Hormone Deficiency Impairs Memory

The brain requires youthful levels of certain hormones to facilitate cell energy metabolism, maintain poor levels of acetyl-choline, and protect brain cell membrane function. As a result, ageing persons often require some hormone replacement to achieve the requisite levels.

HGH (Human Growth Hormone) improves brain cell activity and enhances memory. The daily production of HGH drops from age 26 onwards. Current findings suggest that HGH enhances memory by facilitating the induction of neural plasticity, a condition that permits the neurons (nerve cells of the brain) to change in order to record new memories. HGH is like thyroid, estrogen, testosterone, progesterone, melatonin or DHEA has been shown to help preserve youthful neurological function.

Thyroid hormone deficiency can also cause neurological disturbances such as poor concentration, memory disturbances and depression.

An article in the Journal Obstetrics and Gynecological evaluated 71 postmenopausal women relative to memory function: 28 were taking estrogen hormone replacement therapy. In those taking estrogen, there was significantly better verbal memory function than in those who were not (Kampen et al. 1994).

As men age, their levels of testosterone diminish significantly. Low levels of testosterone in men may contribute to memory impairment and increase vulnerability of the brain to Alzheimer's and related disorders.

One protective mechanism provided by testosterone is against Alzheimer's disease: brain cells are protected from a toxic peptide called beta-amyloid, which can accumulate in certain regions of an ageing brain. Beta-amyloid has been implicated in the development of Alzheimer's disease. An article in Brain Research describes a study in which cultured neurons were exposed to beta-amylod in the presence of testosterone. The resulting toxicity from beta-amyloid was significantly reduced by testosterone (Pike 2001).

What causes the brain to age?

Cognitive impairment has a variety of forms, including short-term memory loss, senility and dementia.

Dementia is a general term for diseases involving nerve cell deterioration. It is defined as a loss in at least two areas of complex behaviour such as language, memory, visual and spatial abilities, and judgement that are severe enough to interfere with a person's daily living. Dementia, the most serious form of age associated mental impairment, is often a slow, gradual process that may take months or even years to become noticeable. Symptoms vary depending on which areas of the brain are affected.

It is important to make a distinction between normal, age-associated mental impairment and conditions such as dementia that signal a disease process. Not all memory difficulties or cognitive complaints indicate the presence of Alzheimer's disease or other mental disorders. Many memory changes are temporary and are linked to environmental factors such as stress rather than to physiological processes.

Neurological diseases such as dementia manifest most commonly in the elderly. The good news is that many of the underlying reasons for why people experience memory loss and other neurological disturbances are correctable. Any one or a combination of the following factors can cause age-associated cognitive dysfunction:

• The damaging effect of chronic inflammation causing injury to both celebral blood vessels and neurons (brain cells).


• Changes in lifestyle and diet leading to nutrient deficiencies (eg. many older people become deficient in critical nutrients)


• Hormonal imbalances and decreased level of key hormones, especially HGH, DHEA, estrogen, testosterone, etc.


• Decrease in oxygen available to brain cells because of impaired circulation due to pathology (e.g. atherosclerosis or heart disease) or a lifetime of poor habits


• Declining energy output of brain cells


• Essential fatty acid deficiencies (the brain is made out of almost entirely of fatty acids)


• The damaging effects of chronic free radical exposure


• Adverse side effects from prescription medications


• Elevated levels of MAO (monomine oxidase)


• Reduced levels of neurotransmitters such as acetyl-choline

Source:Frontline e-Gazette (Sept / October 2008)