The strategy of using antibiotics to fight infections began innocently enough with the introduction of penicillin in the 1940s. However, in the last 70 years, the use of antibiotics has skyrocketed, resulting in indiscriminate, random, and arbitrary overuse of these agents. [1.]
The premise on which antibiotic use is based is simple: Antibiotics are meant to provide chemical weaponry for the selective elimination of targeted pathogenic bacterial species. This chemical warfare is meant to act like a selective cleanup to assist the immune system, which is then free to complete the process and restore health.
The process is a bit more complicated:
• Antibiotics rarely, if ever, completely eliminate a bacterial pathogen from the body, even under ideal conditions. These drugs are effective in eliminating the weaker organisms while sparing the hardy.
• Antibiotics aren't able to selectively eliminate one pathogenic bacterial species over another. Their actions are largely indiscriminate, destroying large numbers of nonpathogenic, probiotic bacterial species in the process.
• The immune system is frequently incapable of finishing the job that's started by the antibiotics, since it has been suppressed in several ways.
Even in controlled in-vitro experiments in the laboratory, antibiotics have been found to induce bacteria to enter dormant states, alter their physiology, and acquire resistance. In the body, the potential for bacteria to evade the effects of these drugs is even more pronounced. These organisms are able to exist in zones of the body inaccessible to antibiotic penetration, thereby achieving asylum.
Antibiotics are unable to target single bacterial species. Even the most "narrow spectrum" agents destroy members of many different species of bacteria, from so-called "friendly fire." In this way they lead to imbalance and dysbiosis on the skin and in the gastrointestinal and respiratory tracts.
Many essential species of bacteria are thereby disturbed and affected by this approach. The broad-spectrum antibiotics are even more effective in destroying a wide range of bacterial species, taking out beneficial bacteria along with pathogenic ones. Opportunistic yeast and monocultures of surviving (and frequently resistant) bacteria are the result. The effects of these disruptions can be widespread and long-lasting.
The use of antibiotics and the subsequent disturbances of bacterial flora in and on the body have been linked to a wide variety of adverse sequelae, including inflammatory bowel disease [2.], pseudomembranous colitis [3.], sudden cardiac death [4.], gastroesophageal reflux disease [5.], inflammatory airway diseases, including asthma [6.] and bronchiectasis [7.], kidney stones, breast cancer [8.], and allergies in later life [9.].
According to researchers at the Drug Safety Clinic at Sunnybrook Health Science Center in Toronto, Canada, antibiotics cause the majority of adverse drug reactions in children. [10.]
The use of antibiotics leads to the emergence of resistance and alters native bacterial flora. It also has direct adverse effects upon the immune system. According to leading pharmacologists, antibiotics directly suppress the immune system through several different pathways, including:
• Decreased leukocyte chemotaxis, the process whereby white blood cells migrate to areas of infection in the body,
• Decreased lymphocyte and monocyte transformation, or cellular immunity, the process whereby inactive white blood cells are activated into cells that attack invading bacterial organisms,
• Decreased antibody production, or humoral immunity, the process of producing specific antibodies against distinct classes of organisms, which enable activated white blood cells to selectively destroy selected bacteria,
• Decreased phagocytosis, the process whereby certain white blood cells actively swallow and digest bacteria,
• Decreased microbiocidal action of polymorphonuclear leukocytes, the process whereby certain white blood cells release toxic chemicals to destroy bacteria. [11.]
The combination of these suppressive factors impair the immune system, making it more susceptible to a wide variety of fungal and viral superinfections while increasing the risk of developing recurrent bacterial infections.
Antibiotics also cause antibiotic resistance in direct proportion to the frequency and duration of their use. Without the use of antibiotics, there would be no crisis of antibiotic resistance. Antibiotic resistance is a direct effect of the way in which these agents work.
Antibiotics eliminate weaker, more fragile and susceptible bacteria and create a type of selective breeding program for stronger, hardier, more resistant, and (in the case of community-acquired MRSA) more aggressive strains. [12.]
Antibiotic-resistant organisms are a predictable and inevitable outcome of antibiotic use. The more prolonged the course of treatment, the more likely that resistant organisms (like MRSA) will develop. The only way to ensure that resistance to antibiotics does not develop is to avoid the use of these agents altogether.
Next week: Part 4 of an eight-part series: Overuse of Antibiotics
References:
1. Wilkoff WG, I'm an Antibiotic Abuser, Guest Ed., Internal Medicine News, April 15, 1997:7.
2. Tlaskalova-Hogenova H, et al, Commensal Bacteria, Mucosal Immunity and Chronic Inflammatory and Autoimmune Diseases, Immunology Letters, 2004, 93:97–108
3. Chico GF, Chico MA, Clostridium Dificile Colitis, GI Consult, Emergency Medicine, 2005, Jan.: 27–32.
4. Ray WA, Murray KT, Meredith S, et al, Oral erythromycin and the risk of sudden death from cardiac causes. New England Journal of Medicine, 2004; 351:1089–96.
5. Blaser M, In a World of Black and White, Helicobacter pylori Is Gray, Annals of Internal Medicine 1999, 130:695–97.
6. Chest. June 2007; 131:1753–1759.
7. Jancin B, Think Bronchiectasis in Frequent Antibiotic Users, Clinical Rounds, Pulmonary Medicine, Internal Medicine News, July 1, 2006:24.
8. O'Connor A, Study Suggests Breast Cancer Is Linked to Use of Antibiotics, New York Times, National, Feb. 17, 2004.
9. McKeever TM, et al, Early Exposure to Infections and Antibiotics and the Incidence of Allergic Disease, Journal of Allergy and Clinical Immunology, 2002, 109:43–50.
10. Quantum Sufficit, American Family Physician, November 1998, 58(8):1734.
11. Gilman AG, Goodman SL, Rall TW, Murad F, Goodman and Gillman's The Pharmacological Basis of Therapeutics, 7th Ed, Macmillan, NY, 1985: 1084.
12. Naimi TS, LeDell DH, Como-Sabetti K, et al, Comparison of community- and health care-associated methicillin-resistant Staphylococcus aureus infection. JAMA 2003; 290:2976-2984.
Ronald D. Whitmont, M.D., is a board-certified internist with a private practice of classical homeopathy in New York.
Dr. Whitmont's Web site
Feeds