Nutritional Modification

It is clear that diet contributes in substantial ways to the development of age-related diseases and that modification of the diet can contribute to their prevention and thus help to improve the quality of life in old age. Macronutrient intake levels can play a significant part in the progression of age-related diseases and affect the quality of life. For example, the total and proportional intakes of polyunsatu-rated fatty acids and saturated fatty acids in the Western diet may have an effect on the incidence of atherosclerosis and cardiovascular diseases.

Our dietary requirements also change as we age and if such changes are not properly addressed this could lead to suboptimal nutritional status. This challenge is compounded by a decrease in the body's ability to monitor food and nutrient intakes. Dietary intake and requirements are complex issues, intertwined with many health and life style issues. However, most research points towards the need for

Biomolecule damaging agents e.g., free radicals

Defense mechanisms that aim to prevent or repair biomolecule damage

e.g., antioxidants

Biomolecule damage may still occur

Nucleic acids

Proteins

Lipids

Altered:

Altered:

Membrane peroxidation and

structure (mutation)

protein structure

destruction leads to

gene expression

biological activity

rigidity of cell membranes,

transcription and translation

Protein aggregation

loss of selective permeability,

Activation of proteolytic enzymes

and loss of membrane integrity.

Protein aggregation

Aggregation with proteins,

DNA - protein cross-links

pigments, and metal ions to

form lipofuscin

Biomolecule damage

Biomolecule damage

Cell with altered biological function - aging cell by chance by chance

Cancer cell

Cell death

Decline in tissue and organ functions

Deveiopment of age-reiated disorders

Cancer cell

Normai ceii

Death

Figure 2 Biomolecule damage and the aging process. (Reproduced with permission from Barnett YA (1994) Nutrition and the aging process. British Journal of Biomedical Sciences 51: 278-287.)

a varied diet as we age, with an increased emphasis on micronutrient intake levels.

An exemplary diet for healthy aging can be found in the traditional diet of Okinawa, Japan. Okina-wans are the longest-living population in the world according to the World Health Organization, with low disability rates and the lowest frequencies of coronary heart disease, stroke, and cancer in the world. This has been attributed to healthy life style factors such as regular physical activity, minimal tobacco use, and developed social support networks as antistress mechanisms, all of which are underpinned by a varied diet low in salt and fat (with monosaturates as the principal fat) and high levels of micronutrient and antioxidant consumption.

Vitamins and micronutrients The mechanisms by which certain vitamins and micronutrients mediate their protective effect in relation to a number of age-related disorders is based in large part upon their abilities to prevent the formation of free radicals or scavenging them as they are formed, either directly (e.g., vitamins C, E, and ^-carotene) or indirectly (e.g., copper/zinc superoxide dismutase, manganese-dependent superoxide dismutase, selenium-dependent glutathione peroxidase). Table 4 summarizes the effects that a variety of vitamins and micro-nutrients can have on age-related disease. Only by exploring more fully the underlying molecular mechanisms of aging and the major classes of anti-oxidants will it be possible to establish the role

Table 3 Major age-related alterations in vivo and the resultant pathological conditions

Body system

Pathological changes

Cardiovascular

Atherosclerosis, coronary heart disease,

hypertension

Central nervous

Reduction of cognitive function,

system

development of various dementias

(e.g., Alzheimer's disease and

Parkinson's disease)

Endocrine

Noninsulin-dependent diabetes,

hypercortisolemia

Hemopoietic

Anemia, myelofibrosis

Immune

General decline in immune system

function, particularly in T cells

Musculoskeletal

Osteoporosis, osteoarthritis, skeletal

muscle atrophy

Renal

Glomerulosclerosis, interstitial fibrosis

Reproductive

Decreased spermatogenesis,

hyalinization of semeniferous tubules

Respiratory

Interstitial fibrosis, decreased vital

capacity, chronic obstructive

pulmonary disease

Sense organs

Cataracts, senile macular degeneration,

diabetic retinopathy

All systems

Cancer

Vitamin or micronutrient

Vitamins B6, E copper, zinc, and selenium

Vitamins C, E, and carotenoids

Carotenoids and zinc

Selenium

Vitamin C, ^-carotene, a-tocopherol, and zinc of, and develop strategies for using various classes of antioxidants to reduce the effects of aging. Other dietary components may also have a beneficial effect in preventing or delaying the onset of age-related disease. For example, as a deterrent against the onset of osteoporosis, adults should ensure adequate calcium and vitamin D intakes.

Dietary energy restriction The effect of caloric restriction on life span has only been convincingly demonstrated in rodents to date. Feeding mice and rats diets that are severely deficient in energy (about 35% of that of animals fed ad libitum, after the initial period of growth) retards the aging of body tissues, inhibits the development of disease and tumors, and prolongs life span significantly. The exact mechanism of action of dietary energy restriction remains to be elucidated, but may involve modulation of free radical metabolism, or the reduced hormone excretion that occurs in dietary restricted animals may lower whole body metabolism resulting in less 'wear and tear' to body organs and tissues.

