How smoking affects your stomach - Research Paper Example

? Effect of smoking on the stomach Introduction The stomach constitutes an important part of the gastro-intestinal system which is responsible for the digestion of food and absorption of nutrients in the body. Tobacco smoke that contains more than 4000 compounds that affect cellular functions in various organs such as the lung and the stomach. Components of cigarette smoke reach the stomach through the circulation or via the gastro-intestinal tract via saliva. Smoking has several known effects on the stomach and is a major contributor to stomach related ailments such as gastro-esophageal reflux disease, delayed emptying of gastric contents, stomach cancer and ulcers. Components of tobacco smoke have also been shown to increase the atrophy of gastric mucosa which is one of the contributing factors to ulceration in the stomach through the secretion of various reactive factors. They have also been found to increase the colonization of Helicobacter pylori in infected individuals (Smoking’s Immediate Effects, 2009; Namiot et al, 2007). Scientific research has also shown that increased secretion of acid in the stomach, which also contributes to peptic ulcer, due to over-expression of the H, K-ATPase found in the parietal cells. (Hammadi et al, 2009). Smoking also increases the risk of developing stomach cancer even after the individual quits the habit as it causes damage to the individual’s DNA which results in tumor formation at a later stage. Cigarette smoke affects the inner lining of the stomach through various mechanisms. Nicotine is the active ingredient in tobacco smoke which is readily absorbed into circulation via the gastro-intestinal tract. Nicotine, which is an oxidant, is known to give rise to free radicals and reactive oxygen and nitrogen species in the tissues where it is present. These radicals in turn react with the tissue cells and cause the breakdown of polyunsaturated fatty acids through oxidative processes giving rise to cytotoxic aldehydes. Cigarette smoking also produces potent superoxides, hydrogen peroxides and hydroxyl radicals which are powerful oxidants that are involved in peroxidation of lipids, oxidation of proteins and causing damage to the DNA within the cells. The damaged DNA generally requires a multi-step process for its repair. This process could involve errors or mutations that may subsequently give rise to abnormal or cancerous cells. In addition, these processes are also considered to be a vital etiological factor for ageing and in the healing of wounds which is known to cause peptic ulcer in the stomach. The reactive molecules produced by the chemicals present in tobacco smoke can lead to oxidative stress within the tissues which also plays a major role in the pathogenesis of diseases such as cancer and heart ailments (Pasupathi, P et al, 2011). The effect of the chemicals from tobacco smoke on the gastro-esophageal reflux mechanism has been well characterized. Under normal conditions the esophageal sphincter which is present at the end of the esophagus prevents the acids secreted within the stomach from reaching the esophagus by regurgitation. In case of individuals who smoke the valve strength or pressure is decreased due to constant contact with the harmful chemicals present in cigarette smoke and this enables the stomach acid to regurgitate back into the esophagus. In addition smoking also increases the secretion of bile salts into the stomach from the intestines which causes additional irritation to the esophageal lining. With the esophagus already damaged due to constant exposure to cigarette smoke the acid reflux adds further injury which could lead to esophageal ulcers or cancer (Smoking’s Immediate Effects, 2009). Another common disease is peptic ulcer which could occur in the stomach or the duodenum. Peptic ulcers are sores which are open and present along the lining of the stomach or the duodenum. Smokers are more prone to develop such ulcers as tobacco smoke increases acid secretion within the stomach and also reduces bicarbonate production by the pancreas which is normally involved in neutralizing the effect of excess acid on the stomach or the intestine. The hydrochloric acid secreted by the parietal cells which are scattered throughout the glands of the stomach is mainly involved in mucosal damage and in the pathogenesis of peptic ulcer. The secretion of this acid is controlled by a proton pump known as the H, K-ATPase which is synthesized by the parietal cells. The expression and activity of this pump has been shown to increase when exposed to cigarette smoke thereby resulting in an excessive secretion of the acid that causes significant damage to the mucosal lining of the stomach. It is also known to be responsible for delayed healing of the peptic ulcer as it decreases blood flow