Here's one (or two) for you, lyndacarol, and maybe Shayk will like them too for the hormone connections.
I had posted on the LDN (low dose naltrexone) forum about a pancreatic cancer case report using LDN as an experimental treatment in one patient, as an example of how LDN papers get published for other diseases, but not, it seems for MS (although plenty of MSers are taking LDN). It got me thinking about whether LDN has anything to do with insulin, and has anyone looked at that, and well, here are two studies on naltrexone and hyperinsulinemia. There are more, but these are most recent.
What this has to do with MS, and people who are not postmenopausal or who don't have polycystic ovary syndrome I don't yet know, but it's interesting, mainly because naltrexone seemed to only impact people's clinical response if they were hyperinsulinemic by normalizing it. It would be an interesting and short term study to neasure gonadotrophins in MS vs normal subjects taking LDN, and see what happens. It might be educational. It might show changes only in some patients with MS, and not others. Then the next question, would such changes correspond with improvement related to MS? The possibilities are out there, and researchers are looking at the effects of naltrexone on a variety of conditions. Why not publish something on MS???? - Lisa
Curr Pharm Des. 2006;12(8):1001-12. Related Articles, Links
Role of opioid antagonists in the treatment of women with glucoregulation abnormalities.
Guido M, Romualdi D, Lanzone A.
Department of Obstetrics and Gynaecology, Universita Cattolica del Sacro Cuore, Roma, Italy. firstname.lastname@example.org
Beta-endorphin were detected in the endocrine pancreas and seem able to influence insulin and glucagon release. Hence, endogenous opioids could have a role in glucoregulation and in the pathogenesis of obesity beyond the previously detected effects on appetite. Metabolic abnormalities, such as hyperinsulinemia, insulin-resistance and obesity, are common features of polycystic ovary syndrome (PCOS), and seem to have a pathogenetic role in this disorder. A link between opioids and PCOS-related hyperinsulinism is suggested by the finding of altered central opioid tone and elevated beta-endorphins levels, directly correlated with body weight, in these patients. Furthermore, naloxone and naltrexone significantly reduce the insulin response to glucose load only in hyperinsulinemic PCOS patients. This effect is obtained chiefly through an improvement of insulin clearance. Naltrexone is also able to ameliorate the abnormal gonadotrophins secretion and to improve the ovarian responsiveness in obese PCOS women undergoing ovulation induction with exogenous GnRH. Such effects are believed to be obtained through an amelioration of hyperinsulinemia. Gonadal steroids modulate the opioid system both centrally and in peripheral districts. Nevertheless, the decline of ovarian function does not abolish the opioidergic control of glucoregulation. Post-menopausal period is characterised by a high prevalence of hyperinsulinemia and insulin-resistance. In particular, an association between hyperinsulinemia and increased opioid activity was found in postmenopausal women showing a central body fat distribution. Both naloxone and naltrexone ameliorate the metabolic imbalance also when it appears in the climacteric period, and mainly by increasing insulin clearance. The benefits of naltrexone may represent in the future a useful tool for the treatment of women with hyperinsulinism in the clinical practice.
PMID: 16533167 [PubMed - in process]
Fertil Steril. 2004 Apr;81(4):1047-54. Related Articles, Links
Use of naltrexone in postmenopausal women with exaggerated insulin secretion: a pilot study.
Cucinelli F, Soranna L, Perri C, Barini A, Cento RM, Mancuso S, Lanzone A.
Department of Obstetrics and Gynecology, Catholic University of Sacred Heart, Rome, Italy.
OBJECTIVE: To determine the effect of naltrexone (an opiate receptor blocker) on insulin metabolism in postmenopausal women with different insulinemic patterns. DESIGN: Randomized placebo-controlled study. SETTING: Academic research environment. PATIENT(S): Forty-one healthy normoinsulinemic or hyperinsulinemic postmenopausal women. INTERVENTION(S): Oral glucose tolerance test (OGTT) before and after 5 weeks of the opioid antagonist (naltrexone, 50 mg/d orally) or the placebo administration; euglycemic-hyperinsulinemic glucose clamp. MAIN OUTCOME MEASURE(S): Glucose, insulin, and C-peptide plasma levels assessed in fasting condition and during the OGTT. Insulin sensitivity was calculated as total body glucose utilization. RESULT(S): Naltrexone reduced fasting and stimulated insulin response to the glucose load while inducing a significant improvement of the hepatic extraction, only in the hyperinsulinemic patients. No differences were found in the C-peptide pancreatic secretion and in the peripheral insulin sensitivity. No net change in the glycoinsulinemic metabolism was observed in normoinsulinemic patients or in placebo-controlled normoinsulinemic and hyperinsulinemic subjects. CONCLUSION(S): Similar to that reported in premenopausal women, endogenous opioid peptides are involved in the modulation of glycoinsulinemic metabolism in postmenopause. Through a prevalent action on liver insulin metabolism, without any clear improvement of insulin resistance and pancreatic beta-cell function, the chronic administration of naltrexone appears to reduce the hyperinsulinemia in those women with an exaggerated insulin response to the OGTT.
Randomized Controlled Trial
PMID: 15066462 [PubMed - indexed for MEDLINE]