PC and Fran and All,
I thought these links to be thought provoking.
Serotonin - The metabolic biosynthetic pathway from tryptophan to serotonin is shown here. Serotonin plays multiple roles in the nervous system, including neurotransmission. It is a precursor to melatonin, which is involved in the regulation of sleepiness and wakefulness. In the intestine, serotonin regulates intestinal peristalsis. Serotonin is also a potent vasoconstrictor, which helps regulate blood pressure.
[
oregonstate.edu]
Plasma tryptophan and total neutral amino acid levels in men: influence of hyperinsulinemia and age.
- Fukagawa NK, Minaker KL, Rowe JW, Young VR
Metabolism 1987 Jul;36(7):683-6.
Because of the well-recognized age-related changes in peripheral tissue sensitivity to insulin and the demonstrated impact of insulin on blood amino acid profiles in young individuals, we evaluated the influence of insulin level and age on the concentrations of tryptophan and its ratio to the sum of the large neutral amino acids (LNAA). The ratio of the plasma concentrations of tryptophan and the LNAA (leucine, isoleucine, valine, tyrosine, and phenylalanine), may be an important determinant of the rate at which tissues synthesize neurotransmitters, such as catecholamines and serotonin. Each of five healthy young (21 to 34 yr) and five healthy old subjects (67 to 85 yr) received, on separate occasions, euglycemic insulin infusions at rates of 6, 10, 30, and 400 mU X m-2 X min-1. Basal plasma tryptophan concentrations and LNAA levels were similar in young and old. Both tryptophan and LNAA levels decreased in an insulin dose-dependent manner (P less than .02). The dose-response effect of insulin on tryptophan levels in the elderly was less than in the young (P less than .03), while the response of the LNAA was similar in both age groups. The ratio of tryptophan to LNAA was less in the old when compared to the young (P less than .03) but increased in the two age groups in an insulin-dose-dependent fashion (P less than .02). Maximal plasma tryptophan decrements were 39% and 32%, and maximal LNAA declines were 58% and 61% in young and old, respectively, during the 400 mU X m-2 X min-1 studies.
[
www.arclab.org]
Depression and Amino Acids
The building blocks of protein, amino acids can affect various central nervous system-controlled mechanisms such as pain threshold, mood, and sleep patterns. Low tyrosine or phenylalanine, for example, can result in abnormal levels of mood regulating chemicals in the brain, such as dopamine and catecholamines. Low tyrosine can also create subnormal levels of thyroid hormone--a well-known cause of depression. This may be why pre-treatment with supplemental tyrosine appears to prevent the behavioral depression observed following an acute stress.1
Because catecholamines rely on S-adenosyl methionine (SAMe) for proper function, low levels of SAMe have been observed in some cases of depression.2 For this reason, it is recommended that the status of the amino acid methionine, the precursor of SAMe, and its various metabolic pathways, be studied in patients with depression.3
Another amino acid, tryptophan, is the body's source material for producing the powerful hormone serotonin, which also influences sleep patterns and mood. Depletion of tryptophan can spur an increase in depressed mood states, particularly in individuals sensitive to affective disorders.4-6 In fact, one study found that a lower tryptophan level corresponded with a higher depression score even for patients who were already under treatment with anti-depressant drugs.7
The Amino Acids Analysis (blood, or 24-hour urine) can reveal deficiencies of tryptophan, tyrosine, methionine and other amino acids which may be significant contributing factors in depression. Should test results uncover important deficiencies, a helpful amino acid supplement schedule is included.
[
www.gsdl.com]
PC, It would seem that low catecholamines could be a possible cause of hypoglycemia, rather than catecholamine induced hypo., due to excess, if I understand you right, which I would propose doesn't cause anxiousness or sweating, but instead, simply, lack of glucagon that should inhibit insulin, as my wife was pondering, and we've been discussing.
This is a very interesting article on the different pathways of neurotransmitters, and I found this highlight, of particular importance in regards to orthostatic problems.
The catecholamines that act as neurotransmitters include dopamine and norepinephrine. Epinephrine is not produced in the central nervous system. The catecholamines share a common synthetic pathway. The rate limiting step is tyrosine hydroxylase. The activity of tyrosine hydroxylase can be modified by phosphorylation. This provides a point of regulation for the neuron. Clinically there are no agents capable of modulating tyrosine hydroxylase. However, treatment with agents such as methyldopa can compete with dopa for further processing. The result is a formation of false neurotransmitters. The false neurotransmitters are packaged in the synapse as though they were the catecholamine but when released into the synapse they are ineffective at the receptor. False neurotransmitters such as octopamine are also thought to be increased in hepatic encephalopathy. The packaging of false transmitters in the periphery is thought to be increased by inhibiting MAO. This is thought to explain the orthostatic blood pressure effects caused by therapeutic doses of MAO inhibitors.
[
www.dendrites.com]
So if the MAO's are being inhibited by lack of, or formation of false neurotransmitters, then could this be the same effect as a MAO inhibitor, which causes the orthostatic problem? More food for thought. Is your plate full yet? I know mine is.
Fran,
This is why you were so hungry.
According to the glucostatic hypothesis, appetite control is determined by the use of glucose by brain cells. If glucose is low, neurons are activated and hunger increases. Conversely, when the rate of glucose is high, the activity of the brain cells sensitive to glucose is diminished, and the sensation of satiation is attained. Unlike peripheral tissues, such as muscles, the brain does not need insulin to metabolize glucose, suggesting further that the metabolism of glucose may have a unique place in the controlling ones appetite.
[
www.matol.com]
Richard