Effects of soy lecithin phosphatidic acid and phosphatidylserine complex (PAS) on the endocrine and psychological responses to mental stress.

Phosphatidylserine, derived from cow brains, has been shown previously to dampen the ACTH and cortisol response to physical stress. Further research investigated the influence of soy lecithin phosphatidylserine supplementation on mood and heart rate when faced with an acute stressor. In this study, we investigated the effects of soy lecithin phosphatidic acid and phosphatidylserine complex (PAS) supplementation on pituitary adrenal reactivity (ACTH, cortisol) and on the psychological response (Spielberger State Anxiety Inventory stress subscale) to a mental and emotional stressor. Four groups of 20 subjects were treated for three weeks with daily dosages of either 400 mg PAS, 600 mg PAS, 800 mg PAS, or placebo before exposure to the Trier Social Stress Test (TSST). Treatment with 400 mg PAS resulted in a pronounced blunting of both serum ACTH and cortisol, and salivary cortisol responses to the TSST, but did not affect heart rate. The effect was not seen with larger doses of PAS. With regard to the psychological response, 400 mg PAS seemed to exert a specific positive effect on emotional responses to the TSST. While the placebo group showed the expected increase in distress after the test, the group treated with 400 mg PAS showed decreased distress. These data provide initial evidence for a selective stress dampening effect of PAS on the pituitary-adrenal axis, suggesting the potential of PAS in the treatment of stress related disorders.

Lower esophageal sphincter relaxation: studies on the neurogenic inhibitory mechanism.

The purpose of this study was to determine the physiological mechanism of lower esophageal sphincter (LES) relaxation. Circular muscle of the esophagus, LES, and stomach were evaluated for their inhibitory response to electrical stimulation during a maintained tonic contraction produced by a superfusion of acetylcholine and physostigmine. Only the circular muscle of the distal esophagus showed an inhibitory response to electrical stimulation. The maximal inhibition of LES muscle was 63.9+/-5.9 (mean+/-SE)% of the acetylcholine produced tension and occurred at 80 V. Upper esophageal and gastric muscle were not inhibited. The inhibitory response of the LES muscle was antagonized by tetrodotoxin and hexamethonium but not by other specific antagonists. Adrenergic nerve destruction following 6-hydroxydopamine also did not abolish the LES inhibition. These data indicate that the distal esophagus, at the zone of the manometrically determined LES, is characterized by a nonadrenergic neural inhibitory system. We suggest that these nerves may mediate LES relaxation.

The site of denervation in achalasia.

Lower oesophageal sphincter supersensitivity to gastrin I and cholinergic stimulation has recently been described in patients with achalasia. To determine the pathogenesis of this finding, the lower oesophageal sphincter was tested to a cholinesterase inhibitor, edrophonium chloride. Edrophonium chloride significantly increased the lower oesophageal sphincter pressure both in normal subjects and in patients with achalasia. The preservation of this response in the presence of denervation supersensitivity suggested intact postganglionic cholinergic nerves and, thus, a preganglionic site of denervation in achalasia.