Tuesday, October 20, 2015

The pharmacology of flatulence

Is it time for a post about drugs and farting?

Of course it's time for a post about drugs and farting.

Drugs do many, many things. Some of these we want, others not so much. The latter get called side effects. One of the less-desired yet relatively benign side effects associated with many drugs is an uptick in the fart department. While perhaps humorous to some, this outcome is generally viewed as unpleasant due to the associated bloating and pain, not to mention the embarrassing sensory assault that is a barrage of toots.

Toots in their nascent form (Source)

Flatulence refers to the mixture of swallowed air and gas produced in the stomach and intestines (by bacterial fermentation of indigestible food components) that eventually makes its way out the bottom end of us as a fart. Normally there is about 150 mL, or a little less than half a can of pop, of gas within our guts. In addition to drug-induced crop dusting, flatulence can result from certain foods (e.g. dairy, legumes, onions, and cruciferous vegetables), poorly-executed soda-fueled burping attempts (or just drinking a lot of carbonated beverages), prebiotics, and/or being afflicted with gastrointestinal diseases such as IBSGERD, or a Giardia infection.

While many drugs enhance one's farting ability, there are also drugs capable of cracking down on crop dusting. Let's look at both groups.


Drugs known to cause flatulence include laxatives, antacids, antibiotics, antidepressants, statins, and an antidiabetes agent called acarbose.

Laxatives are a large and structurally diverse group of molecules capable of causing the contents of your intestines to move through your body more quickly, resulting in the expulsion of gas and other exciting materials. Laxatives include everything from food-based fiber and vitamin C to toxic nasties like calomel and phenolphthalein.

Flatulence has been reported as a major side effect of antibiotics such as chloramphenicol and chlortetracycline. As reported in an old paper I dug up, "the common complaint [of treatment with these drugs] was flatulence..."the wind" troubled them day and night and caused them embarrassment, especially in the general wards. In one case of extreme flatulence the patient could hardly breathe and required the passage of a rectal tube to relive him."

Statins refer to a group of drugs (e.g Lipitor) capable of reducing cholesterol formation by inhibiting the enzyme HMG CoA reductase. This appears to be a good thing in terms of preventing cardiovascular disease. They're among the most commonly prescribed drugs, and one of the most common side effects they cause is flatulence, so I figure they're responsible for a whole lot of the farts out there.

Acarbose is used to treat type 2 diabetes and slow the progression of impaired glucose tolerance toward this disease. It was originally isolated from a bacterium residing in Kenya, and works by inhibiting an enzyme found in your intestine called alpha glucosidase. This slows the release of glucose from larger carbohydrates (e.g. starches), reducing the amount that is absorbed into the blood. It also means that more of the larger carbs end up sticking around in your guts, providing food for bacteria able to convert them into gas.


Moving on from the gas promoters, there are several drugs available to reduce or at least minimize the discomfort associated with flatulence.

Digestive enzymes can be taken to address food-sourced causes of farts. These include lactase (e.g. Lactaid) and alpha-galactosidase (e.g. Beano), which help your body break down lactose and a bunch of polysaccharides and oligosaccharides found in legumes and cruciferous vegetables, respectively. If these carbs aren't digested they can be turned into gas by intestinal microbes. So while acarbose is an enzyme inhibitor that enhances farting by ensuring carbs don't get broken down, digestive enzymes help to break down carbs and thus cut down on farting.

Although some antibiotics can cause flatulence, rifaximin (a derivative of rifamycin used to treat traveler's diarrhea caused by E. coli) appears to help relieve bloating and flatulence, particularly in people with IBS. Rifaximin is interesting because it's really terrible at making its way through the walls of the intestine into the bloodstream, so it mostly just passes through you. It seems that the antibiotic inhibits the growth of hydrogen gas-producing bacteria, thereby reducing fart volumes.

Simethicone (e.g. Gas-X) is a foam inhibitor, which means it can convince small gas bubbles stuck in your intestines to join forces and produce larger bubbles. This doesn't prevent gas production, but it does make it easier to fart (thereby relieving pain and bloating).

There is also some evidence suggesting various spices (e.g. cloves, cumin, coriander, and fennel) and mixtures of bacteria (probiotics) can help reduce gut-based gas production.


Brecević L, Bosan-Kilibarda I, Strajnar F. 1994. Mechanism of antifoaming action of simethicone. Journal of Applied Toxicology 14(3):207-211.

Cappello C, Tremolaterra F, Pascariello A, Ciacci C, Iovino P. 2013. A randomised clinical trial (RCT) of a symbiotic mixture in patients with irritable bowel syndrome (IBS): Effects on symptoms, colonic transit and quality of life. International Journal of Colorectal Disease 28(3):349-358. [Full text]

Chiasson JL et al. 2002. Acarbose for prevention of type 2 diabetes mellitus: The STOP-NIDDM randomised trial. Lancet 359(9323):2072-2077.

Danzl DF. 1992. Flatology. Journal of Emergency Medicine 10(1):79-88.

Sharara AI, Aoun E, Abdul-Baki H, Mounzer R, Sidani S, Elhajj I. 2006. A randomized double-blind placebo-controlled trial of rifaximin in patients with abdominal bloating and flatulence. American Journal of Gastroenterology 101(2):326-333.

Tomaszewski T. 1951. Side-effects of chloramphenicol and aureomycin, with special reference to oral lesions. British Medical Journal 1(4703):388-392. [Full text]

Vaughan CJ, Gotto AM Jr, Basson CT. 2000. The evolving role of statins in the management of atherosclerosis. Journal of the American College of Cardiology 35(1):1-10. [Full text]



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