Endocrine and behavioral responses to methylphenidate in normal subjects

Joyce, Peter R.; Donald, R. A.; Nicholls, M. Gary; Livesey, J. H.; Abbott, Robyn M.

doi:10.1016/0006-3223(86)90282-9

Cited by 35 publications

(19 citation statements)

References 21 publications

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“…For example, cortisol levels are typically highest in the morning, which is when methylphenidate was administered in our study. In contrast, in studies that reported significant increases in cortisol, methylphenidate was administered in the evening, when cortisol levels are typically low [32]. Additionally, physical activity may have enhanced the response to stimulant drugs in some previous studies [29], whereas our subjects were resting.…”

Section: Discussionmentioning

confidence: 57%

“…Similarly, oral methylphenidate at a dose of 20 mg did not alter plasma cortisol levels in healthy subjects [30,31]. In contrast, intravenous methylphenidate at doses of 10 mg (0.12-0.15 mg/kg) or 0.3 mg/kg significantly increased cortisol levels in healthy subjects [32]. Related catecholaminergic substances, such as amphetamine and methamphetamine, have also been shown to elevate cortisol levels in some studies [33,34,35,36] but not others [14].…”

Section: Discussionmentioning

confidence: 99%

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Acute Effects of 3,4-Methylenedioxymethamphetamine and Methylphenidate on Circulating Steroid Levels in Healthy Subjects

et al. 2014

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3,4-Methylenedioxymethamphetamine (MDMA, ‘ecstasy') and methylphenidate are widely used psychoactive substances. MDMA primarily enhances serotonergic neurotransmission, and methylphenidate increases dopamine but has no serotonergic effects. Both drugs also increase norepinephrine, resulting in sympathomimetic properties. Here we studied the effects of MDMA and methylphenidate on 24-hour plasma steroid profiles. 16 healthy subjects (8 men, 8 women) were treated with single doses of MDMA (125 mg), methylphenidate (60 mg), MDMA + methylphenidate, and placebo on 4 separate days using a cross-over study design. Cortisol, cortisone, corticosterone, 11-dehydrocorticosterone, aldosterone, 11-deoxycorticosterone, dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEAS), androstenedione, and testosterone were repeatedly measured up to 24 h using liquid chromatography-tandem mass spectroscopy. MDMA significantly increased the plasma concentrations of cortisol, corticosterone, 11-dehydrocorticosterone, and 11-deoxycorticosterone and also tended to moderately increase aldosterone levels compared with placebo. MDMA also increased the sum of cortisol + cortisone and the cortisol/cortisone ratio, consistent with an increase in glucocorticoid production. MDMA did not alter the levels of cortisone, DHEA, DHEAS, androstenedione, or testosterone. Methylphenidate did not affect any of the steroid concentrations, and it did not change the effects of MDMA on circulating steroids. In summary, the serotonin releaser MDMA has acute effects on circulating steroids. These effects are not observed after stimulation of the dopamine and norepinephrine systems with methylphenidate. The present findings support the view that serotonin rather than dopamine and norepinephrine mediates the acute pharmacologically induced stimulation of the hypothalamic-pituitary-adrenal axis in the absence of other stressors.

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Section: Discussionmentioning

confidence: 57%

Section: Discussionmentioning

confidence: 99%

Acute Effects of 3,4-Methylenedioxymethamphetamine and Methylphenidate on Circulating Steroid Levels in Healthy Subjects

et al. 2014

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“…These differences may be related to the degree of dopaminergic activation. Thus when Joyce et al (1986) administered methylphenidate intravenously to 20 normal subjects behavioural responses were found to vary considerably among individuals ranging from euphoria to dysphoria. As regards endocrine responses, methylphenidate increased plasma noradrenaline briefly, plasma adrenaline demonstrated a marked increase while plasma prolactin gradually declined.…”

Section: Endocrine Autonomic and Subjective Effects Of Methylphenidatementioning

confidence: 96%

“…The behavioural and endocrine effects of methylphenidate may depend on its route of administration (Joyce et al, 1986). Dopamine inhibits prolactin release by direct internuncial neural pathways (Glick et al, 1963) and increases the release of growth hormone.…”

Section: Endocrine Autonomic and Subjective Effects Of Methylphenidatementioning

confidence: 99%

Methylphenidate: a review of its neuropharmacological, neuropsychological and adverse clinical effects

Leonard¹,

McCartan²,

White³

et al. 2004

Human Psychopharmacology

210

145

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“…Indeed, a handful of older studies [42][43][44] have reported an increase in human GH levels with methylphenidate usage. Furthermore, Bereket et al [2] reported methylphenidate to be associated with mild, but transient decreases in serum IGF-1 and IGF binding protein 3 (IGFBP-3) levels, while Toren et al [45] found that boys with ADHD treated with methylphenidate do not differ from untreated boys, or from control subjects, with regards to fasting serum GH, GH binding protein (GHBP) or IGF-1 levels.…”

Section: Stimulants and Growth Hormonementioning

confidence: 99%

Stimulants and growth in children with attention-deficit/hyperactivity disorder

Negrao

Viljoen

2011

Medical Hypotheses

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a b s t r a c tInitial suggestions that suppression of growth may be an intrinsic characteristic of attention-deficit/ hyperactivity disorder (ADHD) have now largely been disproven. Although controversy persists regarding the possible negative effect of adrenergic stimulants on growth in children with ADHD, the consensus that appears to be reached in the scientific literature is that stimulant usage may cause a manageable attenuation of growth in these children. Since it is known that stimulants increase the amount of dopamine and noradrenaline in the synapse, this writing suggests that these increases in dopamine and noradrenaline are responsible for the growth attenuation in these children. It appears that increased amounts of dopamine and noradrenaline have the ability to inhibit the secretion of growth hormone and growth-related hormones such as prolactin, thyroid hormones, sex hormones and insulin. Therefore, it would be reasonable to suggest that the increases in dopamine and noradrenaline caused by stimulant usage can disrupt the homeostasis of both growth hormone and growth-related hormones, generating the potential for the suppression of growth.

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Endocrine and behavioral responses to methylphenidate in normal subjects

Cited by 35 publications

References 21 publications

Acute Effects of 3,4-Methylenedioxymethamphetamine and Methylphenidate on Circulating Steroid Levels in Healthy Subjects

Acute Effects of 3,4-Methylenedioxymethamphetamine and Methylphenidate on Circulating Steroid Levels in Healthy Subjects

Methylphenidate: a review of its neuropharmacological, neuropsychological and adverse clinical effects

Stimulants and growth in children with attention-deficit/hyperactivity disorder

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