Also see:
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
Hypothyroidism and Serotonin
Estrogen Increases Serotonin
Gelatin, Glycine, and Metabolism
Whey, Tryptophan, & Serotonin
Tryptophan, Sleep, and Depression
Menstrual Cycle Related Epilepsy (Catamenial Epilepsy)
Estrogen’s Role in Seizures
The Brain – Estrogen’s Harm and Progesterone’s Protection
Estrogen, Glutamate, & Free Fatty Acids
Women, Estrogen, and Circulating DHA
Epilepsy and Progesterone by Ray Peat, PhD
“In women with preeclampsia, there are abnormally high levels of serotonin, nitric oxide, and lipid peroxidation. In a study of more than 3000 women (Clausen, et al., 2001), the consumption of sugar and polyunsaturated fat was strongly associated with the development of preeclampsia. Women who don’t eat enough protein are likely to substitute sugar and fat for the absent protein, so this study is consistent with Brewer’s work, but it’s very important to see that it was polyunsaturated fats, not saturated or monounsaturated fats, that caused the problem. Eclampsia (pregnancy-related seizures) and preeclampsia are caused by oxidative stress, produced by the excessive unstable fats. The increased serotonin and nitric oxide are exactly what would be expected to result from the high consumption of polyunsaturated fats, especially with a deficiency of protein in the diet.” -Ray Peat, PhD
Hypertension. 2007 Oct;50(4):773-9. Epub 2007 Jul 23.
Pregnant rats treated with a serotonin precursor have reduced fetal weight and lower plasma volume and kallikrein levels.
Salas SP, Giacaman A, Romero W, Downey P, Aranda E, Mezzano D, Vío CP.
Pregnant women with preeclampsia have increased serotonin levels, suggesting a possible role of this amine in abnormal pregnancy. With the hypothesis that an increase in serotonin would reduce volume expansion and cause fetal growth restriction, we evaluated the maternal and fetal effects of the administration of the serotonin precursor 5-hidroxytryptophan (5-HTP) to Sprague-Dawley rats. At pregnancy day 13 (n=19) or in random cycle nonpregnant rats (n=10), animals were assigned to a single injection of 5-HTP (100 mg/kg IP) or to a control group. Animals were studied at day 21, after overnight urinary collection. Additional pregnant rats received ketanserin (1 mg/kg), a 5-HT(2) receptor antagonist, 1 hour before 5-HTP injection. In pregnant rats, 5-HTP lowered plasma volume (control: 22+/-1.1; 5-HTP: 17+/-0.7 mL; P<0.001) and creatinine clearance, whereas serum creatinine and urinary protein excretion were increased; no changes were observed in nonpregnant rats. Systolic blood pressure did not change significantly. Urinary kallikrein activity and plasma aldosterone levels decreased only in pregnant animals. Fetal (control: 5.5+/-0.1; 5-HTP: 4.2+/-0.2 g; P<0.001) and placental weights were reduced. In nonpregnant and pregnant animals, 5-HTP caused profound renal morphological alterations and decreased kallikrein immunostaining. Preadministration of ketanserin abolished all of the changes associated with the use of 5-HTP. These data indicate that the administration of a serotonin precursor to pregnant rats limits plasma volume expansion and fetal growth via 5-HT(2) receptors, suggesting a possible role for serotonin in abnormal pregnancy. We postulate that an increased vascular resistance, both at the placental and renal levels, mediates these effects.
