I can almost hear the moans coming from some of you as you read the title of this post. You’re no doubt thinking, “For real? You haven’t posted in a while, but you’re going to trash what I do to relax and unwind on my night off? Seriously?”

No dear reader, not entirely. Me preaching to someone about drinking alcohol is as good an example of the pot calling the kettle black as you can imagine. I have no desire to emulate the tactics, real or imagined, of Carrie Nation. However, the more I learn about alcohol and the digestive tract, the more cautious I am about abusing it. As a result, my alcohol intake has gone way down.

The reality is that alcohol is a very powerful drug, and not only because it causes some people to prance about a room wearing lampshades on their heads. Neither am I referring to its magical ability to increase the perceived attractiveness of potential sex partners as last call rapidly approaches in whatever watering hole you’re patronizing at the time. Nor because of its often negative effect on judgement that can lead to fighting, murder, drunk driving and accidental falls.

No, what I’m going to write about today is how this liquid drug, when imbibed in excess, either acutely as in a single episode of binge drinking to intoxication, or chronically as in alcoholism, may be one of the most destructive things a person can do to their gastrointestinal flora and the environment these microbes inhabit.

Looking back at the genesis of my own digestive issues, I’m convinced that binge drinking, if not entirely the cause, was certainly a contributing factor.

Now what do I mean by alcohol abuse?

Well, in the case of binge drinking, there is no real global consensus. In the United States, binge drinking is defined as having greater than five drinks if you are a man, and more than four drinks if you are a woman at any one sitting. A drink being defined as one bottle of beer, glass of wine or shot of liquor.

Alcoholism, however, is universally understood to mean compulsive and uncontrolled consumption of alcohol that causes harm to the drinker’s health, interpersonal relationships and social standing.

Women are typically less capable of metabolizing alcohol than men. As a result, blood levels rise quicker in females than in males at lower doses. We can therefore safely conclude that the ill effects of alcohol abuse on all systems of the body, including the reproductive system, hit women harder at comparable levels of alcohol intake then in men.

Be aware that the U.S. definition for binge drinking is considered by some alcohol researchers to be overly permissive. As a result, some are beginning to define binge drinking as having more than two drinks in a single sitting if you are male, and greater than one drink if you are female. These definitions are based on a number of epidemiological findings showing higher rates of morbidity and mortality in those ingesting doses exceeding these levels.

As we are all different, there is little hope of ever arriving at a universal standard that applies to everyone. The reality is that some people are able to metabolize alcohol better than others.

We’ve all met people who become sloppy drunks on a few drinks, and others who show no obvious signs of intoxication at much higher doses. Of the latter, I have a female friend who can easily drink me under the table. Shout-out to you Helen! I even jokingly palpitated her legs once to verify they weren’t hollow.

Of course like most drugs, the more often ingested, the more tolerant to its effects you become. Anyone who has not drunk in while is often surprised by how quickly they feel tipsy. Conversely, one of the hallmarks of alcoholism is the need to drink more in order to attain the same high.

From a wellness perspective, heavy drinkers suffer from a disproportionate number of health problems. And yes, I’m sure most of you know someone who lived to a ripe old age binge drinking the entire time. I know people who lived a long time and smoked all their lives too. Nevertheless, that can never answer whether they would have lived longer and healthier lives had they not drunk or smoked. And for every person who is able to get away with this kind of behavior, there are countless others who die horrible, premature deaths.

Alcohol abuse is quite familiar to those in the medical community. Partly due to the high rates of it in the profession, but mainly because doctors and nurses witness first-hand the harm that chronic and acute drinking causes in many of their patients.

However, it’s always struck me how little alcohol consumption is discussed among those advocating one dietary mode of eating over another. For example, vegetarians and vegans are all too happy to claim that the reason Seventh-day Adventists are healthier than most in the United States is because they don’t eat meat, rarely if ever pointing to the fact that this group also abstains from drinking alcohol and smoking tobacco. (1) Likewise, those taking the opposite side of the argument often highlight the longevity and good health of meat-eating Mormons, yet again fail to mention how observant members of this faith don’t drink or smoke. (2)

Still others claim that the deterioration in health seen in many indigenous cultures after contact with European settlers can be wholly explained by the introduction of refined sugar, white flour, processed foods, etc. to the diets of these native populations. Yet those advocating this viewpoint often fail to bring up the fact that the introduction of distilled spirits like whiskey, vodka, and rum were every bit as alien to these populations as the newly introduced food.

