Does Drinking Alcohol Affect Kidneys

Does Drinking Alcohol Affect Kidneys – Percentage of alcohol-related cancers, by country. Estimated 2020 incidence of cancer (PAF) by alcohol consumption, in both sexes

Alcohol causes cancer of the esophagus, liver, breast, colon, oral cavity, rectum, pharynx, and larynx, and possibly pancreatic cancer.

Does Drinking Alcohol Affect Kidneys

Drinking any amount of alcohol can cause cancer. The more alcohol you drink, the higher your risk of developing cancer.

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Alcoholic beverages were classified as Group 1 carcinogens by the International Agency for Research on Cancer (IRC) in 1988.

Globally, 3.6% of cancer cases and 3.5% of cancer deaths are caused by alcohol consumption (mainly acetaldehyde, a metabolite derived from ethanol).

Also secondary mechanisms of liver inflammation, microbiome dysbiosis, reduced immune system function, retinoid metabolism, increased inflammation levels, 1-carbon metabolism and disruption of folate absorption.

Heavy alcohol consumption, which included 15 or more drinks per week for women or 8 or more drinks per week for women, contributed the most to cancer incidence compared to moderate alcohol consumption. The ratio of alcohol-related cases is 3:1 men:women, especially throat and liver cancer.

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Some countries have introduced warning labels on alcohol packaging informing consumers about alcohol and cancer. The alcohol industry has tried to mislead the public about the potential cancer risk from drinking alcohol, and has argued for repeal of laws requiring alcohol to contain cancer warnings.

In the United States, alcohol-related cancer rates were highest in the following states: Delaware, Colorado, Washington, DC, New Hampshire, and Alaska.

In the year From 2013 to 2016, about 19,000 (4%) cancer-related deaths in the United States were attributable to alcohol consumption each year, with breast cancer and esophageal cancer being the most common causes of death in both women and men.

3.2% of cancer deaths in the United States are due to alcohol consumption. The distribution of mortality by state corresponds to the distribution of incident cases.

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In Europe, approximately 10% and 3% of cancer diagnoses in men and women are alcohol-related.

Europe: A 2011 study found that one in 10 cancers in women and one in 33 in women is due to past or current alcohol consumption.

In the year In 1998, the World Health Organization’s International Agency for Research on Cancer classified alcohol as a carcinogen. The review states: “There is sufficient evidence for the carcinogenicity of alcohol in humans. Alcoholic beverages are carcinogenic to humans (group 1).

After more epidemiological evidence linking alcohol and cancer was discovered, the IARC struck again in 2007. Based on epidemiological studies that showed that the risk of cancer is independent of the type of alcohol and animal studies that show the risk of exposure to ethanol alone, the group concluded that the ethanol in alcoholic beverages is carcinogenic to humans. Alcohol is said to increase the risk of breast cancer, liver cancer, colon cancer, throat cancer, larynx cancer, and mouth cancer. In the year In 2009, the team found that ethanol’s metabolite, acetaldehyde, is also carcinogenic to humans.

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In the year In 2021, the 15th report of the US National Toxicology Program (NTP) classifies alcohol consumption as a “known human carcinogen”, while acetaldehyde is classified as a “reasonably suspected human carcinogen”.

Acetaldehyde is a byproduct of ethanol breakdown in the liver and is produced by alcohol dehydrogenase (ADH), cytochrome P-450 2E1, and bacterial catalase.

The liver normally removes 99% of acetaldehyde. ALDH2 converts acetaldehyde to acetate, a byproduct that can be excreted by the liver. People with ADH1B*1 have a higher rate of conversion of ethanol to acetaldehyde, while people with ALDH2*2 have a slower rate of conversion of acetaldehyde to acetate, leading to rapid accumulation of acetaldehyde.

On average, the liver can process 7 grams of ethanol per hour. For example, it takes 12 hours to remove ethanol in a bottle of wine, which is equivalent to 12 hours or more of exposure to acetaldehyde.

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The acetaldehyde motif can block DNA repair and synthesis mechanisms to change its physical shape or trigger mutations, breaks, and substitutions.

DNA methylation is the addition of a methyl group to the 5th carbon of a nucleotide. The most common site of methylation is on the cysteine ​​in front of the guanine nucleotide.

