It is important to observe that the increase in risk for mortality pertaining to these diseases is greater than the increase in risk for morbidity, especially at lower levels of consumption. This finding suggests that continuous alcohol consumption, be it even in low doses, increases the gravity of liver or pancreas disease by risking yet more severe consequences.
A connection between the concentration of alcohol quota in the blood and almost any sort of unintentional injuries has long been established, as psychomotor fallacies emerge after consuming two to three drinks in one hour. However, Taylor in 2010 indicated that, even at lower BAC values, risk of injury is increased when compared with total lack of alcohol consumption (Rehm, 2011).
The acute effects of alcohol consumption on injury risk are also conditioned by the regularity of the individual's alcohol intake sessions. Gmel et al. consigned in 2010 that people who drink less frequently are more likely to be injured or to injure others at a certain alcohol concentration present in the blood, unlike regular drinkers, presumably because of the formers' diminished tolerance (Rehm, 2011). In addition, Tayor noted in 2008 that it is important to realize that, even if the absolute risk for injury may be relatively small for each occasion of moderate drinking -- moderation being appreciated at 36 grams of pure alcohol in one session, the lifetime risks from such drinking occasions adds up to considerable risk for those who drink at such a high level on a regular basis (Rehm, 2011).
Alcohol consumption is not only correlated with unintentional injury, it has a significant influence on intentional injury, as well. There is a clear connection between alcohol drinking and ensuing aggression, and in 2010 Borges and Loera shared that the average volume of alcohol consumption and the level of drinking before the event have been shown to affect suicide risk. A series of causal pathways that form this link have been identified, most notably biological pathways acting through alcohol's effects on the brain's neurotransmitter substances serotonin and amino butyric acid, or through alcohol's effects on an individual's cognitive capacities (Rehm, 2011).
Another scope of recent epidemiologic research has associated moderate female alcohol consumption with a 10% increase in breast cancer risk, compared to women who don't drink any alcohol. Moreover, women who reported binge-type drinking presented a higher risk to develop breast cancer than those who did not. More studies of this type would be valuable, since binge drinking by young women is on the rise (Brooks et al., 2013). Hence, alcohol consumption is an established risk factor for breast cancer. However, the mechanism that alcohol employs in affecting breast cancer development remains elusive.
Furthermore, it is not clear whether the risk of breast cancer linked twith alcohol consumption is modified by the different levels of estrogen found in pre- and postmenopausal women. A woman's transition from the premenopausal to the postmenopausal phase is associated with a considerable reduction of hormonal estrogen levels throughout the body, and tumor development is, by contrast, associated with accelerated systemic estrogen concentration. In 2012, Wong et al. conducted a study in order to determine whether or not the effects of alcohol on mammary tumor development are modulated in any way by the presence of ovarian estrogen. Surprisingly, the research revealed that an ovariectomy performed on mice subjects -- a procedure of removing the ovaries and ovarian hormone production, lowers the enhancement effect of alcohol on tumor growth as far as 20%. Consequently, these results form two conclusions. Firstly, previous assumptions supporting the fact that alcohol use promotes breast cancer development, through the estrogen signaling pathway, are proven accurate. Secondly, these findings launch the theory that the accelerating effects of alcohol on breast cancer may be prevented by blocking estrogen signaling (Brooks et al., 2013).
In conclusion, it can be asserted that alcohol aggravates the health condition of any human body. As most research from across the past five years appears to illustrate, general concern regarding alcohol's significant contribution to the global burden of disease has justified the direction of investigating further and further into the already known effects of this substance on specific body parts, and thereby delving into a correlative scope that quantifies connections between affected organs, immunity, infectious conditions, gestational risks and injury.
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