Yes, there is no doubt these new foods displaced many of the whole, nutrient-dense staples these populations had consumed for thousands of years. But also displaced were traditionally fermented alcoholic beverages, if they existed at all, of low alcohol content that in many cases were consumed in common, usually only by men, and only during socially regulated celebrations:

“Early Man’s desire to achieve altered states of consciousness through the use of intoxicants would have presented a number of dangers within developing cultures. Alcohol, in the form of the early beers, would have presented the lowest risks because of their relatively low strength and the ability of drinkers to gauge the amount ingested quite accurately. Such beverages also lent themselves most readily to social and group activity rather than solitary consumption. Nonetheless, unrestricted consumption would have presented debilitating states of consciousness which would have outweighed the individual and social benefits, and even the nutritional gains, that beer provided.

It is clearly for this reason that we find early evidence of the integration of alcohol consumption into the core systems of myths and ritual practices within emergent cultures. Such cultural traditions and rules both prescribed the use of alcohol for social and ceremonial functions and proscribed continuous or excessive inebriation. The potential for social disorder arising from the production and consumption of potentially ‘risky’ beverages, and was thus minimized while enabling positive patterns of cultural interaction.” (3)

With the introduction of the “white-man’s firewater,” many of these far less potent beverages and the rituals that regulated their consumption disappeared. To this day, alcohol abuse devastates the lives of many in the indigenous populations of the Americas, New Zealand, Australia, the Pacific Islands and Africa. Any discussion on how nutrition shapes health without reference to alcohol abuse is incomplete at best, deceitful at worst.

I’m certainly not denying the impact devitalized and nutrient-poor foods have on health and longevity. I do, after all, live in the United States, and witness daily how poor dietary choices impact wellness. However, we would all have a far better understanding of how to enhance health and longevity if we also spent some time learning how the world’s favorite recreational drug consistently sabotages both.

A similar myopia afflicts those advocating for low-carb, or low-fat, or high-protein, or low-protein diets. The underlying assumption being that unless you’re a raging alcoholic, there is very little reason to concern oneself with alcohol intake, save as a way to cut out some calories while trying to shed some weight.

That, however, is a very unfortunate assumption to make as you’ll soon see.

According to the National Institute on Alcohol Abuse and Alcoholism, in the United States, 28.8% of women and 43.1% of men over the age of 18 are classified as binge drinkers. (4)  I strongly suspect these figures are vastly understated as I’ll explain in a bit.

While everyone can agree that alcoholism is harmful to health, the belief that one or two weekly binge sessions is harmless is extremely common among the general public. However, more and more research suggests that this pattern of drinking may be far more injurious to health than suspected.

In 2010, a study was published in the British Medical Journal with the catchy title: Patterns of alcohol consumption and ischaemic heart disease in culturally divergent countries: the Prospective Epidemiological Study of Myocardial Infarction (PRIME). This paper reported results from studying the drinking habits of two populations of middle-aged men, one in France, the other in Northern Ireland, and the relationship between these drinking patterns and heart disease risk.

I’ll let the authors of this study speak for themselves: “Regular and moderate alcohol intake throughout the week, the typical pattern in middle aged men in France, is associated with a low risk of ischaemic heart disease, whereas the binge drinking pattern more prevalent in Belfast confers a higher risk.”

Now association is never causation, and the authors of this paper do admit that other confounding variables may be at play here. Nonetheless, as you’ll soon read, binge drinking has well-known negative effects on health, especially gastrointestinal health that can certainly increase the risk of heart disease via increased intestinal permeability, cortisol secretion, endotoxemia and lowered immunity to pathogens.

The pattern of binge drinking seen in Northern Ireland also matches what is seen in the rest of Great Britain, Northern Europe, Canada, the United States, Australia and New Zealand. The pattern of drinking seen in France is more typical of that seen in other Mediterranean countries.

Given the lower incidence of heart disease in Southern Europe, a good case can be made that studying patterns of alcohol intake may offer us more promising avenues of research concerning heart disease risk than focusing solely on the food components of the Mediterranean diet.

OK, enough with the preliminaries. To not overwhelm you or myself, I’ve tackled this topic by reviewing alcohol’s effect on different sections of the digestive tract, beginning with the mouth, throat and esophagus. However, please don’t forget that the digestive tract needs to be viewed as a unified whole.

What occurs further up the old “food chute” oftentimes has knock-on effects further downstream. This caveat will become clearer when I discuss alcohol’s contribution to colon cancer.

Alcohol’s effect on the mouth, throat and esophagus

Alcohol’s impact begins as soon as it enters the mouth. The mouth, like all parts of the digestive tract, is populated by bacteria. Many of these bacteria are deemed commensal, meaning that like beneficial gut flora, their presence helps keep this part of our bodies healthy as well as aid in the digestion of food.

An oral cavity replete with healthy colonies of beneficial bacteria keeps potentially pathogenic organisms at bay by creating an environment that is less conducive to their growth (many times by regulating mucosal pH), and by outcompeting these potential trouble makers for attachment sites.