Current investigations into the effects of dietary energy restriction (of about 30%) on the life spans of primates, squirrels, and rhesus monkeys continue. Caloric restriction in rhesus monkeys leads to reductions in body temperature and energy expenditure consistent with the rodent studies. These investigations should have direct implications for a dietary energy restriction intervention aimed at slowing

Table 4 Effects of vitamins and micronutrients on age-related disorders

Vitamin or micronutrient

Vitamins B6, E copper, zinc, and selenium

Vitamins C, E, and carotenoids

Carotenoids and zinc

Selenium

Vitamin C, ^-carotene, a-tocopherol, and zinc

Selenium, copper, zinc, lithium, vanadium, chromium, and magnesium Vitamins B12, B6, and folate

Chromium

Possible effect on age-related disorder

Impairment of immune function in older humans if inadequate amounts Increased amount in the diet is associated with delayed development of various forms of cataract Protective effect against the development of lung cancer in smokers Dietary supplementation associated with a decreased risk of age-related macular degeneration Absolute or relative deficiency associated with development of a number of cancers (not breast cancer) Dietary supplementation may decrease the rate of development of atherosclerosis Dietary deficits are associated with an increased risk of cardiovascular disease

Adequate levels throughout a lifetime may prevent some of the age-related decrease in cognitive function Deficiency is associated with an increased risk of the development of type 2 diabetes mellitus down the aging process in humans, should any humans wish to extend their life span at such a cost. Once the mechanisms of effects of caloric restriction on longevity are understood it may be possible to develop drugs that act through these mechanisms directly, mitigating the need for diets that interfere with the quality of life.

Molecular Biological Interventions and the Aging Process

Accelerated aging syndromes show degenerative characteristics similar to those appearing during normal aging. The mutations leading to these disorders are being identified and their roles in the aging process are being elucidated. Examining differences in the genetic material from normal elderly people and those with progeria should help to give a better understanding of the genetic mechanisms of aging. Identification of a control gene or genes that inhibit the action of the genes producing the progeroid phe-notype might make it possible to slow down aberrant protein production in normal people as well.

As an example, the genetic defect that predisposes individuals to the development of Werner's syndrome has now been elucidated. Individuals with this disease carry two copies of a mutant gene that codes for a helicase enzyme (helicases split apart or unwind the two strands of the DNA double helix). DNA helicases play a role in DNA replication and repair.

In light of the biological function of these enzymes it has been proposed that the reason for the premature aging in Werner's syndrome is that the defective helicase prevents DNA repair enzymes from removing background DNA damage, which thus becomes fixed as mutations, with consequent deleterious effects on cellular function. It remains to be determined whether increasing the fidelity or activity of helicases in cells will extend their life span.

Since it appears that the loss of telomeric DNA sequences can lead to replicative senescence in dividing cells, in theory by preventing such telomere loss the life span of the cell could be extended. A naturally occurring enzyme, telomerase, exists to restore telomeric DNA sequences lost by replication. Telo-merase is normally only functional in germ cells. Manipulating certain cell types (e.g., cells of the immune system) to regulate the expression telomer-ase may extend their functional life span. Drugs that enhance telomerase activity in somatic cells are currently being developed. However, cellular senescence has been implicated as a tumor suppressor mechanism and it has been found that cancer cells express telomerase. An uncontrolled expression of this enzyme in somatic cells may lead to the onset of malignancy through uncontrolled cell proliferation. Thus, any intervention aiming to increase life span based on the cellular expression of telomerase must strike a balance between maintaining controlled cell division and uncontrolled proliferation.

A number of single gene mutations have been identified that affect metabolic function, hormonal signaling, and gene silencing pathways. In the future it may be possible to develop drugs to mimic the antiaging effects that these genes exert.

See also: Antioxidants: Diet and Antioxidant Defense; Observational Studies; Intervention Studies. Cancer: Epidemiology and Associations Between Diet and Cancer. Coronary Heart Disease: Lipid Theory; Prevention. Fats and Oils. Fatty Acids: Monounsaturated; Saturated. Growth and Development, Physiological Aspects. Lipids: Chemistry and Classification; Composition and Role of Phospholipids. Nucleic Acids. Nutrient Requirements, International Perspectives. Older People: Nutritional Requirements; Nutrition-Related Problems; Nutritional Management of Geriatric Patients. Protein: Synthesis and Turnover; Requirements and Role in Diet; Digestion and Bioavailability. Supplementation: Role of Micronutrient Supplementation.

A Disquistion On The Evils Of Using Tobacco

A Disquistion On The Evils Of Using Tobacco

Among the evils which a vitiated appetite has fastened upon mankind, those that arise from the use of Tobacco hold a prominent place, and call loudly for reform. We pity the poor Chinese, who stupifies body and mind with opium, and the wretched Hindoo, who is under a similar slavery to his favorite plant, the Betel but we present the humiliating spectacle of an enlightened and christian nation, wasting annually more than twenty-five millions of dollars, and destroying the health and the lives of thousands, by a practice not at all less degrading than that of the Chinese or Hindoo.

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    What is nutritional modification?
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