Is Alcohol A Neurotoxin?

Is Alcohol A Neurotoxin
Studies clearly indicate that alcohol is neurotoxic, with direct effects on nerve cells. Chronic alcohol abusers are at additional risk for brain injury from related causes, such as poor nutrition, liver disease, and head trauma.

Is alcohol a toxin to the body?

Alcohol has considerable toxic effects on the digestive and cardiovascular systems. Alcoholic beverages are classified as carcinogenic by the International Agency for Research on Cancer and increase the risk of several cancer types.

Is alcohol a natural toxin?

Alcohol consumption is part of many cultures and wildly so in American culture. Mortality from alcohol-related disease was up 40% from 1999-2017, and in 2020 alcohol intake increased by over 30% by some reports, creating a pandemic of its own. From an evolutionary standpoint intake of alcohol containing fermented liquids and foods may have had an advantage for us.

  • In the primitive world, the fermentation process may have had a preservative role and controlled the pathogen load we might have ingested.
  • Fermentation may have allowed safe hydration in times of clean water scarcity and allowed for some food preservation to bridge times of food scarcity.
  • Alcohol was never a foreign substance to us, as some bacteria in our intestines that we evolved with use fermentation for metabolism and produce alcohol at low levels every day.

Therefore, we evolved with enzymes, most notably alcohol dehydrogenase, that metabolize alcohol and convert it into a usable energy source for us, as well. Another evolutionary advantage. However, the concentration of alcohol in fermented liquids and foods was very low compared to the concentrations we see today from the more complex brewing and distilling processes of the modern world.

  • The concentration of alcohol produced or consumed by us in our prehistoric lives was easily metabolized prior to any significant toxic effects.
  • The alcoholic drinks and the patterns of alcohol consumption we see today can overload our system’s ability to metabolize the alcohol, resulting in intoxication and toxicity.

A recent University of Oxford study concluded that no amount of alcohol is good for you. Moderate alcohol consumption was associated with lower total brain volumes, lower brain grey matter volumes, negative white matter changes, higher blood pressure, and higher body mass index.

Binge drinking made the picture even worse. We have been taught for generations that moderate alcohol consumption may in fact be good for us. The thought has been that the relaxation effect was therapeutic. This rational lead to the common theory that alcohol exerts its effects primarily through our bodies’ neurotransmitter network.

Alcohol has been reported to enhance GABA (gamma amino butyric acid, an inhibitory neurotransmitter) release and act directly at GABA receptors as mechanisms by which alcohol causes relaxation. Alcohol has also been reported to decrease glutamate (an excitatory neurotransmitter) receptor activity, thus furthering a relaxation response.

  1. These combined effects would result in increased inhibition and decreased excitation and would produce a state of overall calm and relaxation, if not sleepiness.
  2. However, people who consume alcohol aren’t always relaxed and subdued: Sometimes they are euphoric, excited, hyperactive, impulsive, disinhibited, and aggressive.

There is some explaining to do. So, the story goes that alcohol also causes the release of dopamine, an activating, feel good, re-enforcing neurotransmitter that stimulates sympathetic nervous system activity, movement, and approach behavior. Which is it? Relaxed? Activated? To make things more complicated, there has been some further thought that serotonin release may be increased as well; yet, in general, alcohol is considered a depressant, which seems inconsistent with this thought.

  1. Acetylcholine is frequently left out of this conversation.
  2. Acetylcholine is the major neurotransmitter in our parasympathetic nervous system, the breed, feed, digest and rest system, and would be a likely candidate for precipitating a relaxation response.
  3. However, acetylcholine seems to be down-regulated by alcohol.

Hmm. In addition, there has been the thought that alcohol may also stimulate the endogenous opioid system to provide a further sense of relaxation, reward, and pleasure. There is an incoherence to this story, in that fundamentally we are first taught alcohol relaxes us (+GABA, feel good) but also stimulates us (+dopamine), feel good, then that it acts as a depressant (-dopamine/-norepinephrine/-serotonin, feel bad).

So what is it: up or down? Feel good or feel bad? Can this incoherence be pulled together into a story with coherence? In fact, it can, and the story that evolves can not only further our understanding of alcohol’s effects on our physiology but shed some light on how we can stay well and healthy overall—unfortunately, not with the use of alcohol.

What if alcohol is simply a toxin? A physical threat to us? Not to discount the findings outlined above, in fact to include and explain most of them, we should look at alcohol as a toxin under the lens of Threat versus Safety and the associated physiologies of threat to see how the story may play out.

  • We humans are not constant even in threat.
  • We are ever-changing in our physiology depending on our environment (extracorporeal and intracorporeal, and extracellular and intracellular).
  • We lack distinct set points, and homeostasis is more of a myth than a reality, but there are patterns of physiologic change that are similar whether we are under a physical attack by a virus, a bear, a toxin, or even another person—whether it be a physical attack or a psychological one.

Even social and cultural attacks such as disenfranchisement, discrimination, and injustice present with similar physiologic changes. The patterns can be viewed as programmed biological survival mechanisms that involve resource conservation and allocation when we are under attack.

  1. With all that in mind, let’s set aside the neurotransmitters for the moment and view alcohol as just a toxin not a ligand, neither an agonist nor an antagonist.
  2. Consider the brain’s dissociation or dissolution process when under the threat of alcohol.
  3. With low levels of threat (consider 1-3 drinks) our system tends towards a mobilization response—something is wrong, so do something.