Now I’m sure most of you have had rubbing alcohol applied to your skin before receiving a vaccination. And the reason for this is to disinfect the site and prevent infection by whatever bacteria happens to be residing on your arm or butt prior to the needle prick.

Alcohol is a very effective bactericidal because it easily disrupts the lipid membrane that encases bacteria. Sadly, however, the alcohol you drink has no magical ability to differentiate between beneficial or harmful oral bacteria. It just goes about its business popping bacterial membranes without a care in the world.

While oral bacteria like gut flora is fairly resistant to bactericidals much as gut flora is somewhat resistant to short courses of antibiotics, there are limits. Limits that are dose dependent, and therefore partly explain the horrific state of dental and oral health that afflict many who abuse alcohol.

Alcohol, apart from effects on oral bacteria, causes direct injury to the mucosal lining of the mouth, throat and esophagus, inviting inflammation and bacteria that thrive in inflamed conditions. Chronic and acute alcohol intake damages the salivary glands and causes interference with saliva secretion. (5) As saliva contains lactoferrin, a glycoprotein that inhibits the growth of oral pathogens, the risk of oral dysbiosis rises with increasing alcohol intake. (6)

Alcoholics and binge drinkers often suffer from glossitis, inflammation of the tongue, as well as stomatitis, inflammation of the mouth. Whether these effects are due to alcohol or its metabolite, acetaldehyde, is still unclear.

I’ll get to acetaldehyde in a moment.

Alcohol affects the esophagus in several ways. Alcohol always diminishes the wave-like motions that propel food along the digestive tract, and this is also true of the peristaltic movements that shuttle food from the throat to the stomach via the esophagus. (7)

Alcohol also weakens the lower esophageal sphincter that exists to prevent stomach acid from entering the esophagus after food has passed. As a result, alcohol always predisposes to gastric reflux. This is dose dependent, so the more you drink the more likely you are to experience this.

Drink enough and often, and you too may experience the joys of what is known as “nutcracker esophagus,” a lovely sensation that mimics a heart attack! (8) Fun times!

Alcoholics and binge drinkers make up a large part of those suffering from Barrett’s esophagus. This condition is characterized by changes in the epithelial lining of the esophagus that results in mucosal inflammation. Barrett’s often precedes esophageal cancer, which isn’t surprising as chronic inflammation is a precursor to many cancers.

Another disorder of the esophagus experienced by alcoholics and binge drinkers is Mallory-Weiss syndrome. (9) This condition involves bleeding caused by tears in the mucosal layer at the junction of the stomach and esophagus. Mallory-Weiss syndrome accounts for between 5% to 15% of upper GI bleeding episodes; and in 20% of these cases, the direct cause is repeated retching and vomiting from a night of binge drinking.

As I hinted earlier, the damage to the mucosal layer of the mouth and esophagus is not solely mediated by alcohol, but also by its metabolite, acetaldehyde. And what, pray tell, is acetaldehyde? Glad you asked.

Acetaldehyde is an intermediary product of ethanol, aka alcohol, metabolism. The enzyme alcohol dehydrogenase metabolizes ethanol into acetaldehyde. Acetaldehyde is then further metabolized by acetaldehyde dehydrogenase into harmless acetate. All of this mostly occurs in the liver, but as you’ll see shortly not entirely.

Unlike acetate, there is nothing harmless about acetaldehyde. Acetaldehyde is a highly toxic and volatile compound, and has shown itself capable of mutating genes and causing cancer in cell cultures and in numerous animal models. (10) Its cancer-causing effects, by the way, are synergistically enhanced by the addition of tobacco smoke. (11)

Acetaldehyde also interferes with DNA repair by inhibiting a protein, O6-methylguanine, involved in this process. (12) As a result, the International Agency for Research on Cancer (IARC) has classified acetaldehyde a carcinogen.

I feel it necessary to bring up the cancer-causing potential of acetaldehyde in this section because of the increased concentrations of acetaldehyde that appear in the mouth and throat shortly after drinking. For you see, while the breakdown of alcohol occurs mainly in the liver, both oral and gut bacteria also metabolize alcohol into acetaldehyde.

After drinking, alcohol is absorbed from the stomach and the duodenum into the portal vein leading to the liver. Due to its high-water solubility, alcohol levels in saliva and the contents of the colon shortly approach those seen in the blood and liver. (13) Because alcohol is metabolized by bacteria to acetaldehyde, levels of this carcinogen are often very high in localized concentrations throughout the digestive tract, including the mouth.

