Alcohol consumption and the risk of breast cancer

Epidemiologic studies addressing the association of alcohol consumption with breast cancer consistently suggest a modest association and a dose-response relationship. The epidemiologic evidence does not point to a single mechanism to explain the association, and several mechanisms have been proposed. Alcohol consumption is shown to increase levels of endogenous estrogens, known risk factors for breast cancer. This hypothesis is further supported by data showing that the alcohol-breast cancer association is limited to women with estrogen-receptor positive tumors. Products of alcohol metabolism are known to be toxic and are hypothesized to cause DNA modifications that lead to cancer. Recent research has focused on genes that influence the rate of alcohol metabolism, with genes that raise blood concentrations of acetaldehyde hypothesized to heighten breast cancer risk. Mounting evidence suggests that antioxidant intake(e.g.folate)mayreducealcohol-associatedbreast cancer risk, because it neutralizes reactive oxygen species, a second-stage product of alcohol metabolism. Diets lacking sufficient antioxidant intake, as a result, may further elevate the risk of breast cancer among alcohol consumers. Given that alcohol consumption is increasing worldwide and especially among women in countries of rapid economic growth, a greater understanding of the mechanisms underlying the known alcohol-breast cancer association is warranted.Avoiding overconsumption of alcohol is recommended, especially for women with known risk factors for breast cancer.

Diversos estudios epidemiológicos muestran la asociación del consumo de alcohol con el cáncer de mama de forma consistente, lo que sugiere una modesta asociación, y una relación de dosis-respuesta.La evidencia no apunta a un mecanismo único para explicar la asociación y varios mecanismos han sido propuestos. El consumo de alcohol incrementa los niveles endógenos de estrógeno, un riesgo conocido para cáncer de mama. Esta hipótesis es apoyada por información que muestra que la asociación entre el alcohol y el cáncer de mama está limitada a mujeres con tumores con receptores positivos de estrógeno. Es conocido que los derivados de la metabolización del alcohol son tóxicos, y se ha pensado que causan modificaciones en el DNA que llevan al cáncer. La investigación reciente se ha enfocado en genes que influencian la velocidad con la que se metaboliza el alcohol, y elevan las concentraciones de acetaldehído que se piensa puede aumentar el riesgo de cáncer de mama. La evidencia actual sugiere que la ingesta de antioxidantes (e.g. folato) puede reducirelriesgode cáncer asociadoalalcohol,porque neutraliza las especies reactivas de oxígeno, un producto de la segunda etapa del metabolismo del alcohol. Las dietas con ingesta insuficiente de antioxidantes,como resultado de esto, pueden elevar el riesgo de cáncer entre los consumidores de alcohol.Dado que el consumo de alcohol está incrementando en todo el mundo, especialmente en mujeres de países con rápido crecimiento económico, un mejor entendimiento de los mecanismos subyacentes a la asociación del cáncer de mama y el alcohol es necesario. Evitar el consumo excesivo es recomendado, especialmente para mujeres con factores de riesgo conocidos para cáncer de mama.

Pharmacodynamics & toxicological profile of PartySmart, a herbal preparation for alcohol hangover in Wistar rats.

BACKGROUND & OBJECTIVE: PartySmart is a herbal preparation intended for the management of alcohol hangover and other related toxic effects in clinical situation. The present study was designed to investigate the pharmacodynamics and oral toxicity of PartySmart, a herbal formulation in rats. METHODS: Effect of PartySmart on blood acetaldehyde and alcohol levels was evaluated at doses of 125, 250 and 500 mg/kg b.wt. in rats. Acute toxicity study was conducted with PartySmart at a limit test dose of 2000 mg/kg b.wt., p.o. In repeated dose 90 day study, PartySmart was administered at doses of 500 and 1000 mg/kg b.wt. once-a-day, orally throughout the study period. RESULTS: PartySmart dose-dependently decreased blood ethanol and acetaldehyde levels as compared to control. PartySmart at a dose of 500 mg/kg b.wt. significantly reduced the area under curve (AUC) of ethanol and acetaldehyde levels. It increased the hepatic alcohol dehydrogenase (ADH) at 500 mg/kg b.wt. and aldehyde dehydrogenase (ALDH) activities at doses of 250 and 500 mg/kg b.w. significantly. Acute toxicity study showed no clinical signs and pre-terminal deaths. The LD(50) of PartySmart was found to be greater than 2000 mg/kg b.wt. No significant differences in PartySmart-treated groups were observed on body weight, food intake, haematological and clinical chemistry, and organ weight ratios as compared to control group in the repeated dose study. Histopathological examination of all target organs showed no evidence of lesions attributing to drug toxicity. INTERPRETATION & CONCLUSION: PartySmart enhanced acetaldehyde metabolism by increasing ADH and ALDH activity without any side effects. These findings indicate that PartySmart may exert beneficial role in the management of alcohol hangover without any toxicity.

Influência da ingestäo aguda de bebidas alcoólicas sobre o aparelho cardiovascular: observaçäo clínica, eletrocardiográfica e laboratorial / Influence of acute intake of alcoholic beverages on the cardiovascular system: clinical, electrocardiographic and laboratory observation

Estudamos os efeitos da ingestäo aguda de bebidas alcoólicas sob o ponto de vista clínico, eletrocardiográfico e laboratorial, em 23 indivíduos, 16 sadios e 7 com antecedentes de cardiopatia, que näo faziam uso habitual de álcool. Todos apresentaram, após a ingestäo alcoólica, aumento significativo das taxas sangüíneas de álcool e acetaldeído. Os níveis séricos de potássio, magnésio e glicose näo sofreram variaçöes importantes, o mesmo ocorrendo com a duraçäo das ondas P e dos intervalos PR, com a morfologia das ondas P e dos complexos QRS, com o eixo elétrico de P e de QRS e com as ondas U. Observamos, em todos os casos, queda da pressäo arterial sistólica, após a ingestäo alcoólica. O grupo de indivíduos com antecedentes de cardiopatia apresentou algumas alteraçöes significativas, caracterizadas por: aumentos da taxa sangüínea de cálcio e de transaminase glutamooxalacética; queda da pressäo arterial diastólica e aumento da freqüência cardíaca; arritmias cardíacas (arritmia sinusal e extra-sistoles ventriculares); diminuiçäo da amplitude dos complexos QRS; aumento do intervalo QT, alteraçöes da repolarizaçäo elétrica ventricular, com aparecimento de ondas T bífidas, invertidas e de baixa voltagem. Esses resultados sugerem que alteraçöes significativas da performance cardíaca conseqüentes à ingestäo alcoólica, ocorreram apenas em indivíduos já portadores de distúrbios cardiovasculares