This methylation is sensed by DNA methyltransferase enzymes, which obtain the methyl group from SAMe. Heavy alcohol consumption causes DNA transcriptional changes by reducing the availability of SAMe and altering DNA methylation patterns.

Oxidative stress and ROS[? ] accumulation plays an important role in the development of cancer. Ethanol metabolism by CYP450 2E1 to acetaldehyde results in ROS. The presence of ROS in the cellular environment leads to lipid peroxidation, which can lead to exocyclic pathways.

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ROS in the tumor microenvironment may also act as an intracellular signal leading to the upregulation of vascular endothelial growth factors and monocyte chemotactic protein 1.

Iron accumulation has been found to be associated with alcohol consumption, which results in higher levels of peroxides and consequent oxidative damage.

High serum hormone levels are associated with alcohol consumption. In particular, estrogen and estrogen can increase transcriptional activity in ER+ cells, which promotes cell proliferation.

People who use progestin contraceptives before menopause have some compensation for high estrogen levels, although people who take more after menopause have a higher risk of breast and estrogen-related cancers.

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Additional mechanisms may contribute to the risk of cancer associated with alcohol consumption. It is believed that heavy alcohol consumption can reduce the availability of folic acid, which may reduce the availability of nucleotides for DNA repair.

In addition, ethanol may reduce the conversion of homocysteine ​​to methionine, an essential amino acid involved in the formation of SAMe.

Alcohol-induced inflammation increases the production of various cytokines, particularly NF-κB.

In addition, alcohol consumption is associated with low levels of vitamin A, which reduces retinoid turnover and signaling.

Does Alcohol Cause Kidney Stones?

People who smoke and drink are more likely to develop oral, pharyngeal, and pharyngeal cancers. Ethanol in cigarettes is believed to be a carcinogen.

Studies have shown that the risk of developing these types of cancer is 35 times higher than that of non-smokers and non-drinkers. This evidence may indicate a cocarcinogenic interaction between alcohol- and tobacco-related carcinogens.

The risk of alcohol-related cancers is high in tissues that are closely related to alcohol consumption, such as the oral cavity, pharynx, and esophagus. This is explained by the fact that ethanol is carcinogenic, and also the metabolite of ethanol (acetaldehyde) produced in the liver is highly carcinogenic, which explains both local (cancer of the mouth, throat, esophagus) and distant (skin, liver). breast cancer). Ethanol is known to cause high levels of cell death in alcoholic beverages. If cells are exposed to 5-10% ethanol or 15-second exposure to 30-40% ethanol for 1-hour in cell culture, a few surviving cells may undergo genetic changes leading to carcinogenesis. However, there is evidence that ethanol’s cytotoxic effect on cells in the mouth, throat, and esophagus activates the division of stem cells deep in the muscle layer to replace dead cells. Every time stem cells divide, they become more susceptible to gotoxic activity from cell division (for example, mutations during DNA replication and chromosomal changes during mitosis) and also to DNA-damaging substances (for example, acetaldehyde and others). Tobacco carcinogens). Alcohol consumption may increase the risk of oral cavity, pharynx, and esophageal cancer by causing accumulation of cell components in stem cells that maintain these tissues in homeostasis. Since the cytotoxic activity of ethanol is concentration-dependent, the risk of these cancers increases not only with increasing ethanol levels, but also with higher doses; An ounce of whiskey is more likely to be carcinogenic undiluted than when mixed with sweetened beverages. The local cytotoxic effect of ethanol may explain the known similarities between alcohol and tobacco consumption in the risk of these cancers.

A study has shown that alcohol promotes epithelial-mesenchymal transition (EMT), which causes normal cancer cells to become more aggressive and begin to spread throughout the body.

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A study on the effect of alcohol consumption on hepatocellular carcinoma (HCC) type C cirrhosis patients showed that alcohol affects the tumor doubling time (TVDT).

A study on chicken embryos suggests that alcohol promotes tumor growth by producing a growth factor that causes blood vessels to form in the tumor.

In the year A 2006 study in mice showed that moderate alcohol consumption led to larger, harder tumors through a process known as angiogenesis.

A study in which rats were given large amounts of alcohol showed that alcohol accelerates the development of cancer by accelerating the accumulation of body fat by suppressing the immune system.

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Acetaldehyde, produced by alcohol metabolism, plays a role in alcohol-induced carcinogenicity, requiring mutations in the enzymes involved.

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