i have only just started having a look at LDN because someone was all stoked with it on an introduction string. what an interesting read. how very interesting that it is an immune system BOOSTER! wow. so anyway, deals with correcting issues with the opioid system (which also happens to be affected in cases of anorexia and bulemia... i'm thinking vegan history could also be implicated???). links to glucose preference and insulin production. this is probably not any kind of news to you, coz i know it was mentioned on your insulin topic, but i thought it was really interesting. here are a couple more abstracts:
An opioid antagonist, naltrexone, reduces preference for sucrose in humans
M. Fantino, J. Hosotte and M. Apfelbaum
Eight healthy nonobese volunteers were asked to rate, on a pleasure-displeasure scale, sucrose and salty solutions as well as alimentary and nonalimentary odors. Effects of intragastric glucose load (vs. water load) and naltrexone (vs. placebo) were tested. Naltrexone produces a significant decrease for sweetened solution on the pleasure scale, a shift even stronger than that of the glucose load itself. Such a decrease is also observed for alimentary odors but not for responses to nonalimentary stimuli. Thus the opioid system is involved in ingestive behavior in humans, and this action is perhaps specific.
Exp Clin Endocrinol Diabetes. 1998;106(5):389-94. Related Articles, Links
Naltrexone effects on insulin sensitivity and insulin secretion in hyperandrogenic women.
Sir-Petermann T, Lopez G, Castillo T, Calvillan M, Rabenbauer B, Wildt L.
Dept of Medicine West Division, School of Medicine Universidad de Chile, Santiago.
A total of 12 women (24.2 +/- 1.6 years old, BMI 36.7 +/- 1.5 Kg/m2) with hyperandrogenism (HA) and with normal glucose tolerance test were studied to evaluate the involvement of endogenous opioids in the pathophysiology of insulin secretion and insulin sensitivity in HA by administering naltrexone, an oral opioid receptor antagonist. Six patients received naltrexone orally (75 mg daily) and another six received placebo for 12 weeks (double-blind study). Before and after therapy a frequently sampled intravenous glucose tolerance test (FSIVGTT) was performed. The insulin sensitivity index (SI) was determined by Bergman's program. SHBG, DHEAS, testosterone, free androgen index (FAI) and plasma concentrations of IGF-I and IGFBP-1 were determined in 3 basal samples, before and after therapy. Treatment with naltrexone in hyperandrogenic patients resulted in a decrease in fasting insulin concentrations of 40% and C-peptide concentrations of 50% (p < 0.05). Insulin and C-peptide from the FSIVGTT displayed a similar pattern with a fall in the area under the curve under naltrexone treatment of 34% for insulin and 35% for C-peptide. Insulin sensitivity did not change under naltrexone (1.26 +/- 0.19 vs 1.32 +/- 0.32 10(-4) x min(-1)/(uU/ml)) or placebo (0.95 +/- 0.19 vs 1.12 +/- 0.28 10(-4) x min(-1)/(uU/ml)) administration. However, glucose effectiveness increased significantly with naltrexone (2.231 +/- 0.002 vs 3.354 +/- 0.006 x 10(-2) min(-1)). Glucose (fasting and area under the curve) was not modified significantly after naltrexone administration. Baseline hormone levels were similar in the two groups, and they did not change after long-term treatment with naltrexone or placebo. In conclusion, these results support the hypothesis of elevated opioid tonus and increased insulin secretion as a possible mechanism of hyperinsulinism in a group of hyperandrogenic women of ovarian origin. This alteration could act as an additional factor in the pathogenesis of insulin resistance found in an important proportion of these patients.