Dr. Raymond Peat’s Views on Ritalin, and How Ritalin Lowers Social Anxiety

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The first study on mice used a human dosage equivalent of about 10 milligrams for a person weighing 60 kilograms or 130 pounds. The researchers found that methylphenidate abolishes testosterone levels, impairs fertility and reduces the number of Leydig cells, which produce testosterone. The higher dosage, equivalent to around 50 milligrams, lowered testosterone less than the smaller dosage. The researchers posited many possible avenues for methylphenidate’s testosterone-lowering effects, but one of the most obvious suggested the drug’s anoretic (appetite-reducing) effects and subsequent lowered caloric intakes, which they argue permanently suppresses pubertal growth in adolescents prescribed the drug. Since dopamine possible that methylphenidate’s dopamine-like effects support testosterone production, whereas a suppression of appetite.11. Fazelipour S, Jahromy MH, Tootian Z, Kiaei SB, Sheibani MT, Talaee N. The Effect of Chronic Administration of Methylphenidate on Morphometric Parameters of Testes and Fertility in Male Mice. J Reprod Infertil. 2012;13(4):232-236.

Weight loss caused by reduced food intake can severely affect growth and pubertal development by perturbing the maturation of not only the hypothalamo –pituitary– gonadal axis but also the axes of the hypothalamus and pituitary with the adrenals, thyroid, and growth hormone.11. Fazelipour S, Jahromy MH, Tootian Z, Kiaei SB, Sheibani MT, Talaee N. The Effect of Chronic Administration of Methylphenidate on Morphometric Parameters of Testes and Fertility in Male Mice. J Reprod Infertil. 2012;13(4):232-236.



However, a study on rats has shown that gavages of hydrochloride cocaine (15 mg/kg), which is structurally similar to MPH, prescribed for 100 days, resulted in testicular weight reduction (12). This study showed the significant reduction of the number of leydig cells in the treatment groups compared with the control group. Some other reports, confirming this finding, have indicated that intraperitoneal injection of hydrochloride cocaine at a dose of 30 mg/kg could cause necrosis and also decrease in the number of interstitial cells of the testes (18). Serum Testosterone secretion showed a significant reduction in the treatment groups of this study. A similar study on the short term effects of MPH on the production of sex-hormone in male mice showed that exposure of mice to MPH causes considerable reduction in testosterone production…” (Fazelipour, et al., 2012). Link: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3719348/



In another study, pre-pubescent children took an average mean daily dosage of 18 milligrams of methylphenidate for a period of four weeks, but they experienced no change in testosterone levels.

Findings suggest that short-term treatment with methylphenidate at usual doses does not significantly alter salivary testosterone levels in attention-deficit/hyperactivity disorder patients.21. Wang L-J, Chou M-C, Chou W-J, et al. Does Methylphenidate Reduce Testosterone Levels in Humans? A Prospective Study in Children with Attention-Deficit/Hyperactivity Disorder. Int J Neuropsychopharmacol. 2016;20(3):219-227. doi:10.1093/ijnp/pyw101

Link: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5408967/

The second study study, done on adolescent primates, specifically Rhesus monkeys, The first study shows that methylphenidate lowers luteinizing hormone (LH) and interferes with the normal menstrual cycle but also could be responsible for its well-known neuroprotective effects. 

“Chronic methylphenidate administration during adolescence perturbs pubertal onset, adversely affects maturation of the female reproductive axis by retarding pituitary LH release, and adversely affects ovarian folliculogenesis. These novel findings may have significant clinical implications in evaluating the effects of methylphenidate abuse on adolescent health.” Reference: https://www.ncbi.nlm.nih.gov/pubmed/16210004

Now, in isolation, a drug’s effect on testosterone tells you little about its desirability in the context of overarching hormonal health.

Dr. Peat has mentioned luteinizing hormone’s contribution to both dementia and cancer.

