An estimated 3.5% of all cancer deaths in the U.S. are cancer related (almost 20,000) deaths yet only one in ten people are aware that alcohol is a carcinogen… in fact, many people are strong proponents for the “benefits of alcohol,” yet as more research is conducted, “The promotion of health benefits from drinking at moderate levels is seen increasingly as disingenuous or irrelevant in comparison to the increase in risk of a range of cancers,” apparently unbeknownst to the public.

“Responsible drinking” has become a 21st-century mantra for how most people view alcohol consumption. But when it comes to cancer, no amount of alcohol is safe. But surely, light drinking doesn’t cause or contribute to cancer? Apparently, it does. In a meta-analysis of 222 studies comprising 92,000 light drinkers and 60,000 nondrinkers with cancer, light drinking was associated with risk for oropharyngeal cancer, esophageal squamous cell carcinoma, and female breast cancer.

So, why isn’t this information viral; why isn’t the public being awared to this pertinent and important information? Well, the information is certainly out there: searching alcohol causes cancer turns up many veritable and scientific affirmations of the search, yet a search for just alcohol effects doesn’t mention cancer outright: one must click on an article and scroll typically to the bottom to see a transient mentioning of cancer, with no explanation for how alcohol directly causes the cancer. I think its exceptionally important to spread this information, as alcohol abuse is largely related, at least in the college age groups as far as I have seen, to the notion that “alcohol is not a drug” when it indeed is—I believe alcohol could be consumed much less or at least more safely if it weren’t perceived as something more playful than what it actually is.

Alcohol has been scientifically proven to be a strong factor in the causation of head, neck, esophageal, colorectal, liver, and breast cancer and a weaker but definite factor in the causation of pancreatic, prostate, and skin (melanoma) cancer. In addition, a study in Chile found a fourfold increase in hemorrhagic stroke in heavy drinkers. While alcohol may contain up to 15 carcinogenic compounds, the predominant and most well-understood mechanism of alcohol’s relation to cancer is the formation of acetaldehyde by alcohol breakdown. Alcohol dehydrogenase breaks ethanol down into acetaldehyde, which is further broken down by acetaldehyde dehydrogenase into acetate, which can be excreted. Acetaldehyde, though, either through buildup via excessive drinking or repeated transient interactions via long-term alcohol consumption, binds with high affinity to many substances, inhibiting metabolic pathways of healthy functioning, as well as increasing liver enzymes, p450 oxidases, which detoxify alcohol metabolism byproducts through oxidating them, generating reactive oxygen species in the process. Aging is quite literally oxidation, which is carried out in deleterious fashions within the body by reactive oxygen species, the direct product of composite exposure to carcinogens, via the oxidation and therefore damaging of DNA, RNA, lipids and proteins. This can not only damage genes, but also impair the bodies ability to repair them. Another mechanism of carcinogenesis is the increase in the production of estrogen, causing women who have at least three drinks a day has 1.5 times the risk of developing breast cancer compared to non-drinkers. The last mechanism of carcinogenesis is direct cellular-level effects on the liver, including the induction of quicker mitosis of hepatocytes as well as causing cirrhosis via chronic inflammation and the accumulation of fatty bodies (see Sugar: The Bitter Truth for the biological mechanism; it is parallel to the metabolism of fructose).

A list of specific pathogeneses of Acetaldehyde(Ah):

-Ah binds to red blood cell integral membrane proteins, stiffening their walls such that they cannot travel through small capillaries and also binds to hemoglobin, reducing its ability to interact with red blood cells causing an ultimate effect of then body being unable to deliver sufficient oxygen to metabolizing organs.

-Antibodies form against the Ah if chronically present, causing an immune response resulting in liver inflammation (contribution to cirrhosis)

-Ah interacts with tubulin such that they can not dimerize to form microtubules effectively. Microtubules provide structural support of nerves, especially dendritic extensions, and a framework upon which nutrients are distributed throughout the neuron. Lack of microtubule integrity leads, ultimately, to dendritic atrophy and death (leading to neural symptoms)

-Ah binds with high affinity to vitamin B1 (Thiamin), which helps to detoxify Ah but is damaged in the process. Thiamin is essential for nerve function and the intracellular production of ATP and acetylcholine (a global neurotransmitter)

-NAD and niacin (B3) also helps detoxify AH and is destroyed in the process. This leads to NADH accumulation, causing reversal or inactivation of basic and integral metabolic pathways, such as the glycolytic pathway leading to fatigue and fat accumulation. Even mild niacin deficiency causes a variety of neurological manifestations.

-Ah binds to pantothenic acid (B5), impairing acetyl CoA and therefore arresting all energy production pathways

-Ah binds with strong affinity to P5P (Pyridoxal-5-Phosphate) and D6D (Delta-6-Desaturase) which are necessary to in the conversion of dietary fatty acids to long chain fatty acids and prostalglandin essential to nerve function which are only supplied via metabolism

-Ah interacts with dopamine and serotonin to form tetrahydro-isoquinolines which are related in structure and presumably function to opiates, explaining the physical addiction to alcohol



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