We turn down the brain functions that won’t help us in an attack, notably the prefrontal cortex (PFC). With the loss of PFC functions, we can become kinetic, reactive, impulsive, and sometimes aggressive. More specifically, whether a bear attack or a toxin attack, the dorsal lateral prefrontal cortex (DLPFC), the part of the brain that helps us to plan and reason and to be contemplative and creative, is not of value and is turned down.

  • It isn’t time to negotiate a settlement nor invent the wheel when being attacked by a bear, and a toxin attack follows suit.
  • Whether a bear attack or a toxin attack, we also turn down the ventral medial prefrontal cortex (VMPFC), the part of the brain that allows us to have empathy for others and to connect and bond with others.

Neither toxins nor angry bears respond well to these functions. Maybe, most important to this discussion is our turning down the medial prefrontal cortex (MPFC) when under attack. This part of the brain is involved in emotional regulation and social calculations, norms, constructs, and constraints.

  • This is the part of the brain involved with our sense of “shoulds”, “musts”, “need to’s” and “have to’s”—the governance of our behavior.
  • In a bear or toxin attack survival is key; who cares what the bear or toxin thinks of us! Resource conservation and allocation rule in an attack.
  • Survival is key.
  • Why is the MPFC so important? The MPFC can directly inhibit the nucleus accumbens (NAc), the tip-top of a part of our brain that integrates our emotions with our cortex and our awareness.

This nucleus is connected all the way down to the midbrain’s ventral tegmentum, and when eMOTIONS arise they create impulses to move and express, seek pleasure and pursue rewards, or just be pissed off and angry and fight, or triggered and kinetic and flee.

It is our MPFC that inhibits these eMOTIONs and says “no, don’t to that”, “you should do this”, “you must do that”, “you need to do this”, or “you have to do that”, thus stifling the eMOTIONs’ impulse or desire for movement, for action. But the eMOTIONs don’t easily go away. They may continue to poke and prod to get out, thus keeping the MPFC and the NAc in a constant tug of war—conflict.

Or our thoughts and eMOTIONS may be suppressed and repressed below awareness where they continue to push our threat and stress buttons. Neither scenario is particularly good for our physiology. With alcohol consumption, the cortical dissociation or dissolution that occurs turns down the MPFC and its control over the NAc, thus releasing the eMOTIONAL network to express itself in a flush of euphoria and excitement.

  • We feel free from the chains of the MPFC.
  • This release feels really good.
  • Perhaps this is why moderate drinkers could possibly live longer—a brief reprieve from the burdens of life, mediated by a toxic retreat of the cortical brain.
  • It is also most certain that this effect, and the brief pleasure associated with it, is a major driver of alcohol addiction,

However, in the background of this initial pleasurable response is the progression of the threat response and toxicity. As the alcohol concentration increases, the threat load increases (consider 3-6 drinks); we see further cortical dissociation in the PFC and the dissociation descends below the PFC into older cortical structures such as the cingulate and insular cortex.

With this we not only see the loss of executive functions ( IQ ) and deterioration in emotional regulation and social integration ( EQ ) but a more generalized fogging and numbing progression into a stuporous state. Consistent with a progressive threat response we can see the transition from a mobilization response to an immobilization response (threat1 to threat2 phenotype).

What we initially saw as disinhibition of our eMOTIONAL system can, with a progressive concentration of alcohol, flip to dissociation or dissolution of both our eMOTIONAL and movement systems. This progression can run through the entirety of the striatum all the way down into the midbrain, as well as, involving the cerebellar structures.

At this point we are progressively stuporous—cognitions, emotions, sensations and coordinated movements are all shutting down. Eventually, it becomes difficult to remain upright and coherent. At this point we can have a desire to lie down or we may simply pass out. More worrisome is when the dissociation or dissolution progresses into the medullary structures of the brain.

Vestibular dysfunction with vertigo is common. The toxin trigger zone for nausea and vomiting will sense too much alcohol and initiate purging. Most worrisome is the down-regulation of the autonomic nervous system’s control of our heart and respiratory rates and rhythms.

  • As brainstem functions slip away due to severe alcohol intoxication, coma is induced and death can follow.
  • In this model one can visualize with increasing alcohol intake and intoxication the progressive dissociation or dissolution of the brain from the tip of the prefrontal cortex to the deeper cortical structures to subcortical structures to the very basal brainstem structures.

Intoxication is the progressive shutting down of the brain (and body) from a toxin that follows the pattern of all progressive threat responses. The elation of the initial MPFC dissociation or dissolution can be followed by a whole lot of hurt. The neurotransmitter model is probably not the right way to look at alcohol intoxication, but as the neurotransmitters are a part of THE SYSTEM and a coordinated threat response, they are involved, just not primary mediators of the response.

  1. The MPFC dissociation or dissolution and release of the NAc restraint will result in a dopamine surge and, less so, a serotonin surge, flowing from the ventral tegmentum and raphe nucleus up the striatum into the cortex.
  2. This surge can explain the euphoric, energized, reinforcing and disinhibited state of early intoxication.
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Note that this state has more to do with alcohol/toxin-induced prefrontal senescence than direct alcohol-induced agonist or antagonist neurotransmission itself. Beyond the initial dopamine and serotonin surge from the dissociation of the PFC, dopamine and serotonin production and signaling are waning with progressive alcohol use and associated toxicity.

Norepinephrine will eventually follow suit. Also, acetylcholine and GABA production and signaling are reduced. Viewing this progression through the neurotransmitters one can see “the relaxation response” is progressive brain dissociation more than neurotransmission, as the relaxation neurotransmitters are being down-regulated.

The outlier neurotransmitter is glutamate, which rises quickly in threat. Glutamate is our most abundant and most primitive neurotransmitter and a primary danger signaler. Glutamate is more persistent than norepinephrine and epinephrine in progressive threat states.

