ethanol
Regulatory sources consulted
Approved indications
- Hand sanitizing to reduce bacteria on the skin when soap and water are unavailable.
Clinical warnings
- Major warning · For external use only. Flammable product: keep away from fire or flame. — FDA/openFDA, SPL set_id 0398573a-44fa-e0c6-e063-6394a90a9924
- Avoid use in the eyes; if contact occurs, rinse thoroughly with water. Stop use and seek advice if irritation or redness persists for more than 72 hours. — FDA/openFDA, SPL set_id 0398573a-44fa-e0c6-e063-6394a90a9924
- Major warning · Keep out of reach of children. If swallowed, get medical help or contact a Poison Control Center immediately. — FDA/openFDA, SPL set_id 0398573a-44fa-e0c6-e063-6394a90a9924
Pregnancy and lactation
No specific pregnancy or breastfeeding recommendation is available.
Recent literature (PubMed)
Approximately 4% of cancers worldwide are caused by alcohol consumption. Drinking alcohol increases the risk of several cancer types, including cancers of the upper aerodigestive tract, liver, colorectum, and breast. In this review, we summarise the epidemiological evidence on alcohol and cancer risk and the mechanistic evidence of alcohol-mediated carcinogenesis. There are several mechanistic pathways by which the consumption of alcohol, as ethanol, is known to cause cancer, though some are still not fully understood. Ethanol's metabolite acetaldehyde can cause DNA damage and block DNA synthesis and repair, whilst both ethanol and acetaldehyde can disrupt DNA methylation. Ethanol can also induce inflammation and oxidative stress leading to lipid peroxidation and further DNA damage. One-carbon metabolism and folate levels are also impaired by ethanol. Other known mechanisms are discussed. Further understanding of the carcinogenic properties of alcohol and its metabolites will inform future research, but there is already a need for comprehensive alcohol control and cancer prevention strategies to reduce the burden of cancer attributable to alcohol.
Alcoholism is a widespread and damaging behaviour of people throughout the world. Long-term alcohol consumption has resulted in alcoholic liver disease (ALD) being the leading cause of chronic liver disease. Many metabolic enzymes, including alcohol dehydrogenases such as ADH, CYP2E1, and CATacetaldehyde dehydrogenases ALDHsand nonoxidative metabolizing enzymes such as SULT, UGT, and FAEES, are involved in the metabolism of ethanol, the main component in alcoholic beverages. Ethanol consumption changes the functional or expression profiles of various regulatory factors, such as kinases, transcription factors, and microRNAs. Therefore, the underlying mechanisms of ALD are complex, involving inflammation, mitochondrial damage, endoplasmic reticulum stress, nitrification, and oxidative stress. Moreover, recent evidence has demonstrated that the gut-liver axis plays a critical role in ALD pathogenesis. For example, ethanol damages the intestinal barrier, resulting in the release of endotoxins and alterations in intestinal flora content and bile acid metabolism. However, ALD therapies show low effectiveness. Therefore, this review summarizes ethanol metabolism pathways and highly influential pathogenic mechanisms and regulatory factors involved in ALD pathology with the aim of new therapeutic insights.
Alcohol is commonly consumed prior to bedtime with the belief that it facilitates sleep. This systematic review and meta-analysis investigated the impact of alcohol on the characteristics of night-time sleep, with the intent to identify the influence of the dose and timing of alcohol intake. A systematic search of the literature identified 27 studies for inclusion in the analysis. Changes in sleep architecture were observed, including a delay in the onset of rapid eye movement (REM) sleep and a reduction in the duration of REM sleep. A dose-response relationship was identified such that disruptions to REM sleep occurred following consumption of a low dose of alcohol (≤0.50 g∙kg-1 or approximately two standard drinks) and progressively worsened with increasing doses of alcohol. Reductions in sleep onset latency and latency to deep sleep (i.e., non-rapid eye movement stage three (N3)) were only observed following the consumption of a high dose of alcohol (≥0.85∙g kg-1 or approximately five standard drinks). The effect of alcohol on the remaining characteristics of sleep could not be determined, with large uncertainty observed in the effect on total sleep time, sleep efficiency, and wake after sleep onset. The results of the present study suggest that a low dose of alcohol will negatively impact (i.e., reduce) REM sleep. It appears that high doses of alcohol may shorten sleep onset latency, however this likely exacerbates subsequent REM sleep disruption. Future work on personal and environmental factors that affect alcohol metabolism, and any differential effects of alcohol due to sex is encouraged.
Breast cancer is one of the main causes of death in women worldwide. In women, breast cancer includes over half of all tumours caused by alcohol. This paper discusses both ethanol metabolism and the mechanisms of mammary tumourigenesis caused by alcohol. Numerous signalling pathways in neoplastic transformation following alcohol consumption in women have been presented. In addition, primary and secondary prevention, phytochemicals, synthetic chemicals, specific inhibitors of enzymes and selective receptor modulators have been described.
To examine the acute and chronic effects of alcohol on blood pressure (BP) and the incidence of hypertension. We discuss the most current understanding of the mechanisms underlining these effects and their associations with the putative cardioprotective effects of consumption of low-to-moderate amounts of alcoholic beverages. A recent meta-analysis confirmed findings of experimental studies, demonstrating an acute biphasic effect of ethanol on BP, decreasing up to 12 h of ingestion and increasing after that. This effect is mediated by vagal inhibition and sympathetic activation. A meta-analysis found that chronic consumption of alcoholic beverages was associated with a high incidence of hypertension in men and women; it also found that, in women, the risk begins at moderate alcohol consumption. The risks of alcohol consumption are higher in Blacks than in Asians or Caucasians. The mechanism underlying the chronic effects of alcohol on BP, and particularly the differential effect on Blacks, is still unknown. Short-term trials showed that alcohol withdrawal promotes BP reduction; however, the long-term effectiveness of interventions that aim to lower BP through the restriction of alcohol consumption has not been demonstrated. The harmful effects of alcohol on BP do not support the putative cardioprotective effect of low-to-moderate consumption of alcoholic beverages. The absence of a tangible mechanism of protection, and the possibility that this beneficial effect is biased by socioeconomic and other characteristics of drinkers and abstainers, calls into question the hypothesis that consuming low amounts of alcoholic beverages improves cardiovascular health. The evidence from investigations with various designs converge regarding the acute biphasic effect of ethanol on BP and the risk of chronic consumption on the incidence of hypertension, particularly for Blacks. These effects do not support the putative cardioprotective effect of consumption of low-to-moderate amou