Also see:
Tryptophan Metabolism: Effects of Progesterone, Estrogen, and PUFA
Estrogen Increases Serotonin
Anti Serotonin, Pro Libido
Gelatin > Whey
Thyroid peroxidase activity is inhibited by amino acids
Whey, Tryptophan, & Serotonin
Tryptophan, Fatigue, Training, and Performance
Carbohydrate Lowers Free Tryptophan
Protective Glycine
Intestinal Serotonin and Bone Loss
Estrogen Increases Serotonin
Gelatin, Glycine, and Metabolism
Whey, Tryptophan, & Serotonin
Tryptophan, Sleep, and Depression
Omega -3 “Deficiency” Decreases Serotonin Producing Enzyme
Serotonin and Autism Connection
Hypothyroidism is a very common cause of increased serotonin (e.g. Henley, et al., 1998), and it the thyroid hormone is supplemented until symptoms are resolved, it’s likely that the serotonin will have been normalized. -Ray Peat, PhD
Hypothyroidism increases the formation of serotonin, as does cortisol (Henley, et al., 1997, 1998; Neckers and Sze, 1976). -Ray Peat, PhD
Synapse 1997 Sep;27(1):36-44.
Thyroid hormones and the treatment of depression: an examination of basic hormonal actions in the mature mammalian brain.
Henley WN, Koehnle TJ.
Numerous clinical reports indicate that thyroid hormones can influence mood, and a change in thyroid status is an important correlate of depression. Moreover, thyroid hormones have been shown to be effective as adjuncts for traditional antidepressant medications in treatment-resistant patients. In spite of a large clinical literature, little is known about the mechanism by which thyroid hormones elevate mood. The lack of mechanistic insight reflects, in large part, a longstanding bias that the mature mammalian central nervous system is not an important target site for thyroid hormones. Biochemical, physiological, and behavioral evidence is reviewed that provides a clear picture of their importance for neuronal function. This paper offers the hypothesis that the thyroid hormones influence affective state via postreceptor mechanisms that facilitate signal transduction pathways in the adult mammalian brain. This influence is generalizable to widely recognized targets of antidepressant therapies such as noradrenergic and serotonergic neurotransmission.
Am J Physiol 1997 Feb;272(2 Pt 2):H894-903.
Hypothyroid-induced changes in autonomic control have a central serotonergic component.
Henley WN, Vladic F.
Three experiments were conducted in unanesthetized rats made hypothyroid (Hypo) or maintained as euthyroid controls (Eu) to examine general cardiovascular responsiveness [experiment I (Exp I)]; responsiveness to a serotonin (5-HT2) agonist, dl-2,5-dimethoxy-4-iodoamphetamine [DOI intracerebroventricularly; experiment II (Exp II)]; or responsiveness to a 5-HT(1A) agonist dl-8-hydroxydipropyl-aminotetralin hydrobromide [8-OH-DPAT intracerebroventricularly; experiment III (Exp III)]. In Exp I, intravenous infusions of phenylephrine and nitroprusside provided little evidence that findings in Exp II and III were caused by generalized impairment in cardiovascular responsiveness in Hypo. In Exp II and III, Eu and Hypo were given either intra-arterial atropine or vehicle. Atropine significantly elevated heart rate (Exp II and III) and mean arterial pressure (Exp II) in Eu only. When compared with Eu, Hypo had a reduced pressor response (5.2 vs. 20.1%), an attenuated pulse pressure response (19.3 vs. 35.4%), and a more robust bradycardia (-17.7 vs. -7.0%) in response to DOI. These differences were atropine sensitive. In Exp III, Hypo had larger decrements in mean arterial pressure (-9.0 vs. -5.1%), heart rate ( -13.9 vs. – 7.7%), and body temperature (-4.5 vs. -2.7%) in response to 8-OH-DPAT in comparison to Eu. Parasympathetic involvement in the differential responses to 8-OH-DPAT was less clear than with DOI. Deranged autonomic control in hypothyroidism may be caused, in part, by changes in central serotonergic activity.
Brain Res 1975 Jul 25;93(1):123-32.
Regulation of 5-hydroxytryptamine metabolism in mouse brain by adrenal glucocorticoids.
Neckers L, Sze
The effects of glucocorticoid hormone on the metabolism of brain 5-hydroxytryptamine (5-HT) were studied in mice. A single injection of hydrocortisone acetate (HCA; 20 mg/kg, i.p.) accelerated the accumulation of 5-HT in whole brain after inhibition of monoamine oxidase activity by paragyline. The hormone did not appear to change brain tryptophan hydroxylase or 5-hydroxytryptophan decarboxylase activity. However, tryptophan levels in brain were elevated by 50% within 1 h after treatment with HCA. The effect of HCA on brain tryptophan levels was localized mainly in the nerve endings. In vitro synaptosomal preparations, HCA at 10(-5)-10(-7)M or corticosterone at 10(-5) M was found to stimulate the uptake of L-[3H]-tryptophan by the synaptosomes while androgenic and progesterone-like steroids were ineffective. These results demonstrate that glucocorticoids may directly act on nerve terminals in the regulation of 5-HT synthesis through an action on the uptake of tryptophan.
Res Commun Chem Pathol Pharmacol. 1975 Jan;10(1):37-50.
Thyroid hormone control of serotonin in developing rat brain.
Schwark WS, Keesey RR.
The influence of thyroid hormone on serotonin was studied in different regions of the rat brain. Surgical thyroidectomy of adult male rats led to significant increases in the level of serotonin in the hypothalamus but had no effect on this biogenic amine in the brain stem and basal ganglia. Experimental cretinism, induced by daily propylthiouracil treatment starting at birth, caused increased serotonin levels in all brain regions studied. In contrast. neonatal hyperthyroidism, produced by daily administration of L-triiodothyronine from birth, had no effect on the ontogenic patterns of serotonin. The turnover of serotonin, estimated by determining the rate of increase of the amine following administration of the monoamine oxidase inhibitor, pargyline, was decreased in the brains of 30-day-old cretinous rats when compared to their control littermates. The data suggest that thyroid hormone may exert an important regulatory influence on serotonin metabolism in the developing brain.