to the injured regions when constantly exposed to cigarette smoke (Hammadi et al, 2009). Smoking also increases a person’s risk to H. pylori infection which is also known to cause peptic ulcers and is also a causative factor for the development of stomach cancer. This organism secretes various products such as urease, protease, phospholipase, ammonia and acetaldehyde that play a role in damaging the gastric mucosa. Through a sequence of events these products can lead to atrophy of the gastric cells followed by intestinal metaplasia and dysplasia and finally to carcinoma. In addition, the organism also produces reactive oxygen and nitrogen species which cause suppression of the antioxidant response of the host thereby leading to potential oxidative damage of the DNA within the cells (Nagini, 2012). The process of wound healing is also delayed in smokers as blood flow to the inner regions of the stomach and the intestine is relatively less and as a result these ulcers remain within the stomach or the duodenum for a long time which can cause terrible pain and also death when left untreated. In individuals already infected with H.pylori, chronic cigarette smoking increases the colonization of the organism and the risk of atrophy of the gastric mucosa and metaplasia of the intestines (Namiot et al, 2007). Tobacco smoke is a major contributing factor to the development of gastric cancer, which is considered to be the leading cause of death due to cancer as the prognosis for the disease is poor due to detection at a later stage leading to a lower survival rate. The cancer can occur at any part of the stomach and when left undetected it can spread throughout the stomach and also to other organs. Several studies have shown a positive correlation between cigarette smoking and the risk of developing gastric cancer. The chemical components of tobacco smoke induce the production of free radicals and reactive molecules that cause damage to the cell DNA. In addition, smoking also decreases the synthesis of prostaglandins which help to maintain the integrity of the gastric mucosa. Tobacco smoke also gives rise to gastric lesions, ulcerations and atrophy of the gastric mucosa which can all contribute to the formation of cancerous tissues within the stomach (Nagini, 2012). A study conducted to examine the effects of exposure to environmental tobacco smoke or second-hand smoke as a causative factor for cancer has concluded that second-hand smoke does increase the risk of stomach cancer even in non-smokers (Strumylaite et al, 2006). Similarly the risks for developing stomach cancer were high in individuals who had already quit smoking as significant damage would have been caused when the body is constantly exposed to cigarette smoke. In conclusion, there is considerable scientific evidence that tobacco smoke has harmful effects on the stomach giving rise to various ailments ranging from gastric refluxes to the more deadly stomach cancer. Hence these evidences are strong warnings for smokers to quit the habit at the earliest and in the case of non-smokers it serves as a reminder to never start smoking. Given the fact that even second-hand smoke when inhaled poses children and adults who do not smoke at a risk of developing cancer, it is up to those who use cigarettes to give up the habit. References 1. Hammadi, M., Adi, M., John, R., Khoder, G. A. K., & Karam, S. M. (2009). Dysregulation of gastric H, K-ATPase by cigarette smoke extract. World Journal of Gastroentrology, 15(32): 4016-4022. Retrieved March 14, 2013, from http://europepmc.org/articles/PMC2731952/reload=0;jsessionid=VbwJ4gmhaPKtumLTbWzJ.0 2. Nagini, S. (2012). Carcinoma of the stomach: A review of epidemiology, pathogenesis, molecular genetics and chemoprevention. World Journal of Gastrointestinal Oncology, 4(7): 156-169. Retrieved March 14, 2013, from http://www.wjgnet.com/1948-5204/full/v4/i7/156.htm 3. Namiot, A., Kemona, A., & Namiot, Z. (2007). Smoking Habit and Gastritis Histology. Advances in Medical Sciences, 52: 191-195. Retrieved March 14, 2013, from http://www.advms.pl/?q=system/files/33_52Namiot.pdf 4. Pasupathi, P et al. (2011). Chronic Tobacco Smoking and Gastric Cancer: A Review. International Journal of Current Biomedical and Pharmaceutical Research, 1(2): 48-66. Retrieved March 14, 2013, from http://cogprints.org/7333/1/Chronic_Tobacco_Smoking_and_Gastric_Cancer_A_Review.pdf 5. Smoking’s Immediate Effects on the Body. (2009). Campaign for Tobacco-Free Kids. Retrieved March 14, 2013, from http://www.tobaccofreekids.org/research/factsheets/pdf/0264.pdf 6. Strumylaite, L., Strazdas, L., & Wright, R. (2006). Environmental Tobacco Smoke and Stomach Cancer Risk. Epidemiology, 17(6): S317-S318. Retrieved March 14, 2013, from http://journals.lww.com/epidem/Fulltext/2006/11001/Environmental_Tobacco_Smoke_and_Stomach_Cancer.836.aspx Read More