  • Common to threat responses is the activation of glutaminergic signaling.
  • While most neurotransmitters are being down-regulated under progressive threat, glutamate signaling irises for a much longer period of time; its production from glucose, alpha-ketoglutarate and glutamine increases.
  • Breakdown of glutamate is decreased, through inhibition of glutamine synthesis.

Too, conversion of glutamate to GABA is blocked. Enzymes, such as the transaminases, are required in this process, and ammonia is a byproduct of glutamate production. In general glutamate is an excitatory neurotransmitter but at times glutamate can have an inhibitory effect.

  • Because of this multiplicity, glutamate can influence different brain structures differently.
  • Glutamate can strengthen certain structures while weakening other structures.
  • In threat, glutamate is initially selectively more excitatory to the more primitive limbic structures of the brain, while having deleterious effects to newer cortical structures.

This model holds up for both acute and chronic alcohol use and helps explain both the acute and chronic physiologic changes, if not disease and illness, associated with alcohol use. The model of progressive threat explains the neurophysiologic changes, including the neurotransmitter changes, seen with alcohol use.

It also explains the increase in endogenous opioids (remember that endogenous opioids are less a part of the pleasure/reward network and very much a part of the threat response). Therefore, as alcohol-induced threat escalates, one would expect endogenous opioids to rise. It is also notable that the classic neurotransmitters—dopamine, norepinephrine, serotonin, acetycholine, GABA, and glutamate—are contextual and can have roles in both threat and safety physiology.

In exploring threat signaling, clarity demands that we leave the neurotransmitters behind and dive into molecular, intracellular, and intercellular networks and signaling. It is at this deeper level where we can really see the toxic effects of alcohol and its stimulation of a danger response.

At this level there are changes in genetic transcription, increases in intercellular signaling by threat cytokines, alterations in mitochondrial structures and metabolism to favor glycolysis and inflammation, all of which can progress to overall cellular alterations and eventual cellular shut down that extends well beyond the brain.

The response to alcohol is one of systemic intoxication and toxicity that comes to our awareness in our brains but has not spared our bodies. Alcohol consumption is associated with obesity, diabetes, cardiovascular disease including arrhythmias, gastrointestinal disease including liver and pancreas diseases, psoriasis, gout, anxiety, depression, dementia, and cancer, just to name a few comorbidities.

It all comes from the same soup and is dictated by total threat load, to which the toxin alcohol can be a substantial contributor. Within this model also consider: Hangovers are less alcohol metabolite- (aldehyde) induced and more threat cytokine-induced. Craving is reverse dissociation or dissolution into a low dopamine, serotonin, acetylcholine, and GABA state (no rush or relief), and a high threat cytokine, glutamate, and norepinephrine state.

Withdrawal is craving in the extreme—high threat cytokines, glutamate, norepinephrine—characterized by headache, body ache, goose flesh, sweating, nausea, vomiting, loss of appetite, fast heart rate, high blood pressure, tremor, anxiety, irritability, disorientation, hallucinations and seizures.

Alcohol is a toxin and little more than a toxin. Alcohol is a threat and creates a threat response. No amount of alcohol is actually good for us even if it makes us feel good. Alcohol intoxication is progressive dissociation or dissolution of the brain. Alcohol has many deleterious effects throughout the body. Cultural constructs and constraints play major roles in the drive for alcohol use. If we decrease the conflict between the medial prefrontal cortex and the nucleus accumbens by other healthy means, we won’t want or “need” alcohol.

Stay Safe and Stay Tuned.

What does alcohol do to neurons?

Short-term alcohol exposure tilts the balance toward inhibition by both enhancing the function of inhibitory neurotransmitters and neuromodulators (i.e., GABA, glycine, and adenosine) and decreasing the function of excitatory neurotransmitters (i.e., glutamate and aspartate).

Is wine a toxin?

Is Your Wine Full Of Toxins? Is Alcohol A Neurotoxin Dry Farm Wines, a wine club that globally sources only from dry-farmed vineyards, is Keto- and paleo-friendly, low-alcohol, low-sulfite and sugar-free,Photo: Karsten Wurth Most wines today are highly processed, just like most foods—filled with toxic trace chemicals that can carry serious health risks.

Almost all modern vineyards spray with chemicals, such as the weed-killer Roundup, whose active ingredient, glyphosate, has shown strong associations with a range of diseases, including cancer and Parkinson’s. As a result of successful lobbying efforts from the wine industry, wine is the only major food product with no ingredients label.

Wines may contain dozens of toxic additives, and you wouldn’t know.U.S. wine producers can legally, and without disclosure, use 76 different FDA-approved additives without disclosing any of them on the bottle—substances like mega purple coloring dye, fish bladders, sulfur dioxide, and dimethyl dicarbonate, which is so toxic that it must be applied by specialists in hazmat suits.

The process of creating these new wines also impacts the environment. More than 95 percent of U.S. vineyards are now irrigated—and irrigation leads to diluted fruit and weaker plants. Fifteen years ago, the average alcohol level in wine was 12.5 percent; today, the average is more than 14 percent. With this higher alcohol content, it’s harder to enjoy wine without a host of negative consequences: hangovers, headaches, stomach issues, brain fog and poor sleep.

The Real Food Movement has us celebrating grass-fed meats, wild-caught fish, organically grown vegetablesand then we pair these wholesome foods with chemical-laced alcoholic concoctions that are high in two substances proven to have an adverse impact on health: sugar and alcohol.

There is a way to ensure that the wine you drink is better for your health, more sustainable for the environment, and more nourishing for your soul: Join the Natural Wine Movement by demanding natural wine, made with no chemical or technological intervention. The word is spreading, and this movement is growing.