As early as the 19th century, heavy drinking was associated with cancer of the esophagus (esophageal cancer) when it was observed that absinth drinkers in France were at high risk for developing these tumors. Subsequent observational studies have shown that both chronic and binge drinking are highly associated with cancers of the mouth, head and neck. (14)

It has been estimated that between 25% to 68% of upper GI cancers can be attributed to drinking alcohol. It is also estimated that abstaining from both alcohol and smoking would result in an 80% reduction in these tumors. (15) (16) Other risk factors for these cancers include poor oral hygiene, nutritional deficiencies and the human papillomavirus.

However, these risk factors are themselves often the result of heavy drinking. Disruption to oral flora is often a precursor to the periodontal disease seen in both alcoholics and binge drinkers.

Likewise, disruption to intestinal flora leads to intestinal dysbiosis predisposing to nutritional malabsorption and deficiencies. I covered how that process works here. And as you’ll read shortly, the immune suppressing effects of alcohol would increase the risk of infection from many bacterial and viral pathogens, including human papillomavirus.


Alcohol’s effect on the stomach

Alcohol’s effects on stomach function are both dependent on alcohol type and dose. In healthy, non-alcoholic subjects, administration of 0.3 to 0.5 grams of alcohol at concentrations of 5% stimulates gastric secretion. However, this is only true for fermented alcoholic beverages like wine, beer, champagne and sherry. Distilled alcoholic beverages like vodka, rum and whiskey do not increase acid secretion. (17)

As I’ve blogged in the past, stomach acid serves a very important barrier function by killing swallowed bacterial pathogens thus preventing them from making their way to your intestine and taking up residence. As ingesting fermented alcoholic beverages like wine and beer increases stomach acid secretion, we would expect this barrier function to be enhanced by small to moderate consumption of these fermented beverages.

At higher doses, however, this beneficial effect disappears. High alcohol consumption, regardless of type, results in an increase in stomach alkalinity that compromises not only your ability to kill swallowed pathogens, but also your capacity to properly digest protein.

While small quantities of alcohol decrease the time food sits in the stomach, large quantities inhibit stomach emptying. (18) The more you drink at any one sitting, the longer food will stay in the stomach.

Pair this with the relaxing of the lower esophageal sphincter, and you can soon experience the unbridled joy of heartburn, acid reflux and re-savoring the food you ate hours earlier. And if you are in just the right position when you finally pass out, choking to death on your own vomit becomes a distinct possibility as was the unfortunate case for John Bonhom.

Alcohol is also known to cause mucosal inflammation in the stomach in those who abuse alcohol. (19) A single bout of heavy drinking has been known to cause stomach inflammation and bleeding lesions.


Alcohol’s effect on the small intestine

Alcoholism and binge drinking are risk factors for small intestinal bacterial overgrowth (SIBO). This shouldn’t come as a shock for as I just explained, excess alcohol consumption reliably impairs gastric-barrier function opening the door to intestinal infection from swallowed pathogens.

Pathogens that are not killed in the stomach will merrily make their way to the intestinal tract. As alcohol in large quantities is also quite adept at obliterating colonies of beneficial bacteria that live in the duodenum, the risk that swallowed pathogens adhere to and colonize the mucosal lining of this part of the small intestine increases.

Alcohol also does the same thing to the mucus layer of the small intestine as it does in the mouth, throat, esophagus and stomach, i.e. it inflames it. Inflammation, as those of you who read my SIBO series recall, creates a most excellent environment for pathogens to thrive in. The more inflammation, the greater the likelihood of contracting SIBO.

Alcohol and acetaldehyde have been shown in in vitro, animal and human studies to increase intestinal permeability in the small intestine and colon. (20) Modes for doing so involve activation of cell-signaling pathways that disrupt tight junction proteins, initiation of oxidative stress via inflammation and physical changes to the cell structures lining the digestive tract. The more permeable the gut wall, the higher the translocation of gut endotoxins to the liver and systemic circulation.

In a study of 198 people who were confirmed to have SIBO via hydrogen breath testing, 95% were discovered to be moderate alcohol drinkers. (21) And how was moderate drinking defined? As no more than two drinks a day for men, and one drink a day for women.

Now, does this prove that moderate drinking causes SIBO? Not necessarily. If there is one thing I’ve learned since I’ve been studying nutrition is that people very often lie about what they claim to eat and drink, and I suspect more than a bit of that was going on here.

A recent study in Great Britain found that the British underestimate their consumption of alcohol by around 40%. (22) I can assure you that those figures are comparable to many other countries, including the United States, hence my skepticism about the U.S. binge drinking statistics I cited earlier.

So I take the results from this SIBO study the same way I take most studies utilizing food-frequency questionnaires, with a huge grain of salt.

In the case of light to moderate drinkers, compromised gastric-barrier function is not likely to be an issue due to increases in gastric secretion assuming, of course, that the liquor of choice was fermented like wine or beer. However, it is within the realm of possibility that for some, the increase in mucosal inflammation and resulting intestinal permeability would encourage the growth of pathogens in the small intestine.

