Progesterone – Substance Use Disorder * Biotin – Hormone Lab Results * Vitamin E – HPA-Axis

progesterone in substance use disorderRole of Exogenous Progesterone in the Treatment of Men and Women with Substance Use Disorders: A Narrative Review

Progesterone and it’s metabolite allopregnanolone show promise in substance use disorder, specifically with nicotine and cocaine.

“…progesterone, attenuates the craving for and the euphoric effects of drugs of abuse. Research to date has demonstrated that progesterone may modulate responses to drugs of abuse and may have utility as a novel treatment for SUDs. A literature search was conducted to identify and examine studies that administered exogenous progesterone. Sixteen publications were identified, exploring the utility of exogenous progesterone or its metabolite, allopregnanolone, among a range of substances, including amphetamines (one study), benzodiazepines (one study), cocaine (nine studies), and tobacco/nicotine (five studies). Results indicated that exogenous progesterone and, its metabolite allopregnanolone, demonstrated preliminary efficacy as a treatment for substance use in both men and women. Notably, progesterone appears to target negative affect and augment cognitive functioning, especially among female substance users.

Cocaine: (1)(2)(3)(4)(5)(6)(7)(8)

Suspected Testosterone-Producing Tumor in a Patient Taking Biotin Supplements

Biotin (vitamin B7) is known for it’s ability to give false readings on thyroid blood tests (TSH). This report chronicles alterations in other hormone results, including testosterone. These abnormal results led to unnecessary referrals and suspicion of a hormone producing tumor.

“A perimenopausal woman presented with palpitations, hirsutism, and inability to lose weight. Laboratory tests revealed an unusual endocrine hormonal profile including pituitary hormones (TSH, ACTH, and prolactin) below reference intervals and gonadal (testosterone) and adrenal (cortisol) hormones above reference intervals. Ultimately, after a comprehensive workup including a scheduled surgical procedure, abnormal laboratories were determined due to biotin interference…This case is unique due to the abnormalities observed not only in the well-described TSH “sandwich” immunoassay, but also in tests for gonadal steroids, adrenal, and pituitary hormones. Falsely high as well as falsely low results can be ascribed to biotin. Competitive immunoassays (Fig. 1A)— in this case, tests used initially for serum cortisol and testosterone— can demonstrate falsely high results…
Biotin effect on our patient’s endocrine testing led to decidedly abnormal findings, unnecessary medical referrals and diagnostic studies, and comprehensible psychological distress. Interference with one immunoassay, TSH, persisted a full 2 weeks after discontinuation of biotin; indeed, some tests demonstrate sensitivity to lesser quantities of biotin.

HPA-axis vitamin E aging
Elevation by Oxidative Stress and Aging of Hypothalamic-Pituitary-Adrenal Activity in Rats and Its Prevention by Vitamin E

Vitamin E prevents oxidative stress induced dysfunction of the HPA-axis,

“a complex set of direct influences and feedback interactions among three components: the hypothalamus, the pituitary gland (a pea-shaped structure located below the thalamus), and the adrenal (also called “suprarenal”) glands (small, conical organs on top of the kidneys).
These organs and their interactions constitute the HPA axis, a major neuroendocrine system that controls reactions to stress and regulates many body processes, including digestion, the immune system, mood and emotions, sexuality, and energy storage and expenditure.(W)

The study, in rats, used 200mg/kg of natural α-Tocopherol form of vitamin E (R,R,R-alpha-tocopherol).

“The present study was conducted in order to determine whether oxidative stress during aging involves dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis in association with the emergence of cognitive deficits. When young rats were subjected to oxidative stress … reactive substances, conjugated diene and lipid hydroperoxides increased markedly in the HPA axis.
Vitamin E inhibited such increases in lipid peroxides in each organ. Levels of corticotrophin-releasing hormone (CRT/CRF) in the hypothalamus and plasma levels of adrenocorticotrophic hormone (ACTH) and corticosterone were markedly elevated in young rats exposed to hyperoxia. However, young rats fed vitamin E-supplemented diets showed no abnormal hormone secretion, even after being subjected to hyperoxia. Furthermore, glucocorticosteroid receptors (GR) in pyramidal cells in the Cornus ammonis 1 region of the hippocampus in young rats were markedly decreased by oxidative stress. Similar phenomena were also observed in normal aged rats and young rats fed vitamin E-deficient diet kept in a normal atmosphere. Vitamin E supplementation prevented the decrease in GR in the hippocampus and the increase in corticosterone secretion caused by hyperoxia. These results suggest that oxidative stress induces oxidative damage in the hippocampus and the HPA axis during aging, resulting in a cognitive deficit in rats, and that negative-feedback inhibition on HPA activity was markedly dampened due to an increase in corticosterone levels caused by loss of GR.”