Growth hormone and its releasers: a hope for Alzheimer’s?

The growth hormone (GH) secretion declines as we age (by 14% per decade), the process called somatopause. Drugs like pyridostigmine (an acetylcholinesterase inhibitor) are able to enhance GH secretion, but its clinical use is limited due to the strong side effects. Rivastigmine, a drug for Alzheimer’s disease (AD), was found to enhance GH release (Gerontology. 2003;49:191–195).
Oral administration of certain amino acids (arginine, glutamine, glycine, and lysine)  increased the release of endogenous GH (Nutrition. 2002;18:657–661); the doses of arginine were 0.5 or 1 g/kg body weight increased GH level (J Clin Endocrinol Metab, 2011 ; Vol. 43 (3): 582-586) or roughly 35 to 70 g a day.
Arginine dissolved in distilled water was infused over a thirty-minute period in doses 1/12, 1/6 and 1/4 g. per pound of body weight. Only the highest dose (average 37.5 g total) was found to be effective in this administration mode. Interestingly, the responses of GH among females remain significantly higher than those among males (N Engl J Med 1967; 276:434-439).
The mixture of L-arginine, L-glutamine, L-lysine, and glycine at a ratio of 37:30:18.5:14.5) added as 5% of the daily meals total has been found to increase the release of endogenous GH. When mice were fed a diet containing GH-releasing supplements they had significantly fewer memory impairments and changes in acetylcholine level in hippocampus induced by Alzheimer’s amyloid beta 1–42  (J Pharmacol Sci; 2005, 99, 117 – 120).
Recently, a clinical target for improving the conditions of AD may be the activation not of GH alone but the entire GH/insulin-like growth factor-I (IGF-I) brain axis. IGF-I alone is also considered a physiological regulator of brain amyloid levels with therapeutic potential (Nature Medicine, 2002;  8, 1390 – 1397)

The growth hormone (GH) secretion declines as we age (by 14% per decade), the process called somatopause. Drugs like pyridostigmine (an acetylcholinesterase inhibitor) are able to enhance GH secretion, but its clinical use is limited due to the strong side effects. Rivastigmine, a drug for Alzheimer’s disease (AD), was found to enhance GH release (Gerontology. 2003;49:191–195).

Oral administration of certain amino acids (arginine, glutamine, glycine, and lysine)  increased the release of endogenous GH (Nutrition. 2002;18:657–661); the doses of arginine were 0.5 or 1 g/kg body weight increased GH level (J Clin Endocrinol Metab, 2011 ; Vol. 43 (3): 582-586) or roughly 35 to 70 g a day.

Arginine dissolved in distilled water was infused over a thirty-minute period in doses 1/12, 1/6 and 1/4 g. per pound of body weight. Only the highest dose (average 37.5 g total) was found to be effective in this administration mode. Interestingly, the responses of GH among females remain significantly higher than those among males (N Engl J Med 1967; 276:434-439).

The mixture of L-arginine, L-glutamine, L-lysine, and glycine at a ratio of 37:30:18.5:14.5) added as 5% of the daily meals total has been found to increase the release of endogenous GH. When mice were fed a diet containing GH-releasing supplements they had significantly fewer memory impairments and changes in acetylcholine level in hippocampus induced by Alzheimer’s amyloid beta 1–42  (J Pharmacol Sci; 2005, 99, 117 – 120).

Recently, a clinical target for improving the conditions of AD may be the activation not of GH alone but the entire GH/insulin-like growth factor-I (IGF-I) brain axis. IGF-I alone is also considered a physiological regulator of brain amyloid levels with therapeutic potential (Nature Medicine, 2002;  8, 1390 – 1397)

What does marijuana do to our bodies and brains?

Brain Basics — 7:20 am

Question: Hi. Please, before you claim this as outside of your expertise I would really appreciate your answer even if it is only a little information, you can send it to my email privately at too if you wish. So, I was wondering, what does marijuana do to our bodies and brains? How dangerous can it be?

