Binge drinking is known as the pattern of drinking that raises blood alcohol concentration (BAC) levels to 0.08 g/dL [3]. Typically, the pattern occurs after 4 drinks for women and 5 drinks for men in the period of 2 hours [3]. According to Shukla et. al, alcohol overconsumption through binge drinking is an emerging major health concern common in young adult population in US and generally around the globe. The Centers for Disease Control and Prevention estimates that one in six adults binge drinks about four times each month [1]. The progression of alcoholic steatosis (infiltration of liver cells with fat) to alcoholic hepatitis (diseased and inflammatory condition of the liver) has known to occur due to heavy binge drinking in people who have
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The seven-week-old male rats weighing approximately 250-300 grams were kept under 12-hour light/12-hour darkness cycle [1]. After allowing the rats to acclimatize to their new environments, they were divided into two groups and given either a control diet or ethanol liquid diet [1]. Initially, the ethanol was introduced at 1.25% in accordance to their weight/volume ratio on day 1 [1]. Afterwards, the ethanol content was further increased to 1.67% on day 2, and eventually raised to 2.5 % on days 3 and 4 [1]. Finally, the ethanol group was placed on final high level of 5% weight/volume ratio, which was maintained for 4 weeks [1]. During the post 4-week period, the rats were divided [1]. The control received water, chronic-ethanol which received water, control-binge, and chronic-ethanol binge group [1]. Both the control-binge and chronic ethanol binge group received three doses of ethanol binge in accordance with 5 gram/kg body weight ratio [1]. The liver tissues for rats from each group was obtained 4 hours after the last ethanol binge …show more content…
Although it was supposed to be an overview, the main conclusion of the popular press article was more broadly connected to liver injury possibly because histone H3S10 phosphorylation was associated with transcription of TNFα expression. Moreover, suppression of TNFα expression in chronic ethanol binge group may be clinically relevant since the endotoxin tolerance may contribute to increased susceptibility to infections in chronic alcoholics with binge drinking habits. The authors were credited more on their statements rather than their findings and interpretation of the results. The results of the original literature seemed more interesting than suggested by the press article. One important point that should have been included in the press article is progression of liver injury by adenosine receptor antagonists, which supports the role of adenosine signaling in damage progression. The popular press article also lacked advisory caution regarding numerous other causes and altered levels of proteins which may be equally responsible for liver injury
The seven-week-old male rats weighing approximately 250-300 grams were kept under 12-hour light/12-hour darkness cycle [1]. After allowing the rats to acclimatize to their new environments, they were divided into two groups and given either a control diet or ethanol liquid diet [1]. Initially, the ethanol was introduced at 1.25% in accordance to their weight/volume ratio on day 1 [1]. Afterwards, the ethanol content was further increased to 1.67% on day 2, and eventually raised to 2.5 % on days 3 and 4 [1]. Finally, the ethanol group was placed on final high level of 5% weight/volume ratio, which was maintained for 4 weeks [1]. During the post 4-week period, the rats were divided [1]. The control received water, chronic-ethanol which received water, control-binge, and chronic-ethanol binge group [1]. Both the control-binge and chronic ethanol binge group received three doses of ethanol binge in accordance with 5 gram/kg body weight ratio [1]. The liver tissues for rats from each group was obtained 4 hours after the last ethanol binge …show more content…
Although it was supposed to be an overview, the main conclusion of the popular press article was more broadly connected to liver injury possibly because histone H3S10 phosphorylation was associated with transcription of TNFα expression. Moreover, suppression of TNFα expression in chronic ethanol binge group may be clinically relevant since the endotoxin tolerance may contribute to increased susceptibility to infections in chronic alcoholics with binge drinking habits. The authors were credited more on their statements rather than their findings and interpretation of the results. The results of the original literature seemed more interesting than suggested by the press article. One important point that should have been included in the press article is progression of liver injury by adenosine receptor antagonists, which supports the role of adenosine signaling in damage progression. The popular press article also lacked advisory caution regarding numerous other causes and altered levels of proteins which may be equally responsible for liver injury