From an elegant French ploussard, to a bolder South African syrah, to a tall, slender bottle of an Austrian grüner veltliner, the Natural Wine Movement is really a journey to rediscovering wine. Real wine. Natural wine isn’t easy to find. To enjoy wine that agrees with my ketogenic lifestyle, I started Dry Farm Wines, a wine club that globally sources only from dry-farmed vineyards that use no irrigation.

  • Following strict health and taste criteria, we perform independent lab tests on every wine for purity and alcohol content.
  • Eto- and paleo-friendly, Dry Farm Wines are low alcohol, low sulfite and sugar-free.
  • The more alcohol there is in a wine, the bolder and richer it will be.
  • When you eat clean on a regular basis, you start to crave wines that are also cleaner, fresher and lighter.

The standard American diet deadens the palate—but consistently eating clean repairs the palate, so natural wines end up tasting better, and we feel better after drinking them. If you’re passionate about healthier living, higher taste, supporting sustainable farmers, and tapping into the deep connection that wine represents, join the Natural Wine Movement.

Is beer a toxin?

Last week I attended a discussion group chaired by the Observer’s health correspondent Denis Campbell where one of the other experts, a public health doctor, asserted that alcohol should be treated differently from tobacco (and by inference other drugs) because there is no safe dose of tobacco whereas alcohol is safe until a person’s drinking gets to “unsafe” levels.

  • Its health benefits for the cardiovascular system are also often used to support the claim that in low doses alcohol is safe, for how else could it be health-promoting? The myth of a safe level of drinking is a powerful claim.
  • It is one that many health professionals appear to believe in and that the alcohol industry uses to defend its strategy of making the drug readily available at low prices,

However, the claim is wrong and the supporting evidence flawed. There is no safe dose of alcohol for these reasons: Alcohol is a toxin that kills cells such as microorganisms, which is why we use it to preserve food and sterilise skin, needles etc. Alcohol kills humans too.

  1. A dose only four times as high as the amount that would make blood levels exceed drink-driving limits in the UK can kill,
  2. The toxicity of alcohol is worsened because in order for it to be cleared from the body it has to be metabolised to acetaldehyde, an even more toxic substance.
  3. Any food or drink contaminated with the amount of acetaldehyde that a unit of alcohol produces would be immediately banned as having an unacceptable health risk.

Although most people do not become addicted to alcohol on their first drink, a small proportion do. As a clinical psychiatrist who has worked with alcoholics for more than 30 years, I have seen many people who have experienced a strong liking of alcohol from their very first exposure and then gone on to become addicted to it.

We cannot at present predict who these people will be, so any exposure to alcohol runs the risk of producing addiction in some users. The supposed cardiovascular benefits of a low level of alcohol intake in some middle-aged men cannot be taken as proof that alcohol is beneficial. To do that one would need a randomised trial where part of this group drink no alcohol, others drink in small amounts and others more heavily.

Until this experiment has been done we don’t have proof that alcohol has health benefits. A recent example of where an epidemiological association was found not to be true when tested properly was hormone replacement therapy. Population observations suggested that HRT was beneficial for post-menopausal women, but when controlled trials were conducted it was found to cause more harm than good,

For all other diseases associated with alcohol there is no evidence of any benefit of low alcohol intake – the risks of accidents, cancer, ulcers etc rise inexorably with intake, Hopefully these observations will help bring some honesty to the debate about alcohol, which kills up to 40,000 people a year in the UK and over 2.25 million worldwide in the latest 2011 WHO report,

We must not allow apologists for this toxic industry to pull the wool over our eyes with their myth of a safe alcohol dose, however appealing it might be to all us so-called “safe” drinkers. Remember these words of a man whose great family wealth and influence was built on illegal alcohol: “The great enemy of the truth, is very often not the lie – deliberate, contrived and dishonest – but the myth – persistent, persuasive and unrealistic.

Is alcohol A Carcinogen?

Alcohol and Cancer Risk Fact Sheet Alcohol is the common term for ethanol or ethyl alcohol, a chemical substance found in alcoholic beverages such as beer, hard cider, malt liquor, wines, and distilled spirits (liquor). Alcohol is produced by the fermentation of sugars and starches by yeast.

  1. Alcohol is also found in some medicines, mouthwashes, and household products (including vanilla extract and other flavorings).
  2. This fact sheet focuses on cancer risks associated with the consumption of alcoholic beverages.
  3. According to the, a standard alcoholic drink in the United States contains 14.0 grams (0.6 ounces) of pure alcohol.
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Generally, this amount of pure alcohol is found in:

  • 12 ounces of beer
  • 8–10 ounces of malt liquor
  • 5 ounces of wine
  • 1.5 ounces, or a “shot,” of 80-proof distilled spirits (liquor)

These amounts are used by public health experts in developing health guidelines about alcohol consumption and to provide a way for people to compare the amounts of alcohol they consume. However, they may not reflect the typical serving sizes people may encounter in daily life.

  • According to the federal government’s, individuals who do not drink alcohol should not start drinking for any reason.
  • The Dietary Guidelines also recommends that people who drink alcohol do so in moderation by limiting consumption to 2 drinks or less in a day for men and 1 drink or less in a day for women.