What is not an inconceivable mechanism, however, is the consistent effect drinking has on intestinal motility or peristalsis. In both normal and alcoholic subjects, the administration of alcohol reliably reduces peristaltic movement in the small intestine. As I wrote in this post:

“But just as importantly, peristalsis prevents bacteria from the colon from migrating up to the small intestine and colonizing it. A valve forms the physical barrier between the remote or distal end of the small intestine and the colon. This valve is called the ileocecal valve. It’s thought to prevent colonic contents and bacteria from refluxing back into the small intestine. However, studies in animals have failed to confirm this after resection surgery lending support to the theory that what prevents colonic bacteria from entering and colonizing the small intestine is the paristaltic movement of the small intestine.

So anything that impairs this housekeeping function in the presence or absence of chyme will also predispose you to SIBO.”

Alcohol certainly fits the bill as a substance capable of doing this. It is, after all, a nervous system depressant, and like all depressants dampens the the intestinal nerves responsible for moving things along.

It’s not the only thing that does this, but it sure as hell is a very common cause of impaired intestinal movement whose effects would be amplified by the simultaneous ingestion of gluten-containing grains, a very common practice for those enjoying their favorite bread-based food while imbibing. Recall that the digestion of gluten results in the production of five separate opioid peptides, and the formation of the neuroinhibitory transmitter adenosine. (23) (24) Opioids and adenosine both slow intestinal movement.

Apart from promoting SIBO, animal studies have shown how acute alcohol consumption inhibits the absorption of water, sodium, glucose, fat and certain amino acids. (25) Malabsorption of nutrients is a common finding in alcoholics and binge drinkers.

Malabsorption has mostly to do with small bowel dysbiosis. You can’t properly digest and absorb food unless the the hair-like structures lining the folds of the small intestine are healthy, regardless of how wholesome or nutrient dense your diet happens to be, and these structures can never be healthy in the presence of gut pathogens.

Now, I doubt these effects are entirely caused by alcohol alone. I suspect acetaldehyde is a large culprit here as gut flora metabolizes alcohol to this intermediary, which in turn would increase levels of this metabolite throughout the length of the GI tract, including the small intestine. As such, this highly inflammatory and carcinogenic substance may help explain why colonization of the gut wall with pathogens is common in those who overindulge.

Candida overgrowth is also extremely prevalent in alcoholics and binge drinkers. It’s not uncommon for those who wake up with a hangover the morning after to notice a coated tongue when staring at their bleary selves in the mirror. If it’s that bad on the tongue, you can imagine what’s happening in areas of the digestive tract you can’t see.

Finally, any bacterial or yeast overgrowth in this part of the intestinal tract caused by alcohol intake cannot be wholly explained without reference to alcohol’s well known immune-suppressing effects. So before moving on to the colon and rectum, I need to cover briefly how alcohol negatively impacts immune function.


Alcohol’s effect on the immune system

The immune response to an invading pathogen occurs in two phases. The first phase involves the initiation of an inflammatory response, and this primarily involves a number of white blood cells that ingest and destroy microorganisms. These cells are known as phagocytes.

Several different types of phagocytes exist. Neutrophils are one such type that ingest and destroy pathogens. Monocytes either circulate in blood or become sentinels once they enter tissue (macrophages), and they too ingest and destroy pathogens. Monocytes can also present protein fragments from pathogens to other immune cells like T and B cells to activate them. Finally, these cells secrete signaling molecules known as cytokines that help regulate immune activity.

Natural killer cells are another type of phagocyte. Their role is to eliminate cells in the body that have been infected by parasites. They are also tasked with eliminating cells that have turned cancerous.

All of these cells are hard-wired in us to respond to threats, and are part of what is called the innate immune system in that everyone has the same inborn defenses. There is another arm of our immunity, however, called adaptive immunity. This is the part of the immune system that learns to guard against specific threats unique to us that we encounter over the course of our lives.

The most important cells involved in the adaptive arm of the immune system are the T lymphocytes (T cells) and B lymphocytes (B cells). While too complex a subject to cover here, just be aware that the ability of the immune system to form specific, long-lasting antibodies to various threats, involves this arm of the immune system. It is this part of the immune system that is stimulated by vaccination, for example.

Alcohol negatively impacts both arms of the immune system. (26) Chronic or acute alcohol consumption reduces the ability of phagocytes to ingest and destroy pathogens as they enter the body.

In alcoholics, levels of inflammatory-invoking signaling molecules (cytokines) are consistently elevated resulting in increased metabolism, fever, weight loss, protein in the liver and malnutrition. However, in binge drinkers, alcohol temporarily reduces the production of these same cytokines significantly compromising the innate immune defense against threats. Two of the worst colds I ever came down with were due not only to the viruses I was exposed to, but to lowered immunity from previous episodes of binge drinking.

