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Injury is defined as physical damage or harm that is done or sustained. The potential of injuring oneself or others can be increased after consuming alcohol due to the certain short term effects related to the substance such as lack of coordination, blurred vision, and slower reflexes to name a few. [95]
Extreme levels of consumption can cause alcohol poisoning and death; a concentration in the blood stream of 0.36% will kill half of those affected. [2] [3] [4] Alcohol may also cause death indirectly by asphyxiation, caused from vomiting. Alcohol can greatly exacerbate sleep problems.
Alcohol and cortisol have a complex relationship. While cortisol is a stress hormone, alcoholism can lead to increased cortisol levels in the body over time. This can be problematic because cortisol can temporarily shut down other bodily functions, potentially causing physical damage.
Alcohol crosses the placental barrier and can stunt fetal growth or weight, create distinctive facial stigmata, damaged neurons and brain structures, and cause other physical, mental, or behavioural problems. [222] Fetal alcohol exposure is the leading known cause of intellectual disability in the Western world. [223]
Alcohol-related brain damage [1] [2] alters both the structure and function of the brain as a result of the direct neurotoxic effects of alcohol intoxication or acute alcohol withdrawal. Increased alcohol intake is associated with damage to brain regions including the frontal lobe , [ 3 ] limbic system , and cerebellum , [ 4 ] with widespread ...
Based on responses, researchers estimated that 94 million Americans felt politics caused significant stress, 44 million lost sleep, 30 million suffered physical health harm, and 11 million had ...
The long-term impact of alcohol on the brain has become a growing area of research focus. While researchers have found that moderate alcohol consumption in older adults is associated with better cognition and well-being than abstinence, [1] excessive alcohol consumption is associated with widespread and significant brain lesions.
This presents a novel indirect mechanism and suggests that a metabolite, not the ethanol itself, could cause the behavioural or symptomatic effects of alcohol intoxication. Many of the primary targets of ethanol are known to bind PIP 2 including GABA A receptors, [ 30 ] but the role of PEth needs to be investigated further.