Heavy alcohol drinking is defined as having 4 or more drinks on any day or 8 or more drinks per week for women and 5 or more drinks on any day or 15 or more drinks per week for men. Is Alcohol A Neurotoxin There is a strong scientific consensus that alcohol drinking can cause several types of cancer (, ). In its, the National Toxicology Program of the US Department of Health and Human Services lists consumption of alcoholic beverages as a known human,

  • The evidence indicates that the more alcohol a person drinks—particularly the more alcohol a person drinks regularly over time—the higher his or her risk of developing an alcohol-associated cancer.
  • Even those who have no more than one drink per day and binge drinkers (those who consume 4 or more drinks for women and 5 or more drinks for men in one sitting) have a modestly increased risk of some cancers (–).

Based on data from 2009, an estimated 3.5% of cancer deaths in the United States (about 19,500 deaths) were alcohol related (). Clear patterns have emerged between alcohol consumption and the development of the following types of cancer:

: Moderate to heavy alcohol consumption is associated with higher risks of certain head and neck cancers. Moderate drinkers have 1.8-fold higher risks of (excluding the lips) and (throat) cancers and 1.4-fold higher risks of (voice box) cancers than non-drinkers, and heavy drinkers have 5-fold higher risks of oral cavity and pharynx cancers and 2.6-fold higher risks of larynx cancers (, ). Moreover, the risks of these cancers are substantially higher among persons who consume this amount of alcohol and also use tobacco ().

: Alcohol consumption at any level is associated with an increased risk of a type of esophageal cancer called esophageal, The risks, compared with no alcohol consumption, range from 1.3-fold higher for light drinking to nearly 5-fold higher for heavy drinking (, ). In addition, people who inherit a deficiency in an that metabolizes alcohol have been found to have substantially increased risks of esophageal squamous cell carcinoma if they consume alcohol ().

  • : Epidemiologic studies have consistently found an increased risk of breast cancer with increasing alcohol intake. Pooled data from 118 individual studies indicates that light drinkers have a slightly increased (1.04-fold higher) risk of breast cancer, compared with nondrinkers. The risk increase is greater in moderate drinkers (1.23-fold higher) and heavy drinkers (1.6-fold higher) (, ). An analysis of data for 88,000 women participating in two US concluded that for women who have never smoked, light to moderate drinking was associated with a 1.13-fold increased risk of alcohol-related cancers (mostly breast cancer) ().
  • : Moderate to heavy alcohol consumption is associated with 1.2- to 1.5-fold increased risks of cancers of the colon and rectum compared with no alcohol consumption (,, ).

Numerous studies have examined whether there is an association between alcohol consumption and the risk of other cancers. For cancers of the ovary, prostate, stomach, uterus, and bladder, either no association with alcohol use has been found or the evidence for an association is inconsistent.

However, evidence is accumulating that alcohol consumption is associated with increased risks of melanoma and of prostate and pancreatic cancers (, ). Alcohol consumption has also been associated with decreased risks of (–) and (, ) in multiple studies. However, any potential benefits of alcohol consumption for reducing the risks of some cancers are likely outweighed by the harms of alcohol consumption.

In fact, a recent study that included data from more than 1,000 alcohol studies and data sources, as well as death and disability records from 195 countries and territories from 1990 to 2016, concluded that the optimal number of drinks to consume per day to minimize the overall risk to health is zero ().

  • That study did not include data on kidney cancer or non-Hodgkin lymphoma.
  • Alcohol consumption may also be associated with an increased risk of,
  • For example, a of data from 19 studies showed that among patients with cancer of the upper (UADT)—which includes the oral cavity, pharynx, larynx, and esophagus—for every 10 grams of alcohol consumed per day before the first UADT cancer diagnosis there was a 1.09-fold higher risk of a second primary UADT cancer ().

It is less clear whether alcohol consumption increases the risk of second primary cancers at other sites, such as the breast (–). Researchers have hypothesized multiple ways that alcohol may increase the risk of cancer, including

  • metabolizing (breaking down) ethanol in alcoholic drinks to acetaldehyde, which is a toxic chemical and a probable human ; acetaldehyde can damage both (the genetic material that makes up ) and
  • generating (chemically reactive molecules that contain oxygen), which can damage DNA, proteins, and lipids (fats) in the body through a process called
  • impairing the body’s ability to break down and absorb a variety of nutrients that may be associated with cancer risk, including ; nutrients in the, such as ; ; ; ; and
  • increasing blood levels of, a sex hormone linked to the risk of breast cancer

Alcoholic beverages may also contain a variety of carcinogenic contaminants that are introduced during fermentation and production, such as, fibers,, and, The mechanisms by which alcohol consumption may decrease the risks of some cancers are not understood and may be indirect.

  1. Shows that people who use both alcohol and tobacco have much greater risks of developing cancers of the, (throat),, and than people who use either alcohol or tobacco alone.
  2. In fact, for oral and pharyngeal cancers, the risks associated with using both alcohol and tobacco are multiplicative; that is, they are greater than would be expected from adding the individual risks associated with alcohol and tobacco together (, ).

A person’s risk of alcohol-related cancers is influenced by their, specifically the genes that encode involved in metabolizing (breaking down) alcohol (). For example, one way the body metabolizes alcohol is through the activity of an enzyme called alcohol dehydrogenase, or ADH, which converts ethanol into the carcinogenic acetaldehyde, mainly in the liver.

  1. Recent evidence suggests that acetaldehyde production also occurs in the oral cavity and may be influenced by factors such as the oral (, ).
  2. Many individuals of East Asian descent carry a version of the gene for ADH that codes for a “superactive” form of the enzyme.
  3. This superactive ADH enzyme speeds the conversion of alcohol (ethanol) to toxic acetaldehyde.

Among people of Japanese descent, those who have this form of ADH have a higher risk of pancreatic cancer than those with the more common form of ADH (). Another enzyme, called aldehyde dehydrogenase 2 (ALDH2), metabolizes toxic acetaldehyde to nontoxic substances.

