Long-Term Use of Methamphetamine Disrupts the Menstrual Cycles and Hypothalamic-Pituitary-Ovarian Axis

Shen, Wenwen; Zhang, Yisheng; Li, Long-hui; Liu, Yu; Huang, Xian-ni; Chen, Linghong; Zhou, Wenhua

doi:10.1097/adm.0000000000000021

Cited by 13 publications

(8 citation statements)

References 28 publications

(32 reference statements)

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“…In addition, estrogen is known to protect the heart from ischemic injury [36–37]. Shen et al [38] recently reported that function of the hypothalamic-pituitary-ovarian axis is disrupted in women who chronically use methamphetamine and that it remains disrupted following several months of abstinence from the drug. Thus, methamphetamine might negate the cardioprotective benefit of being female by disrupting the hypothalamic-pituitary-ovarian axis and suppressing the production of cardioprotective ovarian hormones.…”

Section: Discussionmentioning

confidence: 99%

Repeated exposure to methamphetamine induces sex-dependent hypersensitivity to ischemic injury in the adult rat heart

et al. 2017

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BackgroundWe previously reported that adult female, but not male rats that were prenatally exposed to methamphetamine exhibit myocardial hypersensitivity to ischemic injury. However, it is unknown whether hypersensitivity to ischemic injury develops when rats are exposed to methamphetamine during adulthood. The goal of this study was to determine whether methamphetamine exposure during adulthood sensitizes the heart to ischemic injury.MethodsAdult male and female rats received daily injections of methamphetamine (5 mg/kg) or saline for 10 days. Their hearts were isolated on day 11 and subjected to a 20 min ischemic insult on a Langendorff isolated heart apparatus. Cardiac contractile function was measured by an intraventricular balloon, and infarct size was measured by triphenyltetrazolium chloride staining.ResultsHearts from methamphetamine-treated females exhibited significantly larger infarcts and suppressed postischemic recovery of contractile function compared to hearts from saline-treated females. In contrast, methamphetamine had no effect on infarct size or contractile recovery in male hearts. Subsequent experiments demonstrated that hypersensitivity to ischemic injury persisted in female hearts following a 1 month period of abstinence from methamphetamine. Myocardial protein kinase C-ε expression, Akt phosphorylation, and ERK phosphorylation were unaffected by adult exposure to methamphetamine.ConclusionsExposure of adult rats to methamphetamine sex-dependently increases the extent of myocardial injury following an ischemic insult. These data suggest that women who have a heart attack might be at risk of more extensive myocardial injury if they have a recent history of methamphetamine abuse.

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Section: Discussionmentioning

confidence: 99%

Repeated exposure to methamphetamine induces sex-dependent hypersensitivity to ischemic injury in the adult rat heart

et al. 2017

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“…Remarkably, cardiovascular toxicity due to prenatal METH exposure in adult offspring exhibits significant sex differences but the reason for this discrepancy is unknown. Shen reported that chronically abused METH disrupts the hypothalamic-pituitary-ovarian axis in women Shen et al (2014), indicating that METH exposure during pregnancy may affect estrogen secretion in female offspring and damage its protective effects on the heart. Gender has different effects on the pharmacokinetics of METH in the placenta.…”

Section: Cardiovascular Toxicitymentioning

confidence: 99%

The Adverse Effects of Prenatal METH Exposure on the Offspring: A Review

Liu

Zhang

et al. 2021

Front. Pharmacol.

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Abuse of methamphetamine (METH), an illicit psychostimulant, is a growing public health issue. METH abuse during pregnancy is on the rise due to its stimulant, anorectic, and hallucinogenic properties. METH can lead to multiple organ toxicity in adults, including neurotoxicity, cardiovascular toxicity, and hepatotoxicity. It can also cross the placental barrier and have long-lasting effects on the fetus. This review summarizes neurotoxicity, cardiovascular toxicity, hepatotoxicity, toxicity in other organs, and biomonitoring of prenatal METH exposure, as well as the possible emergence of sensitization associated with METH. We proposed the importance of gut microbiota in studying prenatal METH exposure. There is rising evidence of the adverse effects of METH exposure during pregnancy, which are of significant concern.

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“…It is unclear why fetal exposure to methamphetamine produces sex dependent effects in the hearts of adult offspring. Shen et al (47) reported disruption of the hypothalamicpituitary-ovarian axis in women who chronically used methamphetamine. This suggests that prenatal exposure to methamphetamine may disrupt ovarian function, resulting in a loss of estrogen-dependent cardioprotection.…”

Section: Methamphetaminementioning

confidence: 99%

Does Prenatal Exposure to CNS Stimulants Increase the Risk of Cardiovascular Disease in Adult Offspring?

Rorabaugh

2021

Front. Cardiovasc. Med.

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Prenatal exposure to an adverse uterine environment can have long lasting effects on adult offspring through DNA methylation, histone acetylation, and other epigenetic effects that alter gene expression and physiology. It is well-known that consumption of CNS stimulants such as caffeine, nicotine, amphetamines, and cocaine during pregnancy can adversely impact the offspring. However, most work in this area has focused on neurological and behavioral outcomes and has been limited to assessments in young offspring. The impact of prenatal exposure to these agents on the adult cardiovascular system has received relatively little attention. Evidence from both animal and human studies indicate that exposure to CNS stimulants during the gestational period can negatively impact the adult heart and vasculature, potentially leading to cardiovascular diseases later in life. This review discusses our current understanding of the impact of prenatal exposure to cocaine, methamphetamine, nicotine, and caffeine on the adult cardiovascular system.

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Long-Term Use of Methamphetamine Disrupts the Menstrual Cycles and Hypothalamic-Pituitary-Ovarian Axis

Abstract: The present data demonstrate that long-term use of MA results in the disruption of menstrual cycles and dysfunction of hypothalamic-pituitary-gonadal axis in women.

Cited by 13 publications

References 28 publications

Repeated exposure to methamphetamine induces sex-dependent hypersensitivity to ischemic injury in the adult rat heart

Repeated exposure to methamphetamine induces sex-dependent hypersensitivity to ischemic injury in the adult rat heart

The Adverse Effects of Prenatal METH Exposure on the Offspring: A Review

Does Prenatal Exposure to CNS Stimulants Increase the Risk of Cardiovascular Disease in Adult Offspring?

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