Aging and Senior Health issues

Unlike cells in other organ systems, cells in the nervous system cannot reproduce. For example, damaged cells in liver, lung, or bowel may regenerate in part, but brain cells disappear if they become atrophied or injured. New cells cannot be produced, and damaged cells usually wither and die.

The number of nerve cells decreases with normal aging. In some areas (eg, brain stem nuclei) the cell loss is minimal, while in others (eg, the hippocampus) the loss is profound. Overall, brain weight gradually declines (about 10%) from the second or third decade to the age of 90. Compared with the entire intracranial contents, the area of the cerebral ventricles may enlarge on cross section three to four times from the third decade until the ninth decade. The clinical implications of these changes are difficult to judge, since brain weight and ventricular size are not well correlated with intelligence. Also, severe dementia may exist in those whose ventricular size may be normal for their age.

Other changes in the brain include deposition of the aging pigment lipofuscin in nerve cells, deposition of amyloid in blood vessels and cells, and appearance of senile plaques and, less frequently, neurofibrillary tangles. Although plaques and tangles are the hallmark of Alzheimer’s disease, they also appear in the brains of older people without clinical evidence of dementia (albeit in lesser numbers). This finding has led to the idea that Alzheimer’s disease is actually accelerated aging. However, the recent demonstration of genetic linkages in many patients with this disorder makes that argument less tenable. The role of anti aging hormones like HGH should be emphasized over here as scientists claim to have found positive impacts of growth hormones like DHEA on brain and their significant role in brain activities and neuroprotection.

Changes in neurotransmitter systems, particularly the dopaminergic and less so the cholinergic system, occur with aging. For example, levels of choline acetylase, cholinergic receptors, gamma-aminobutyric acid, serotonin, and catecholamines are lower. While the significance of these reduced levels is not completely understood, abnormally low levels of some enzymes and neurotransmitters may be associated with functional changes (eg, low choline acetyltransferase levels in Alzheimer’s disease or low dopamine levels in Parkinson’s disease). Conversely, the activity of other enzymes, such as monoamine oxidase, may increase. Inhibitors of monoamine oxidase may forestall the onset of disability in patients with Parkinson’s disease.

Certain properties of the brain may mitigate these adverse changes. DHEA can help brain cell activities. First is a property called redundancy, ie, many more nerve cells exist than are needed. For example, diabetes insipidus (which arises from a lack of antidiuretic hormone) does not appear until > 85% to 90% of the nerve cells in the supraoptic and paraventricular nuclei have been destroyed. Furthermore, hydrocephalic patients who have only a thin cerebral cortical mantle may still have normal intelligence. The number of cells required for certain functions is not known, so the extent of redundancy is difficult to estimate.

Second, compensatory mechanisms may appear if the brain is damaged. For example, when speech centers in the dominant hemisphere are damaged, the nondominant hemisphere may compensate and speech function may gradually return. Large areas of the cerebellum may be destroyed by injury, vascular disease, or tumor, and recovery is often seen as other motor systems take over. Compensatory mechanisms are more effective in the higher centers, so that the spinal cord, for example, has less ability than the brain to compensate after injury. In addition, myelinated peripheral nerves regenerate slowly. Although few functional changes are noted in peripheral nerves with aging, conduction times do decrease.

Neurologic diseases encountered in old age fall into three categories. First are those that occur nearly exclusively in the elderly–the degenerative and cerebrovascular disorders. Degenerative disorders encompass those in which the cause is unknown; some diseases (eg, familial Alzheimer’s disease) may be classified differently as more is learned about them. Second are disorders that occur at any age but have different implications, manifestations, treatment, and prognosis in the elderly. For example, seizures occurring for the first time in the elderly are more likely than those occurring in the young to be the result of some identifiable structural abnormality. Third are diseases that more typically occur in younger persons such as muscular dystrophy, demyelinating disease, and migraine. When they occur in late life, the cause may be unusual or the diagnosis may be incorrect.

Neurologic disorders are common in the elderly. The most serious, usually stroke or dementia, account for more than half of all disabilities requiring supervision in a nursing home. Acute conditions such as delirium are also common and serious, but they may be treatable. Yet, even less severe and potentially treatable neurologic conditions, such as movement disorders, are burdensome for the elderly and their caregivers. Neurologic diseases often rob elders of independence, productivity, drive, and personality.

New modes of therapy can successfully prevent or ameliorate some neurologic disorders. The incidence of cerebrovascular disease has decreased markedly in the USA, largely because of detection and treatment of hypertension. Advances in the treatment of Parkinson’s disease have helped tens of thousands of people. The second most common type of dementia in the elderly, vascular (multi-infarct) dementia, is now more easily detectable with new imaging techniques, and this dementia may be prevented or ameliorated with appropriate treatment of hypertension and diabetes.

Noninvasive means of visualizing the nervous system are providing more knowledge about many neurologic diseases, and advances in research techniques have been applied extensively to diseases of the nervous system. For example, advances in molecular biology have been used to identify sites on three chromosomes associated with familial Alzheimer’s disease. Genetic mutations that result in overproduction of amyloid, which may be a factor in Alzheimer’s disease, have also been identified. Other so-called degenerative diseases afflicting the elderly (eg, motor neuronal disorders, Huntington’s chorea, spinocerebellar degeneration) are now clearly established as genetic disorders.

Previously called adult-onset, maturity-onset, or ketosis-resistant diabetes, type II diabetes mellitus involves relative insulin deficiency and resistance to insulin action. The combination of normal or high insulin levels and hyperglycemia implies insulin resistance. Both increased insulin levels and decreased insulin action have been documented in the two groups at increased risk for type II diabetes–the obese and the elderly.

If pancreatic beta-cell reserve is sufficient, hyperinsulinemia preserves normal glucose levels. Eventually, impaired glucose tolerance occurs, although hyperinsulinemia continues. This state of mild glucose intolerance with near-normal fasting blood glucose levels may persist indefinitely. But in patients in whom insulin secretion is subsequently impaired, plasma glucose levels increase to those consistent with diabetes, and plasma insulin levels fall to normal or below. These patients are thought to have an increased genetic susceptibility to decreased beta-cell reserve.

Type II diabetes is distinguished by an absence of ketosis, which indicates that the patient has some effective insulin. About 35% of patients with type II diabetes use exogenous insulin. But unlike patients with type I diabetes, they do not need exogenous insulin to sustain life.

Obesity and age are independent risk factors for type II diabetes mellitus. Some 80% to 90% of type II diabetic patients are obese, and the prevalence doubles for every 20% increase over desirable body weight and for each decade after the fourth, regardless of weight. The prevalence in persons ages 65 to 74 is about 15%. An even higher percentage of people beyond the eighth decade may have type II diabetes mellitus. Type II diabetes is more prevalent in certain populations, eg, American Indians, blacks, and those of Hispanic ancestry.
Secondary Diabetes Mellitus

This category includes diabetes mellitus resulting from diseases that destroy the pancreas (eg, hemochromatosis, pancreatitis, and cystic fibrosis), certain endocrine diseases in which excess hormones interfere with insulin action (eg, growth hormone in acromegaly, cortisol in Cushing’s syndrome, and catecholamines in pheochromocytoma), and certain drugs that suppress insulin secretion (eg, phenytoin) or inhibit insulin action (eg, estrogens or glucocorticoids).