  1. Some people, particularly those of East Asian descent, carry a variant of the gene for ALDH2 that encodes a defective form of the enzyme.
  2. In people who produce the defective enzyme, acetaldehyde builds up when they drink alcohol.
  3. The accumulation of acetaldehyde has such unpleasant effects (including facial flushing and heart palpitations) that most people who have inherited the ALDH2 variant are unable to consume large amounts of alcohol and therefore have a low risk of developing alcohol-related cancers.

However, some individuals with the defective form of ALDH2 can become tolerant to the unpleasant effects of acetaldehyde and consume large amounts of alcohol. Epidemiologic studies have shown that such individuals have a higher risk of alcohol-related esophageal cancer, as well as of head and neck cancers, than individuals with the fully active enzyme who drink comparable amounts of alcohol ().

  1. These increased risks are seen only among people who carry the ALDH2 variant and drink alcohol—they are not observed in people who carry the variant but do not drink alcohol.
  2. The plant secondary compound, found in grapes used to make red wine and some other plants, has been investigated for many possible health effects, including cancer prevention.

However, researchers have found no association between moderate consumption of red wine and the risk of developing prostate cancer () or colorectal cancer (). Most of the studies that have examined whether cancer risk declines after a person stops drinking alcohol have focused on and on,

  • In general, these studies have found that stopping alcohol consumption is not associated with immediate reductions in cancer risk.
  • The cancer risks eventually decline, although it may take years for the risks of cancer to return to those of never drinkers.
  • For example, ex-drinkers still had higher risks of and cancers than never drinkers even 16 years after they stopped drinking alcohol, although it was lower than before they stopped drinking ().

One study estimated that it would take more than 35 years for the higher risks of and pharyngeal cancers associated with alcohol consumption to decrease to the level of never drinkers (), As with most questions related to a specific individual’s cancer treatment, it is best for patients to check with their health care team about whether it is safe to drink alcohol during or immediately following treatment.

