Also see:
Bowel Toxins Accelerate Aging
Endotoxin: Poisoning from the Inside Out
Protection from Endotoxin
Protective Bamboo Shoots
The effect of raw carrot on serum lipids and colon function
Linoleic Acid and Serotonin’s Role in Migraine
Hypothyroidism and Serotonin
Estrogen Increases Serotonin
Gelatin, Glycine, and Metabolism
Whey, Tryptophan, & Serotonin
Tryptophan, Sleep, and Depression
Anti-Serotonin, Pro-Libido
Serotonin and Melatonin Lower Progesterone
Res Clin Stud Headache. 1978;6:110-6.
Role of individual free fatty acids in migraine.
Anthony M.
Total plasma free fatty acids, platelet serotonin content and plasma stearic, palmitic, oleic and linoleic acids were estimated in 10 migraine patients before, during and after a migraine attack. Total and individual plasma free fatty acid levels rose and platelet serotonin content fell in most patients. The highest rise was observed in linoleic acid, which is known to be a potent liberator of platelet serotonin in vitro and is the only precursor of all prostaglandins in the body. It is suggested that the rise in plasma levels of linoleic acid in migraine could be responsible for the platelet serotonin release observed during the attack. At the same time, it may also serve as a source of increased prostaglandin E1 synthesis, which has a powerful vasodilating effect. It is realized that both suggestions have to be confirmed by relevant investigations, as outlined in the body of this paper.
Clin Exp Neurol. 1978;15:190-6.
Individual free fatty acids and migraine.
Anthony M.
Total plasma free fatty acids (FFAs), platelet serotonin content and plasma stearic, palmitic, oleic and linoleic acids were estimated in 10 migrainous patients before, during and after a migraine attack. Total and individual plasma FFA levels rose and platelet serotonin fell in most patients. Comparison of the pre-headache and headache mean values showed that of the FFAs linoleic acid rises most during headache. 10 non-migrainous controls had platelet serotonin content estimated before and after the ingestion of 20g linoleic acid. All showed a significant fall in platelet serotonin in the post-ingestion period. It is shown that linoleic acid releases platelet serotonin in vitro, and this study suggests that it has the same action in vivo. Further, it is the precursor of all prostaglandins in the body and its marked elevation during migraine may serve as a source of increased prostaglandin E1 (PGE1) synthesis. It is suggested that linoleic acid plays an important role in the biochemical process of the migraine attack, acting both as a serotonin releasing factor and a source of PGF1, the vasodilating action of which can aggravate the clinical symptoms of migraine.
Headache. 2006 Sep;46(8):1230-45.
Serotonin in trigeminal ganglia of female rodents: relevance to menstrual migraine.
Berman NE, Puri V, Chandrala S, Puri S, Macgregor R, Liverman CS, Klein RM.
OBJECTIVES:
We examined changes in the serotonin system across the estrous cycle in trigeminal ganglia of female rodents to determine which components are present and which are regulated by the variations in levels of ovarian steroids that occur during the estrous cycle.
BACKGROUND:
Migraine is 2-3 times more prevalent in women than in men and attacks are often timed with the menstrual cycle, suggesting a mechanistic link with ovarian steroids. Serotonin has been implicated in the pathogenesis of migraine, and the effectiveness of triptans, selective 5HT-1B/D/F agonists, has provided further support for this concept. It is not known whether serotonin, its rate-limiting enzyme tryptophan hydroxylase (TPH), or its receptors are regulated by ovarian steroids in trigeminal ganglia.
METHODS:
We used reverse transcription-polymerase chain reaction to examine gene expression in cycling mice, Western blots to examine protein expression, double-labeling immunohistochemistry using markers of nociceptors and nonnociceptors and confocal microscopy to identify specific types of neurons, and primary tissue culture to examine effects of estrogen on trigeminal neurons in vitro.
RESULTS:
In C57/BL6 mice mRNA levels of TPH-1, the rate-limiting enzyme in serotonin synthesis, were over 2-fold higher and protein levels were 1.4-fold higher at proestrus, the high estrogen stage of the cycle than at diestrus, the low estrogen stage. TPH protein also was present in primary trigeminal cultures obtained from female Sprague-Dawley rats, but levels were not affected by 24-hour treatment with physiological levels (10(-9) M) of 17beta-estradiol. Gene expression of 5HT-1B and 5HT-1D receptors in trigeminal ganglia was not regulated by the estrous cycle. Serotonin was present in trigeminal neurons containing CGRP, a potent vasoactive neuropeptide, peripherin, an intermediate filament present in neurons with unmyelinated axons, neurofilament H, which is present in neurons with myelinated axons, and in neurons binding IB4, a marker of nonpeptidergic nociceptors. Serotonin was also present in neurons containing 5HT-1B. The serotonin-positive population was significantly larger in diameter than the serotonin-negative population.
Conclusions.-Expression of the rate-limiting enzyme required for serotonin synthesis is regulated during the natural estrous cycle, and serotonin is present in larger trigeminal neurons of all the major subtypes. Colocalization of serotonin with 5HT-1B suggests that this receptor functions as an autoreceptor to regulate serotonin release. Cyclical changes in serotonin levels in trigeminal ganglia could contribute to the pathogenesis of menstrual migraine.
Cluster headaches have also responded well to LSD and similar drugs (Sewell, et al., 2006). -Ray Peat, PhD
[LSD is a serotonin antagnoist]
Neurology. 2006 Jun 27;66(12):1920-2.
Response of cluster headache to psilocybin and LSD.
Sewell RA, Halpern JH, Pope HG Jr.
The authors interviewed 53 cluster headache patients who had used psilocybin or lysergic acid diethylamide (LSD) to treat their condition. Twenty-two of 26 psilocybin users reported that psilocybin aborted attacks; 25 of 48 psilocybin users and 7 of 8 LSD users reported cluster period termination; 18 of 19 psilocybin users and 4 of 5 LSD users reported remission period extension. Research on the effects of psilocybin and LSD on cluster headache may be warranted.
