase enzyme regenerates telomeres, prevents senescence (replicative senescence) and immortalizes cell cultures. Cancer cells are known to activate telomerase.
(b) Damage due to a variety of other factors, including DNA damage (stress-induced senescence).
Free radical - production of free radicals during oxidative metabolism which damages fat, protein and DNA.
Wear and tear - cumulative damage from normal injury/stress which is unable to repair itself.
Apoptosis theory - programmed cell death due to genetic events

System theories

These theories involve loss in the function of neuroendocrine or immune systems with consequent age-related physiological changes and an increase in autoimmunity.

Whole body metabolism and energy expenditure theory proposes that there is a fixed limit to the cumulative energy expenditure and metabolism during a lifetime, so that if this limit is reached quickly the lifespan is short. Energy restriction in rodents reduces energy expenditure and prolongs lifespan, but there is a lack of studies in primates or humans.

Evolutionary theories

Cumulative mutation - mutations that accumulate during the lifetime act in older age rather than during the active reproductive period (for which there is evolutionary selection), producing pathology and senescence. The theory was initially based on the observation that Huntington's disease, a dominant lethal mutation which typically manifests itself between 35 and 55 years, allows affected individuals to reproduce.
Disposable soma - the somatic body is maintained to ensure reproductive success, after which it is disposable. Factors that may enhance reproductive success may have detrimental effects on ageing - a possible example being androgen secretion, which may be beneficial to reproduction but potentially detrimental with development of prostatic cancer and cardiovascular disease in later life.
Several of these theories have strong nutritional components. Disability and dependency in older humans are at least partly due to poor nutrition, and correction of deficiencies or nutrient imbalances can prevent the decline in function from falling below the disability threshold. In this way some loss of function may be prevented or reversed, especially if other measures, such as physical activity, which increases muscle mass and strength are undertaken.

Early origins of health and disease in older adults

A low birth weight (and or length) is associated with reduced height, as well as reduced mass and fat-free mass in adult life. These relationships can occur independently of genetic factors, since the smaller of identical twins becomes a shorter and lighter adult. Relationships have also been reported between growth of the fetus and a variety of diseases and risk factors for disease in adults and older people. These include cardiovascular disease, especially ischaemic heart disease, hypertension, and diabetes, and even obesity and fat distribution. However, the strength of association for some of these conditions is in some cases weak. Animal studies involving dietary modifications during pregnancy or early postnatal life (e.g. protein, zinc), even within the normal range of intakes, have clearly demonstrated effects, such as hypertension, which persist through the lifetime of the offspring, and even their offspring. The extent to which these apply to humans is uncertain, and the mechanisms are poorly understood. Since relationships with cardiovascular disease in old age have also been related to growth in the first few years of life as well as starvation during puberty, it is likely that cumulative environmental stresses, including nutritional, from the time of implantation of the fertilized egg, to fetal and postnatal growth and development, and adult life, summate to produce an overall disease risk.

Nutritional requirements in the elderly

These are qualitatively similar to the requirements of younger adults, but as energy expenditure is less, there is a lower energy requirement. However, maintaining physical activity is required for the overall health of the elderly.

The daily energy requirement of 'elderly people' (aged 60 and above, irrespective of age) has been set to be approximately 1.5 × BMR. The BMR is reduced, owing to a fall in the fat-free mass, from an average of 60 kg to 50 kg in men and from 40 kg to 35 kg in women. In disease, physical activity is usually decreased. The diet should contain approximately the same proportions of nutrients, and essential nutrients are still required. Although disabilities and diseases are common in older people, the RNIs are intended for healthy people without disease. The nutrient requirements for those with disease are less well defined.

Nutritional deficits in the elderly are common and may be due to many factors, such as dental problems, lack of cooking skills (particularly in widowers), depression and lack of motivation. Significant malnourishment in developed countries is usually secondary to social problems or disease. In the elderly who are institutionalized, multiple nutrient deficiencies are common. Vitamin D supplements may be required because often these people do not go into the sunlight. Owing to the high prevalence of osteoporosis in elderly people, daily calcium intake of 1-1.5 g/day is often recommended.