  1. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans., IARC Monographs on the Evaluation of Carcinogenic Risks in Humans 2010; 96:3–1383.
  2. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. IARC Monographs on the Evaluation of Carcinogenic Risks in Humans 2012; 100(Pt E):373–472.
  3. Bagnardi V, Rota M, Botteri E, et al. Light alcohol drinking and cancer: a meta-analysis. Annals of Oncology 2013; 24(2):301–308.
  4. Bagnardi V, Rota M, Botteri E, et al. Alcohol consumption and site-specific cancer risk: A comprehensive dose-response meta-analysis. British Journal of Cancer 2015; 112(3):580–593.
  5. Cao Y, Willett WC, Rimm EB, Stampfer MJ, Giovannucci EL. Light to moderate intake of alcohol, drinking patterns, and risk of cancer: Results from two prospective US cohort studies. BMJ 2015; 351:h4238.
  6. Chen WY, Rosner B, Hankinson SE, Colditz GA, Willett WC. Moderate alcohol consumption during adult life, drinking patterns, and breast cancer risk. JAMA 2011; 306(17):1884–1890.
  7. White AJ, DeRoo LA, Weinberg CR, Sandler DP. Lifetime alcohol intake, binge drinking behaviors, and breast cancer risk. American Journal of Epidemiology 2017; 186(5):541–549.
  8. Nelson DE, Jarman DW, Rehm J, et al. Alcohol-attributable cancer deaths and years of potential life lost in the United States. American Journal of Public Health 2013; 103(4):641–648.
  9. LoConte NK, Brewster AM, Kaur JS, Merrill JK, Alberg AJ. Alcohol and cancer: A statement of the American Society of Clinical Oncology. Journal of Clinical Oncology 2018; 36(1):83–93.
  10. Hashibe M, Brennan P, Chuang SC, et al. Interaction between tobacco and alcohol use and the risk of head and neck cancer: Pooled analysis in the International Head and Neck Cancer Epidemiology Consortium. Cancer Epidemiology, Biomarkers & Prevention 2009; 18(2):541–550.
  11. Wu C, Wang Z, Song X, et al. Joint analysis of three genome-wide association studies of esophageal squamous cell carcinoma in Chinese populations. Nature Genetics 2014; 46(9):1001–1006.
  12. Grewal P, Viswanathen VA. Liver cancer and alcohol. Clinics in Liver Disease 2012; 16(4):839–850.
  13. Petrick JL, Campbell PT, Koshiol J, et al. Tobacco, alcohol use and risk of hepatocellular carcinoma and intrahepatic cholangiocarcinoma: The Liver Cancer Pooling Project. British Journal of Cancer 2018; 118(7):1005–1012.
  14. Fedirko V, Tramacere I, Bagnardi V, et al. Alcohol drinking and colorectal cancer risk: An overall and dose-response meta-analysis of published studies. Annals of Oncology 2011; 22(9):1958–1972.
  15. Zhao J, Stockwell T, Roemer A, Chikritzhs T. Is alcohol consumption a risk factor for prostate cancer? A systematic review and meta-analysis. BMC Cancer 2016; 16(1):845.
  16. Mahabir S, Leitzmann MF, Virtanen MJ, et al. Prospective study of alcohol drinking and renal cell cancer risk in a cohort of Finnish male smokers. Cancer Epidemiology, Biomarkers & Prevention 2005; 14(1):170–175.
  17. Rashidkhani B, Akesson A, Lindblad P, Wolk A. Alcohol consumption and risk of renal cell carcinoma: A prospective study of Swedish women. International Journal of Cancer 2005; 117(5):848–853.
  18. Lee JE, Hunter DJ, Spiegelman D, et al. Alcohol intake and renal cell cancer in a pooled analysis of 12 prospective studies. Journal of the National Cancer Institute 2007; 99(10):801–810.
  19. Tramacere I, Pelucchi C, Bonifazi M, et al. Alcohol drinking and non-Hodgkin lymphoma risk: A systematic review and a meta-analysis. Annals of Oncology 2012; 23(11):2791–2798.
  20. Psaltopoulou T, Sergentanis TN, Ntanasis-Stathopoulos I, et al. Alcohol consumption and risk of hematological malignancies: A meta-analysis of prospective studies. International Journal of Cancer 2018; 143(3):486–495.
  21. GBD 2016 Alcohol Collaborators. Alcohol use and burden for 195 countries and territories, 1990-2016: A systematic analysis for the Global Burden of Disease Study 2016. Lancet 2018; 392(10152):1015–1035.
  22. Druesne-Pecollo N, Keita Y, Touvier M, et al. Alcohol drinking and second primary cancer risk in patients with upper aerodigestive tract cancers: A systematic review and meta-analysis of observational studies. Cancer Epidemiology, Biomarkers & Prevention 2014; 23(2):324–331.
  23. Simapivapan P, Boltong A, Hodge A. To what extent is alcohol consumption associated with breast cancer recurrence and second primary breast cancer?: A systematic review. Cancer Treatment Reviews 2016; 50:155–167.
  24. Park SM, Li T, Wu S, et al. Risk of second primary cancer associated with pre-diagnostic smoking, alcohol, and obesity in women with keratinocyte carcinoma. Cancer Epidemiology 2017; 47:106–113.
  25. Knight JA, Fan J, Malone KE, et al. Alcohol consumption and cigarette smoking in combination: A predictor of contralateral breast cancer risk in the WECARE study. International Journal of Cancer 2017; 141(5):916–924.
  26. Turati F, Garavello W, Tramacere I, et al. A meta-analysis of alcohol drinking and oral and pharyngeal cancers: Results from subgroup analyses. Alcohol and Alcoholism 2013; 48(1):107–118.
  27. Druesne-Pecollo N, Tehard B, Mallet Y, et al. Alcohol and genetic polymorphisms: Effect on risk of alcohol-related cancer. Lancet Oncology 2009; 10(2):173–180.
  28. Stornetta A, Guidolin V, Balbo S. Alcohol-derived acetaldehyde exposure in the oral cavity. Cancers 2018; 10(1):20.
  29. Fan X, Peters BA, Jacobs EJ, et al. Drinking alcohol is associated with variation in the human oral microbiome in a large study of American adults. Microbiome 2018; 6(1):59.
  30. Kanda J, Matsuo K, Suzuki T, et al. Impact of alcohol consumption with polymorphisms in alcohol-metabolizing enzymes on pancreatic cancer risk in Japanese. Cancer Science 2009; 100(2):296–302.
  31. Yokoyama A, Omori T., Alcohol 2005; 35(3):175–185.
  32. Vartolomei MD, Kimura S, Ferro M, et al. The impact of moderate wine consumption on the risk of developing prostate cancer. Clinical Epidemiology 2018; 10:431–444.
  33. Chao C, Haque R, Caan BJ, et al. Red wine consumption not associated with reduced risk of colorectal cancer. Nutrition and Cancer 2010; 62(6):849–855.
  34. Rehm J, Patra J, Popova S. Alcohol drinking cessation and its effect on esophageal and head and neck cancers: A pooled analysis. International Journal of Cancer 2007; 121(5):1132–1137.
  35. Ahmad Kiadaliri A, Jarl J, Gavriilidis G, Gerdtham UG. Alcohol drinking cessation and the risk of laryngeal and pharyngeal cancers: A systematic review and meta-analysis. PLoS One 2013; 8(3):e58158.
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Do humans naturally have alcohol?

Why Do Our Bodies and Brains React with Alcohol? – What most people don’t realize is that we are naturally exposed to alcohol from day one! Our bodies produce about 3 to 4 grams of alcohol per day. This is equivalent to about ¼ of a standard alcoholic beverage.

  • Alcohol is produced in our gastrointestinal tract through the action of bacteria and fungi (yeasts) as a by-product of carbohydrate metabolism.
  • Some researchers believe alcohol can also be produced by cells outside the GI tract.
  • However, the body identifies alcohol as a toxin that needs to be rapidly broken down into harmless components.

Thus, the liver, the first organ to encounter alcohol after it leaves the GI tract, has evolved various enzymes to convert alcohol to carbon dioxide and water. Some people have an illness called “auto-brewery syndrome” where the GI tract contains excessive amounts of yeast that create intoxicating levels of alcohol in the blood stream.

What is the most toxic type of alcohol?

Case resolution – You recognize that methyl alcohol is also known as methanol. You order fomepizole to block the patient. You obtain an osmolar gap of 49.0 mOsm/kg. You also obtain methanol, ethylene glycol and isopropanol levels, which showed a methanol level of 130 mg/dL.

Methanol Ethylene Glycol Isopropanol
Potential routes of exposure Oral, inhalation, dermal Oral Oral, inhalation, dermal
Anion Gap Metabolic Acidosis Yes Yes No
Toxic metabolites Formic acid, formaldehyde Glycolic acid, Glyoxylic acid, oxalic acid Acetone
Clinical effects
  1. CNS Depression
  2. Visual changes
  3. Liver injury
  4. Pancreatitis
  5. Rhabdomyolysis
  6. Seizure
  • CNS Depression
  • Nephrotoxicity
  • Cranial Nerve palsies
  • Cerebral edema
  • Seizure
CNS Depression Hemorrhagic gastritis
Adjunctive treatments Folate, sodium bicarbonate Thiamine, Pyridoxine None

Does long term alcohol use destroy neurons?