Alcohol is known to tamper inflammatory cytokine production by increasing anti-inflammatory interleukin 10 (IL-10). (27) IL-10 is vital for helping to turn off an immune response when a threat has passed. However, secreted too soon, it can also hamper the immune system’s ability to fight off an ongoing threat.

Alcohol also interferes with both T and B cells. Alcoholics have lower-than-normal numbers of all subsets of T cells. They also exhibit aberrant B cell functioning.

I suspect that a good part of the compromised immunity experienced by both binge drinkers and alcoholics can be explained by the effect chronic or acute alcohol consumption has on intestinal permeability. Due to alcohol’s/acetaldehyde’s ability to increase gut leakiness in both the small and large intestine, endotoxin translocation to systemic circulation is elevated, which in turn stimulates the hypothalamic-pituitary-adrenal (HPA) axis. (28)

This results in higher cortisol secretion that further undermines not only gut-wall integrity, but the immune system. Recall that cortisol always suppresses immune function.

The practical effect of all this is that the more alcohol consumed, the less well the immune system works. As a result, binge drinkers and alcoholics are at higher risk for a number of infectious diseases like pneumonia and tuberculosis. (29) (30) In the case of bacterial pneumonia, alcoholics suffer mortality rates that far exceed the non-alcoholic population even when treated with the best antibiotics available.

Alcoholics are also at increased risk for contracting viral infections, including the human papillomavirus and HIV. (31) And most relevant to today’s discussion, alcoholics and binge drinkers are at elevated risk for coming down with infections of the small and large bowel as elevations in cortisol secretion would dampen the normal immune defenses against pathogens invading these areas of the digestive tract.

Finally, the consistent association between heavy drinking and numerous cancers can be partly attributed to decreases in natural killer cell activity. In lab animals, chronic alcohol consumption leads to a reduction in the number and activity of these cells and increases tumor metastasis. (32)

Therefore, due to the carcinogenic effects of acetaldehyde, coupled with a decrease in natural killer cell activity, it shouldn’t be surprising that chronic and acute drinking are highly associated with cancers of the mouth, head, neck, throat, esophagus, liver, breast, small bowel, colon and rectum.

La Chaim!

Alcohol’s effect on the colon

Alcoholics, and some binge drinkers, are often plagued by diarrhea. This is explained by the fact that alcohol consumption significantly reduces the frequency and strength of the peristaltic muscle contractions that occur in the colon. This leads to a reduction in both compaction and transit time and predisposes to diarrhea. (33)

That said, I believe there is much more going on here than mere effects on colonic motility. As I’ve hammered home on many occasions, you cannot divorce what occurs in the colon with what happens further up the digestive tract.

For example, failure to digest fat, whether because of small intestinal dysbiosis, undiagnosed celiac disease or gallbladder problems, for example, will always lead to changes in how feces is formed, its consistency and its frequency. Changes will also be reflected in the composition of colonic gut flora due to changes in the food substrates that reach this part of the GI tract.

The fact that chronic or acute alcohol drinkers are far more likely to develop small intestinal bacterial and fungal overgrowth, would be expected to have knock-on effects in the colon. And many of those effects are going to be reflected in the composition of colonic gut flora.

While I haven’t come across any studies regarding colonic dysbiosis and alcoholism, I suspect that as a group both alcoholics and binge drinkers exhibit decreased populations of both beneficial bifidobacteria and lactobacillus species in this part of their digestive tract. If so, disordered gut flora in the colon may be a better explanation for why these populations often suffer from chronic diarrhea.

Alcohol abuse is also a significant risk factor for diverticulosis as reported in a recently published study:


Courtesy: Alcohol Consumption Is a Risk Factor for Colonic Diverticulosis

Courtesy: Alcohol Consumption Is a Risk Factor for Colonic Diverticulosis (34)


While the authors of this study were careful to note that association can never prove causality, they nonetheless noted that the association between levels of alcohol consumption and diverticulosis was stronger than any other dietary component studied. This, of course, doesn’t mean that everyone who comes down with diverticulosis consumes alcohol, but it appears to enhance the probability of this outcome in those who do drink.

As the colon has the largest number of bacteria of any part of the digestive tract, acetaldehyde levels after drinking are found in the highest concentrations here. (35) I consider it highly doubtful that chronically or acutely elevated levels of this volatile metabolite is healthy for the beneficial gut flora that lives here.

Alcohol abuse is consistently associated with both colon and rectal cancer. While the association appears stronger between alcohol abuse and rectal cancer, there is still plenty of suggestive evidence that colon cancer risk is elevated in those who consistently abuse alcohol.

