Urinary isoflavone and lignan phytoestrogen levels and risk of uterine fibroid in Jamaican women.

BACKGROUND: Isoflavones and lignans are phytoestrogens, and therefore, are able to bind to and activate estrogen receptors. The resultant estrogenic or antiestrogenic effect is dependent on the concentration of these phytoestrogens relative to endogenous estrogens and the site of their action, among others. Thus, isoflavones and lignans act as selective estrogen receptor modulators; having a beneficial effect in some tissues while simultaneously causing deleterious changes in others. OBJECTIVE: This case-control study investigates the relationship between urinary concentrations of genistein, daidzein, equol, and enterolactone, and the presence of uterine leiomyomas (fibroids) in Jamaican women. DESIGN: Phytoestrogen concentration in spot urine samples from 157 uterine fibroid cases and 171 fibroid-free controls diagnosed by ultrasonography, were assessed by Time-resolved Fluoroimmnoassay. Statistical evaluations were performed using SPSS 12.0. RESULTS: The median concentration of urinary enterolactone was significantly different between uterine fibroid cases and controls (p=0.029). However, this was not observed to affect risk of uterine fibroid, as trends across quartiles of urine enterolactone did not differ significantly between cases and controls. Median urinary genistein (p=0.510), daidzein (p=0.838), equol (p=0.621), total isoflavones (0.510) and total phytoestrogens (p=0.084) were similar for both groups. Binary logistic regression analysis of quartiles of urine genistein, daidzein, equol, enterolactone, total isoflavones, and total phytoestrogens showed no association with uterine fibroid. CONCLUSIONS: Uterine fibroid cases had a higher median urine concentration of enterolactone compared with controls. However, this was not observed to affect ones risk of fibroid. Neither was urine genistein, daidzein, equol total isoflavones, and total phytoestrogens observed to be associated with risk of uterine fibroid.

Chemical analyses of some Jamaican preparations of cannabis

The major cannabinoids present in Jamaican samples of herbal cannabis and derived resin were determined by gas-liquid chromatography. Their qualitative and quantative profiles were not unusual, but in 3 of the 4 samples, there was an unexpectedly low content of 1 tetrahydrocannabinol, the main psychoactive ingredient (AU)

Fatty acids generate dicarboxylic acids in hypoglycin poisoning - abstract

We investigated the metabolic origin of certain dicarboxylic acids which appears in urine of hypoglycin poisoned subjects (Jamaican vomiting sickness). These include hexanedioic (adipic), octanedioic (suberic) and decanedioic (sebacic) acids which, with unsaturated variants, are also excreted in some rare congenital diseases (glutaric acidaemia Type II, generalized dicarboxlic acidaemias), and in ketosis. Long-chain fatty acids have been established as precursors only in the case of diabetic, ketotic rats. In one report, evidence for this origin was negative for the case of hypoglycin poisoning, but no alternative precursors appear likely and the problem has remained unresolved since 1972. The present work utilized palmitic acid labelled either with Tritium, or with 14c at various atoms of the molecule as a tracer in hypoglycin-treated rats. Suberate and sebacate, isolated from urines by gas liquid chromatography, were found to be radioactively labelled, and hence, significant conversion of fatty acid to dicarboxylic acid was demonstrated. A further conclusion emerged from the relative labelling yielded by [1-14C] - and [16-14C] palmitic acid. After chain shortening by 3 -4 cycles of fatty acid á-oxidation, w-oxidation appears to intervene as a consequence of inhibition of the former process by the hypoglycin metabolite methylenecyclopropylacetyl-CoA. This sequence is in contrast to the ketotic animal, in which initial w-oxidation of fatty acid apparently precedes bilateral á-oxidation. In fasted hypoglycin-poisoned rats, excretion of each of these compounds is not insignificant, being about 7 - 33 mg/24 hr(1 - 4 mg/mg creatinine) (AU)