“…one of the ways testosterone works is to lower the luteinizing hormone, and people are now thinking that this gonadotropin pituitary hormone itself has a big role in forming Alzheimer’s disease. For example, they’ve created transgenic mice that can’t produce any of the LH pituitary hormone and they are free of Alzheimer’s disease. If they are crossed to the strain that to produce dementia, if they don’t have the luteinizing hormone, LH, they don’t get demented.”

Dr. Ray Peat, PhD in the Herb Doctors: Dementia and Progesterone Around 00:22:58 on

The pituitary hormones have diverse functons, including effects on epithelial tissues, other than their “classical” functions.  Growth hormone, ACTH (Lostroh and Li, 1957), and ACTH with prolactin (Tullner, 1963) stimulate prostate growth.  Prolactin–which is increased by estrogen–stimulates growth of the rat’s lateral prostate (Holland and Lee, 1980), and stimulates the growth of human prostate epithelial cells in vitro (Syms, et al., 1985).  LH (luteinizing hormone) increases when progesterone or testosterone is deficient, and growth hormone and prolactin (which are closely associated in evolution) both increase under a variety of stressful situations, and with estrogenic stimulation.  Prostate cancer patients who had higher levels of LH and lower testosterone died most quickly. 
(Harper, et al., 1984.)  Also, a high ratio of testosterone to estradiol or of testosterone to prolactin corresponded to better survival (Rannikko, et al., 1981.)  Considered separately, patients with higher testosterone levels had a better prognosis than those with lower levels, and patients with lower growth hormone levels did better than those with higher growth hormone levels. (Wilson, et al., 1985.)  Has anyone ever tried testosterone therapy for prostate cancer?  Or, more practically, a generalized antiestrogenic therapy, using thyroid, progesterone, and pregnenolone?  Other drugs (naloxone, bromocriptine, gonadotropin-releasing hormone agonists, and anti-growth hormone druges, e.g.) are available to regulate the pituitary hormones, and might be useful therapeutically or preventively.  (See Blaakaer, et al., 1995.)  Biskind and Biskind’s work (1944) with ovarian tumors might be relevant to both testicular and prostate cancer.”   References Fazelipour, Simin, et al. “The Effect of Chronic Administration of Methylphenidate on Morphometric Parameters of Testes and Fertility in Male Mice.” Journal of Reproduction & Infertility, vol. 13, no. 4, 2012, pp. 232–36.Wang, Liang-Jen, et al. “Does Methylphenidate Reduce Testosterone Levels in Humans? A Prospective Study in Children with Attention-Deficit/Hyperactivity Disorder.” International Journal of Neuropsychopharmacology, vol. 20, no. 3, Dec. 2016, pp. 219–27. PubMed Central, doi:10.1093/ijnp/pyw101.

Dr. Raymond Peat has mentioned caffeine as a treatment from attention-deficit hyperactivity disorder (ADHD), as the drug has a similar effect in the brain as methylphenidate. Caffeine has been shown to have anxiogenic (anxiety-producing effects), whereas methylphenidate (the extended-release version) has been shown to actually improve social anxiety in adults with ADHD.

“The relationship between social anxiety disorder (SAD) and attention-deficit/hyperactivity disorder (ADHD) is a subject which has recently become a topic of interest for research.
In this study, 20 patients with comorbid SAD and adult ADHD who were treated with extended-release methylphenidate monotherapy were evaluated retrospectively.
Clinical response for both ADHD and SAD symptoms was observed in 17 of 20 patients. Overall, one patient did not respond to treatment and two patients dropped out of treatment at the beginning due to adverse effects.
Extended-release methylphenidate improved both SAD and ADHD symptoms and was generally well tolerated. Further studies are required to investigate the relationship between SAD and ADHD.”
Koyuncu, Ahmet, et al. “Extended-Release Methylphenidate Monotherapy in Patients with Comorbid Social Anxiety Disorder and Adult Attention-Deficit/Hyperactivity Disorder: Retrospective Case Series.” Therapeutic Advances in Psychopharmacology, vol. 7, no. 11, Nov. 2017, pp. 241–47. PubMed Central, doi:10.1177/2045125317714193.

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