In a very recently published paper, researchers identified the bacteria Fusobacterium nucleatum as being involved in the genesis and progression of colon cancer. (36) These researchers have demonstrated how this bacteria adheres to the epithelium of the colon, and induces cell mutations and inflammation. Genetic markers for this bacteria in colon tumors was found to be 10 to 100 higher than in healthy controls.

What’s fascinating to me about these findings is the origin of this pathogen. It is not a typical constituent of colonic flora. Rather, its normal environment is the oral cavity, i.e. the mouth.

So the million-dollar question is how does this bacteria end up in the colon?

For colonization of this bacteria to occur in the colon, two things must happen: compromised gastric-barrier function and large bowel dysbiosis. Compromised gastric-barrier function in order for the pathogen to survive transit through the stomach, colonic dysbiosis to allow it to adhere to the gut wall and begin its inflammatory mayhem.

But how does this relate to alcohol intake?

Well, both chronic and acute alcohol consumption reduces the acidity of stomach acid. The more alkaline stomach pH, the less likely swallowed bacteria is killed before reaching the intestinal tract.

Remember that those who abuse alcohol suffer from high rates of periodontal disease, especially if they smoke. As oral dysbiosis is quite common in this group, there is no shortage of F. nucleatum in the mouths of alcoholics and binge drinkers. (37)

Now couple this steady stream of swallowed oral bacteria with a colon depleted of beneficial bifidobacteria and lactobacillus, and it’s easy enough to envision how this pathogen could attach itself to the colon or rectum. The inflammation it would induce would further create an environment hospitable not only to itself, but to other inflammation-loving bacteria like E. coli.

Finally, add elevated levels of acetaldehyde and reduced natural killer cell activity, and it’s not difficult to see how this can all end very badly. This is as clear an illustration as I can offer that the digestive tract needs to be viewed as an interrelated whole. What occurs in the mouth, esophagus, stomach or small intestine will affect the colon and the large populations of gut flora that inhabit it.

A Votre Sante!

Final thoughts

Most of the negative effects from alcohol use are dose dependent. The more you drink, and the more you drink at any one time, the more adversely alcohol will impact health for the worse.

Many people who imbibe on occasion, or one or two drinks a day, probably need not fear any long-term disruption to GI health, although no one really knows for sure. Again, we’re all different and come to the “bar” with preexisting genetic, gender and gut flora variations that make uniform predictions regarding alcohol’s impact on gastrointestinal health impossible to make.

For certain subsets of the population, any amount of alcohol can be harmful. I’m referring to those who lack the genes necessary for the production of class II aldehyde dehydrogenase (ALDH2). This is the enzyme needed to metabolize acetaldehyde to harmless acetate. Individuals lacking this enzyme experience far higher levels of acetaldehyde toxicity after drinking, and all the negative consequences that flow from that.

ALDH2-deficiency is extremely common in Asian populations, far more so than in Caucasians. For example, about 50% of the Japanese population are ALDH2 deficient. (38)

Individuals with total ALDH2 deficiency caused by receiving this genetic variant from both parents suffer from flushing of the face and body, rapid heart rate, a drop in blood pressure, headache and nausea after consuming alcohol.

I vividly recall an instance when a Vietnamese co-worker drank what she thought was a virgin piña colada at lunch. Within seconds, she was passed out on the floor as the rest of us tried to revive her. Luckily, she came to shortly afterwards, but not without putting the fear of God into both the waitress and bartender.

These people rarely abuse alcohol for obvious reasons. This, of course, brings up the intriguing possibility that the longevity and generally positive health markers seen in many Japanese may be partly due less to diet, than to lower rates of chronic or acute alcohol intake in some members of that society.

However, those that receive this genetic variant from only one parent are able to metabolize some acetaldehyde, although never to the same extent as those lacking ALDH2 deficiency. Sadly, some of these folks do go on to become binge drinkers or alcoholics. As a result, these people are at an especially high risk for developing digestive-tract cancers. (39)

Of the alcoholic beverages available to drink, the research suggests that wine, both red and white, is the safest option. As I said, small to moderate quantities of wine increases gastric secretion, and therefore improves gastric-barrier function and digestion.

Wine also contains abundant polyphenols, far more than what is found in beer or hard liquor. Many of the polyphenols in wine have been shown to have both antioxidant and anticancer properties. The three most studied wine-containing polyphenols are quercetin, rutin and resveratrol.

