The Transgenerational Consequences of the Interaction Between Humans and Molecules: Alcohol as a Cultural Artifact

Granato, Alberto

doi:10.3389/fpsyg.2020.00061

Cited by 2 publications

(2 citation statements)

References 42 publications

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“…Notably, Hausknecht et al (2015) reported an enhanced excitatory synaptic strength in the ventral tegmental area dopamine neurons associated with drug addiction due to PAE that persists from infancy through to adulthood in rats (2–12 weeks). This implies that PAE modifies the reward system such that its plastic responses are persistently altered (Granato, 2020). Hence, the mu‐opioid receptor (MOR) may be involved in the programming effect of PAE as alcohol‐induced β‐endorphins stimulate the MOR believed to cause the release of dopamine in the brain reward system (Herz, 1997).…”

Section: Prenatal Alcohol Consumption: Mechanisms To Aldmentioning

confidence: 99%

Early‐lifeexposure to alcohol and the risk ofalcohol‐inducedliver disease in adulthood

Asiedu

Nyakudya

Lembede

et al. 2021

Birth Defects Research

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Alcohol consumption remains prevalent among pregnant and nursing mothers despite the well‐documented adverse effects this may have on the offspring. Moderate‐to‐high levels of alcohol consumption in pregnancy result in fetal alcohol syndrome (FAS) disorders, with brain defects being chief among the abnormalities. Recent findings indicate that while light‐to‐moderate levels may not cause FAS, it may contribute to epigenetic changes that make the offspring prone to adverse health outcomes including metabolic disorders and an increased propensity in the adolescent‐onset of drinking alcohol. On the one hand, prenatal alcohol exposure (PAE) causes epigenetic changes that affect lipid and glucose transcript regulating genes resulting in metabolic abnormalities. On the other hand, it can program offspring for increased alcohol intake, enhance its palatability, and increase acceptance of alcohol's flavor through associative learning, making alcohol a plausible second hit for the development of alcohol‐induced liver disease. Adolescent drinking results in alcohol dependence and abuse in adulthood. Adolescent drinking results in alcohol dependence and abuse in adulthood. Alterations on the opioid system, particularly, the mu‐opioid system, has been implicated in the mechanism that induces increased alcohol consumption and acceptance. This review proposes a mechanism that links PAE to the development of alcoholism and eventually to alcoholic liver disease (ALD), which results from prolonged alcohol consumption. While PAE may not lead to ALD development in childhood, there are chances that it may lead to ALD in adulthood.

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Section: Prenatal Alcohol Consumption: Mechanisms To Aldmentioning

confidence: 99%

Early‐lifeexposure to alcohol and the risk ofalcohol‐inducedliver disease in adulthood

Asiedu

Nyakudya

Lembede

et al. 2021

Birth Defects Research

View full text Add to dashboard Cite

show abstract

“…In support of this hypothesis, lacosamide, an antiepileptic drug, prohibits CRMP2-mediated microtubule assembly which underlies addiction-like behavior. 76 Given mounting evidence that FASD is associated with increased propensity for substance use disorders, 78 this could be a critical mechanism to investigate.…”

Section: Introductionmentioning

confidence: 99%

White matter abnormalities in fetal alcohol spectrum disorders: Focus on axon growth and guidance

Mathews

Dewees

Diaz

et al. 2021

Exp Biol Med (Maywood)

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Fetal Alcohol Spectrum Disorders (FASDs) describe a range of deficits, affecting physical, mental, cognitive, and behavioral function, arising from prenatal alcohol exposure. FASD causes widespread white matter abnormalities, with significant alterations of tracts in the cerebral cortex, cerebellum, and hippocampus. These brain regions present with white-matter volume reductions, particularly at the midline. Neural pathways herein are guided primarily by three guidance cue families: Semaphorin/Neuropilin, Netrin/DCC, and Slit/Robo. These guidance cue/receptor pairs attract and repulse axons and ensure that they reach the proper target to make functional connections. In several cases, these signals cooperate with each other and/or additional molecular partners. Effects of alcohol on guidance cue mechanisms and their associated effectors include inhibition of growth cone response to repellant cues as well as changes in gene expression. Relevant to the corpus callosum, specifically, developmental alcohol exposure alters GABAergic and glutamatergic cell populations and glial cells that serve as guidepost cells for callosal axons. In many cases, deficits seen in FASD mirror aberrancies in guidance cue/receptor signaling. We present evidence for the need for further study on how prenatal alcohol exposure affects the formation of neural connections which may underlie disrupted functional connectivity in FASD.

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The Transgenerational Consequences of the Interaction Between Humans and Molecules: Alcohol as a Cultural Artifact

Cited by 2 publications

References 42 publications

Early‐lifeexposure to alcohol and the risk ofalcohol‐inducedliver disease in adulthood

Early‐lifeexposure to alcohol and the risk ofalcohol‐inducedliver disease in adulthood

White matter abnormalities in fetal alcohol spectrum disorders: Focus on axon growth and guidance

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