Deal in the womb: fetal opiates, parent-offspring conflict, and the future of midwifery.

This paper argues that parent-offspring conflict is mediated by placental beta-endorphins in placental mammals, i.e., foetuses make their mothers endorphin-dependent then manipulate them to increase nutrient allocation to the placenta. This hypothesis predicts that: (1) anatomic position of endorphin production should mirror its presumed role in fetal-maternal conflict; (2) endorphin levels should co-vary positively with nutrient carrying capacity of maternal blood system; (3) postpartum psychological symptoms (postpartum blues, depression and psychosis) in humans are side-effects of this mechanism that can be interpreted as endorphin-deprivation symptoms; (4) shortly after parturition, placentophagia could play an adaptive role in decreasing the negative side-effects of fetal manipulation; (5) later, breast-feeding induced endorphin excretion of the maternal pituitary saves mother from further deprivation symptoms. Finally, whatever the molecular mechanism of fetal manipulation is, widespread and intense medical care (such as caesarean section and use of antidepressants) affects the present and future evolution of mother-foetus conflict in the human species (and also in domestic animals) to increase 'fetal aggressiveness' and thus technology-dependency of reproduction.

No evidence for endorphin deficiency in fibromyalgia following investigation of cerebrospinal fluid (CSF) dynorphin A and Met-enkephalin-Arg6-Phe7.

The CSF levels of Met-enkephalin-Arg6-Phe7 and dynorphin A were measured in patients with fibromyalgia. The mean CSF Met-enkephalin-Arg6-Phe7 level was 35.1 +/- 2.4 fmol/ml (mean +/- S.E.M.). The mean CSF level of dynorphin A was 14.3 +/- 0.9 fmol/ml. Regression analysis showed a statistically significant correlation between Met-enkephalin-Arg6-Phe7 and dynorphin A (r = 0.5369, P = 0.001). When correlated to the previously measured CSF levels of beta-endorphin, a statistically significant correlation was found with Met-enkephalin-Arg6-Phe7 (r = 0.5055, P = 0.03) but not with dynorphin A (P greater than 0.05). The Met-enkephalin-Arg6-Phe7 and dynorphin A levels are elevated compared to the levels available for comparison groups. Therefore, a lack of endorphin secretion does not seem to be the basis for the hyperalgesia observed in these patients.

Altered neuroendocrine regulation of luteinizing hormone secretion in postmenopausal women with Parkinson's disease.

The secretion of gonadotropins and the role exerted by the endogenous opioid system on luteinizing hormone (LH) secretion were investigated in 6 postmenopausal women affected by idiopathic Parkinson's disease (PD) as well as in 6 age- and weight-matched normal postmenopausal women as controls. The mean plasma follicle-stimulating hormone (FSH) and LH levels were evaluated both under basal conditions and after 20 days of conjugated estrogen administration (1.25 mg/day). At the same time, the activity of the endogenous opioid system was evaluated, as well as the LH response to the 4-hour infusion of the opioid antagonist naloxone (1.6 mg i.v. bolus followed by 1.6 mg/h). Both before and during estrogen administration, plasma FSH levels were similar in the two groups of subjects, whereas plasma LH levels were significantly lower (p less than 0.01) in parkinsonian than in control women. In each subject estrogen administration significantly blunted (p less than 0.01) plasma FSH levels. Plasma LH levels were reduced only in controls (p less than 0.05), but not in women with PD. In each subject, before estrogen administration, the plasma LH levels did not vary during naloxone infusion. In control women after 20 days of estrogen administration, the plasma LH levels significantly increased during naloxone infusion (p less than 0.01). By contrast, in women with PD, conjugated estrogens failed to restore the LH response to naloxone. The present results suggest that the neurotransmitter mechanisms, which regulate LH secretion, are altered, and, in particular, the activity of the endogenous opioid system is deficient in women with PD.

Opioid peptides and psychiatric illness.

In the 10 years since Hughes et al (1975) identified from porcine brain two related pentapeptides with potent opiate activity, abnormalities of endorphin and enkephalin production or metabolism have been postulated in many disease states. The possibility of an advance in our understanding of the aetiology of functional psychiatric illness has led to a considerable body of research, which is discussed in this paper.

Biochemical basis of alcoholism: statements and hypotheses of present research.

Experimental results and theoretical considerations on the biology of alcoholism are devoted to the following topics: genetically determined differences in metabolic tolerance; participation of the alternative alcohol metabolizing systems in chronic alcohol intake; genetically determined differences in functional tolerance of the CNS to the hypnotic effect of alcohol; cross tolerance between alcohol and centrally active drugs; dissociation of tolerance and cross tolerance from physical dependence; permanent effect of uncontrolled drinking behavior induced by alkaloid metabolites in the CNS; genetically determined alterations in the function of opiate receptors; and genetic predisposition to addiction due to innate endorphin deficiency. For the purpose of introducing the most important research teams and their main work, statements from selected publications of individual groups have been classified as to subject matter and summarized. Although the number for summary-quotations had to be restricted, the criterion for selection was the relevance to the etiology of alcoholism rather than consequences of alcohol drinking.

Neonatal monosodium glutamate differentially alters two models of behavioral activity in conjunction with reduced hypothalamic endorphins.

Neurotoxic doses of monosodium glutamate were administered to neonatal male and female Sprague-Dawley rats for five days postpartum. The rats were tested at 6 months for alterations in two forms of activity--initial activity in an open field and overnight activity in a familiar cage. In comparison with age-, sex- and handling-matched littermate controls, experimental subjects exhibited increased open field behaviors and reduced overnight activity. Subsequent histology indicated marked reductions in arcuate and periarcuate cells which included but probably were not limited to beta-endorphin containing neurons. These findings indicate that neonatal MSG has long-term behavioral and neurological consequences, that some changes occur within behaviorally discrete systems, and that they may be associated with functional alterations within endogenous opioid systems, inter alia.