A PERSON EXPERIENCING:• FATIGUE• THIRST• EXTRA SENSITIVITY TO LIGHT• NAUSEA OR VOMITING• LACK OF CONCENTRATION• DIZZINESS

• ACHES• SLEEPLESSNESS• DEPRESSION• ANXIETY• IRRITABILITY• RAPID HEARTBEAT

IS FEELING

HANGOVEROR "DISCOMFORT FOLLOWING OVERINDULGENCE"

ETHANOL VS. LIVER ENZYMES

Ethanol metabolism. A: ethanol metabolism occurs in two steps: ethanol is metabolized quickly by alcohol dehydrogenase (ADH) to generate acetaldehyde. Acetaldehyde is then metabolized by the mitochondrial aldehyde dehydrogenase 2 (ALDH2) to acetate. The first step of metabolism, catalyzed by ADH, is a reversible reaction. The second step, catalyzed by ALDH2, is the rate-limiting step in ethanol metabolism, and it takes ∼1 h to metabolize the amount of ethanol that is found in a single alcoholic beverage. B: ethanol metabolism occurs mainly in the liver. In normal ALDH2 individuals, acetaldehyde is quickly oxidized to nontoxic acetate. In ALDH2 enzyme-deficient (ALDH2*2) individuals, a significant amount of acetaldehyde is rapidly accumulated even after a moderate amount of alcohol ingestion. Acetaldehyde, which is very diffusible and crosses biological membranes, can be circulated in the blood and metabolized in all tissues, as ALDH2 is present in all mitochondria.

Diseases in which activators of ALDH2 may be beneficial. Red highlights diseases where the evidence for ALDH2 role came from preclinical proof-of-concept studies. Blue highlights diseases where ALDH2 role was supported by clinical observations. Black highlights diseases where evidence from both preclinical studies and from human epidemiological or pathohistological studies supports a role for ALDH2.

Ethanol-induced cardiotoxicity. ALDH2 confers protection against ethanol toxicity by affecting the activity of key proteins in cardiac myocytes. The scheme summarizes data from transgenic mice that elucidated the potential pathways that are regulated by ALDH2 and acetaldehydes. Activation of ALDH2 or ALDH2 overexpression were found to confer cardiac protection by regulating autophagy and apoptosis through the balance between AKT and AMPK and their downstream substrates, such as MTOR, STAT3, NOTCH1, PP2A, and PP2C (93, 98, 112).

THERE IS NO CURE TO HANGOVERS. IT WOULD APPEAR IT’S LINKED TO

AN IMMUNE SYSTEM RESPONSE. IN VERY SIMPLE TERMS,

GETTING BLIND DRUNK IS A LITTLE LIKE SELF-IMPOSED FLU. DRINKING PLENTY OF FLUIDS WON’T DO YOU ANY HARM, BUT IT’S NOT ACTUALLY A

SOLUTION.

REFERENCES:

• HTTP://SKOLYAR-STUDENT.RU/PHOTOS/GOLOVNYE-BOLI-POSLE-PRIEMA-ALKOGOLYA-NA-UTRO-121106-LARGE.JPG

• HTTPS://EN.WIKIPEDIA.ORG/WIKI/HANGOVER

• HTTP://WWW.MAYOCLINIC.ORG/DISEASES-CONDITIONS/HANGOVERS/BASICS/SYMPTOMS/CON-20025464

• HTTP://PHYSREV.PHYSIOLOGY.ORG/CONTENT/94/1/1

• HTTPS://CHRONICLEFLASK.COM/2015/08/29/DOES-DRINKING-ALCOHOL-ACTUALLY-CAUSE-DEHYDRATION/

• HTTP://DISINHERITED.COM/WHERE-THERE-WILL-I-WANT-BE-IT-CAN-I-SAY-NO/DONT-WANT-IT/

• HTTP://DISINHERITED.COM/WHERE-THERE-WILL-I-WANT-BE-IT-CAN-I-SAY-NO/DONT-WANT-IT/