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Vitamins C and E to prevent Alzheimer’s

In 1980s, 65% of all East Boston residents over the age of 65 were recruited in the study of neuroprotective effects of vitamins C and E. None of the people taking vitamin C or vitamin E developed Alzheimer’s disease when followed up in 4.5 years while among vitamin C non-users, 85% developed the disease. Among vitamin E non-users, 14% developed Alzheimer’s (1)
I was shown that supplementation with vitamin E and/or vitamin C might be useful in maintaining brain acetylcholinesterase (footnote a) activity at the normal level and serotonin (footnote b) concentration for some extent under the condition to induce experimental dementia in experimental animals (2)
High intake of vitamin E from food (tocopherol), but not from supplements (which usually contain alpha-tocopherol), is shown to reduce incidence of Alzheimer’s disease. The most common alpha-tocopherol alone may not be sufficient in the protective effects (3)
Sources
MC Morris et al, Vitamin E and Vitamin C Supplement Use and Risk of Incident Alzheimer Disease. Alzheimer Disease & Associated Disorders, 1998 – V12 – 3
LEE Lilha et al., Effect of supplementation of vitamin E and vitamin C on brain acetylcholinesterase activity and neurotransmitter levels in rats treated with scopolamine, an inducer of dementia, Journal of nutritional science and vitaminology, 2001, vol. 47, no5, pp. 323-328
MC  Morris et. al., Relation of the tocopherol forms to incident Alzheimer disease and to cognitive change. Am J Clin Nutrition, Vol. 81, No. 2, 508-514, February 2005
Footnotes
a) Acetylcholinesterase (AChE) is an enzyme that degrades  the neurotransmitter acetylcholine at neuromuscular junctions and cholinergic synaptic transmission in the brain.
b) Serotonin is a neurotransmitter found in the central nervous system. It is best known as a “happiness hormone” though it’s no hormone but monoamine.

In 1980s, 65% of all East Boston residents over the age of 65 were recruited in the study of neuroprotective effects of vitamins C and E. None of the people taking vitamin C or vitamin E developed Alzheimer’s disease when followed up in 4.5 years while among vitamin C non-users, 85% developed the disease. Among vitamin E non-users, 14% developed Alzheimer’s (1)

I was shown that supplementation with vitamin E and/or vitamin C might be useful in maintaining brain acetylcholinesterase (footnote a) activity at the normal level and serotonin (footnote b) concentration for some extent under the condition to induce experimental dementia in experimental animals (2)

High intake of vitamin E from food (tocopherol), but not from supplements (which usually contain alpha-tocopherol), is shown to reduce incidence of Alzheimer’s disease. The most common alpha-tocopherol alone may not be sufficient in the protective effects (3)

Sources

  1. MC Morris et al, Vitamin E and Vitamin C Supplement Use and Risk of Incident Alzheimer Disease. Alzheimer Disease & Associated Disorders, 1998 – V12 – 3
  2. LEE Lilha et al., Effect of supplementation of vitamin E and vitamin C on brain acetylcholinesterase activity and neurotransmitter levels in rats treated with scopolamine, an inducer of dementia, Journal of nutritional science and vitaminology, 2001, vol. 47, no5, pp. 323-328
  3. MC  Morris et. al., Relation of the tocopherol forms to incident Alzheimer disease and to cognitive change. Am J Clin Nutrition, Vol. 81, No. 2, 508-514, February 2005

Footnotes

a) Acetylcholinesterase (AChE) is an enzyme that degrades  the neurotransmitter acetylcholine at neuromuscular junctions and cholinergic synaptic transmission in the brain.

b) Serotonin is a neurotransmitter found in the central nervous system. It is best known as a “happiness hormone” though it’s no hormone but monoamine.

New at Brain Fuels

Brain Basics — 5:55 am

The theory of mind presumes that we can only imagine that others have a mind because we have no direct access to the mind of another. In the late 1980s, this theory seemed to be fortified by experimental data describing a population of brain cells (named by researchers “mirror neurons”) – becoming active when a monkey watched another animal act

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