In vitro studies have also found wine to contain bacterialcidal properties that are deadly to pathogens like Salmonella typhimurium, Shigella sonnei and Escherichia coli—all common causes of intestinal infections and traveler’s diarrhea. (40) (41)

However, caution must be exercised when extrapolating in vitro studies to intake by humans. I’d warn anyone away from relying on wine consumption as a preventative for eating improperly handled food while on a vacation. (42)

As far as cancer risk is concerned, an epidemiological study followed 15,117 males and 13,063 females for 13.5 years to determine the relation between the consumption of different alcoholic beverages and cancers of the mouth, throat, esophagus, stomach and upper respiratory tract. (43)

What they found was that those people who drank wine were at lowest risk of developing these tumors in contrast to those who drank beer or spirits. The authors concluded that moderate wine consumption probably doesn’t increase the risk of oral and esophageal cancer, whereas moderate beer and hard liquor consumption considerably increases the development of these tumors.

However, remember that this is an epidemiological study replete with confounding variables. As a rule wine drinkers tend to come from more affluent classes, and more income tends to equate with higher education and generally better health outcomes.

And even if these results are true, it’s no argument to begin drinking wine if you are a teetotaler. Nor does it mean you won’t get these cancers if you drink wine, and certainly not if you abuse it.

While low to moderate drinking may have no obvious adverse effects on a friend or family member, it may not be the case for you. Speaking from my experience, more than two glasses of wine at any sitting disturbs my sleep. I believe it does so because it increases my cortisol levels during the night, which tells me that it made my gut more permeable to endotoxins.

So a good question to ask yourself is: Is the quantity of alcohol you now consume affecting your sleep for the worse? If so, you may need to reconsider your drinking habits as sleep disturbances are very often an early indicator of higher cortisol secretion caused by translocating gut pathogens.

What you eat also has an impact on how harmful alcohol proves to be. Being malnourished is good for no one, especially someone who abuses alcohol. However, it’s extremely common in many alcoholics who would rather spend their time and energies drinking than eating.

High intake of polyunsaturated fats (PUFAs), especially omega 6s, along with alcohol will enhance liver damage via lipid peroxidation. Inflammation and PUFAs are never a good mix, and few things are more inflammatory to the liver than chronic or binge drinking. Research in animals has consistently found that saturated fats are far more protective of the liver in the presence of high alcohol intake than PUFAs. (44) (45) (46) (47) (48)

Likewise, combining copious quantities of alcohol with gluten grain or refined sugar consumption is not a very good idea. As I said, gluten will enhance the peristaltic inhibiting effects of alcohol.

Nor, might I add, is it good practice to take antacids, proton-pump inhibitors, licit or illicit opiates, acetaminophen or non-steroidal anti-inflammatories during or after copious alcohol intake. All of these drugs can adversely affect gastrointestinal or liver function, and their combination with alcohol will only amplify these effects. And as mentioned, tobacco smoke has a decidedly negative synergistic effect, especially in the mouth, throat and upper respiratory tract when paired with alcohol.

Finally, I need to discuss the elephant in the room regarding the observational finding that low to moderate drinking is associated with lower coronary-disease risk. The key word in that sentence is “associated.” These results have not been derived from randomly controlled clinical trials, but from epidemiology.

So while this association may be true, just be aware that you are basing your drinking behavior on something that has not been proven to be true. Adding to further confusion, a pair of Chinese studies have thrown some doubt on this commonly accepted benefit of drinking. (49) (50)

As I said at the beginning of this post, it’s not my intention to turn all of you into teetotalers, although some of you may be questioning that declaration after reading this post. For better or worse, alcohol is part of the social fabric that binds many of us together, and it isn’t going away anytime soon.

Many of my happiest memories revolve around having a great meal, home cooked or at a good restaurant, surrounded by friends and family while enjoying alcohol. Such social interaction is extremely beneficial to health, and our lives would be poorer without it. While I have no scientific proof of this, I truly believe that beneficial gut flora do not thrive in humans experiencing social isolation.

Nevertheless, too much of a good thing always turns into its opposite. For those of you looking for explanations about why you may have developed the gut problems you have, or why they may have recurred, it may behoove you to examine your level of alcohol intake and adjust it accordingly.

It’s more than obvious that alcohol is incapable of explaining all the digestive issues that afflict many people, especially infants and children who’ve never touched a drop of liquor. Nevertheless, for those who are adults, and entered life already at a gut flora disadvantage due to Caesarian birth or formula feeding or both, and have been subjected to repeated courses of antibiotics, the addition of this drug to your recreational repertoire is entirely capable of tipping the scales in a direction you didn’t plan on. (51) (52)

And yes, fortifying and encouraging the growth of beneficial gut flora will help mitigate the damage caused by excess alcohol intake. I already wrote about that here. So by all means, consume probiotics, prebiotics and fermented foods especially if you drink with any regularity.

However, even these measures have limits. When it comes to alcohol, moderation is key. If this isn’t possible for you, then it’s time to seek help to achieve total abstinence or I can assure you that your current indigestion, gas, bloating, diarrhea or constipation will be the least of your worries going forward.



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