The gut connection: ulcers, reflux and the disease smoking makes worse

A ring of muscle at the bottom of the oesophagus, the lower oesophageal sphincter, is supposed to stay shut except when you swallow. Nicotine relaxes it.

Smoking also reduces saliva production, and saliva is your natural acid neutralizer. The combination is chronic heartburn: acid climbing where it does not belong, more often and for longer.

Long-term reflux damages the lining of the oesophagus and can lead to Barrett's oesophagus, a precancerous change. Smoking independently raises the risk of oesophageal cancer as well.

The stomach protects itself from its own acid with a bicarbonate-rich mucus layer and constant blood flow to the lining. Smoking reduces bicarbonate secretion and constricts those vessels.

Most peptic ulcers involve the bacterium Helicobacter pylori or anti-inflammatory drugs, but smoking makes ulcers more likely to form, slower to heal and more likely to come back after treatment. It also raises the risk of the two dangerous complications: bleeding and perforation.

Smoking is the most important modifiable risk factor in Crohn's disease. Smokers with Crohn's have more flares, more need for steroids and immunosuppressants, more surgery, and more disease recurrence after surgery.

Gastroenterologists routinely tell patients that quitting smoking is comparable to adding a medication to their regimen. This is one of the few areas of medicine where a lifestyle change has drug-level impact.

Curiously, ulcerative colitis behaves differently in studies, but that is never a reason to smoke: the cancer and cardiovascular arithmetic overwhelms any theoretical benefit.

Smoking is a recognized risk factor for pancreatic cancer, one of the deadliest cancers, and for colorectal cancer and polyps.

It also worsens liver disease progression and is linked to gallstones. The carcinogens that enter your bloodstream have to be processed by the liver and excreted by the kidneys, exposing both.