Wernicke-Korsakoff Syndrome – Long-term alcohol abuse can lead to various forms of alcohol dementia. Among them is Wernicke-Korsakoff syndrome, a serious neurological disorder linked to alcohol use that does result in the loss of brain neurons. The syndrome is characterized by memory problems, amnesia, and lack of muscle coordination.

Is beer the most unhealthy alcohol?

Drinking Hard Liquor vs. Beer: Which Is the More Addicting and Damaging Type of Alcohol? – Alcohol is generally made up of the same compounds, so beer and hard liquor both pose similar risks to a person’s health. The only catch is that hard liquor comes with a higher threat because it contains a higher alcohol content than beer.

What alcohol actually does to your body?

Drinking too much – on a single occasion or over time – can take a serious toll on your health. Here’s how alcohol can affect your body: Brain: Alcohol interferes with the brain’s communication pathways, and can affect the way the brain looks and works.

Cardiomyopathy – Stretching and drooping of heart muscle Arrhythmias – Irregular heart beat Stroke High blood pressure

Liver: Heavy drinking takes a toll on the liver, and can lead to a variety of problems and liver inflammations including:

Steatosis, or fatty liver Alcoholic hepatitis Fibrosis Cirrhosis

Pancreas: Alcohol causes the pancreas to produce toxic substances that can eventually lead to pancreatitis, a dangerous inflammation and swelling of the blood vessels in the pancreas that prevents proper digestion. Cancer: According to the National Cancer Institute: “There is a strong scientific consensus that alcohol drinking can cause several types of cancer.

In its Report on Carcinogens, the National Toxicology Program of the US Department of Health and Human Services lists consumption of alcoholic beverages as a known human carcinogen. “The evidence indicates that the more alcohol a person drinks–particularly the more alcohol a person drinks regularly over time–the higher his or her risk of developing an alcohol-associated cancer.

Even those who have no more than one drink per day and people who binge drink (those who consume 4 or more drinks for women and 5 or more drinks for men in one sitting) have a modestly increased risk of some cancers. Based on data from 2009, an estimated 3.5% of cancer deaths in the United States (about 19,500 deaths were alcohol related.” Clear patterns have emerged between alcohol consumption and increased risks of certain types of cancer:

Head and neck cancer, including oral cavity, pharynx, and larynx cancers.

Esophageal cancer, particularly esophageal squamous cell carcinoma. In addition, people who inherit a deficiency in an enzyme that metabolizes alcohol have been found to have substantially increased risks of esophageal squamous cell carcinoma if they consume alcohol.

Liver cancer.

Breast cancer: Studies have consistently found an increased risk of breast cancer in women with increasing alcohol intake. Women who consume about 1 drink per day have a 5 to 9 percent higher chance of developing breast cancer than women who do not drink at all.

Colorectal cancer.

For more information about alcohol and cancer, please visit the National Cancer Institute’s webpage ” Alcohol and Cancer Risk ” (last accessed October 21, 2021). Immune System: Drinking too much can weaken your immune system, making your body a much easier target for disease.

What is the alcohol toxin called?

The Chemical Breakdown of Alcohol – Image The chemical name for alcohol is ethanol (CH3CH2OH). The body processes and eliminates ethanol in separate steps. Chemicals called enzymes help to break apart the ethanol molecule into other compounds (or metabolites), which can be processed more easily by the body.

Some of these intermediate metabolites can have harmful effects on the body. Most of the ethanol in the body is broken down in the liver by an enzyme called alcohol dehydrogenase (ADH), which transforms ethanol into a toxic compound called acetaldehyde (CH3CHO), a known carcinogen. However, acetaldehyde is generally short-lived; it is quickly broken down to a less toxic compound called acetate (CH3COO-) by another enzyme called aldehyde dehydrogenase (ALDH).

Acetate then is broken down to carbon dioxide and water, mainly in tissues other than the liver.

Is alcohol poison and toxic?

Overview – Alcohol poisoning is a serious — and sometimes deadly — result of drinking large amounts of alcohol in a short period of time. Drinking too much too quickly can affect breathing, heart rate, body temperature and gag reflex. In some cases, this can lead to a coma and death.

What is toxin in human body?

Toxins are substances created by plants and animals that are poisonous (toxic) to humans. Toxins may also include some medicines that are helpful in small doses, but poisonous in large amounts. Most toxins that cause problems in humans come from germs such as bacteria.

  • For example, the symptoms of cholera are caused by a toxin made by cholera bacteria.
  • Other toxins that cause problems include metals, such as lead, and certain chemicals in the environment. Lee WM.
  • Toxin- and drug-induced liver disease.
  • In: Goldman L, Schafer AI, eds.
  • Goldman-Cecil Medicine.26th ed.
  • Philadelphia, PA: Elsevier; 2020:chap 141.

Meehan TJ. Approach to the poisoned patient. In: Walls RM, Hockberger RS, Gausche-Hill M, eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice,9th ed. Philadelphia, PA: Elsevier; 2018:chap 139. Updated by: David C. Dugdale, III, MD, Professor of Medicine, Division of General Medicine, Department of Medicine, University of Washington School of Medicine.

What toxin buildup from alcohol?

Alcohol-induced hepatitis is inflammation of the liver caused by alcohol use. Too much alcohol overloads the liver with toxins that injure the tissues. People with this condition should ask their healthcare providers for help to quit drinking in order to prevent further liver damage.

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