The Foreskin Advantage

and toxic condoms

Benefits enjoyed by males who are intact (not circumcised)

1. Full penis length and circumference. The “prepuce” (foreskin) constitutes 50% or more of the skin system of the penis [1]. If unfolded and spread flat, the average adult foreskin measures 60-90 square centimeters (10-14 square inches) [2], or about the size of an index card [see illustration]. The foreskin creates a visibly longer penis, especially when the foreskin extends beyond the head of the penis. Also, the double-layered tissue of the foreskin engorges with blood during erection and creates a visibly and sensually thicker shaft and glans.When the engorged foreskin retracts behind the coronal ridge of the glans, it often creates a wider and more pronounced “ridge” that many partners find especially stimulating during penetrative intercourse. The circumcised penis appears truncated and thinner than a full-sized intact penis.

2. Protection. The sleeve of tissue known as the foreskin normally covers the glans and protects it from abrasion, drying, callusing (keratinization), and environmental contaminants. The glans is intended by nature to be a protected internal organ, like the female clitoris [see illustration]. The effect of an exposed glans and resulting keratinization on human sexual response has never been studied. Increasing reports by circumcised men indicate that keratinization causes a loss of sexual sensation, pleasure and fulfillment [3, 4].

3. Ridged bands. The inner foreskin contains bands of densely innervated, sexually responsive tissue [1]. They constitute a primary erogenous zone of the human penis and are important for realizing the fullness and intensity of sexual response [5].

4. Gliding action.  The foreskin is the only moving part of the penis. During any sexual activity, the foreskin and glans work in unison; their mutual interaction creates a complete sexual response. In heterosexual intercourse, the non-abrasive gliding of the penis in and out of itself within the vagina facilitates smooth and pleasurable intercourse for both partners [see illustration]. Without this gliding action, the corona of the circumcised penis can function as a one-way valve, dragging vaginal lubricants out into the drying air and making artificial lubricants essential for non-painful intercourse [6].

5. Specialized sensory tissue. In addition to the “ridged bands” mentioned above, thousands of coiled fine-touch receptors (Meissner’s corpuscles) constitute the most important sensory component of the penis [1]. The foreskin contains branches of the dorsal nerve and between 10,000 and 20,000 specialized erotogenic nerve endings of several types, which are capable of sensing slight motion and stretch, subtle changes in temperature, and fine gradations in texture [7, 8, 9, 10, 11, 12].

6. The frenulum. This is a highly nerve-laden web of tissue that tethers the inner foreskin to the underside of the glans [see photo]. It is similar to the frenula found under the tongue, the upper lip and the clitoral hood (female foreskin). For many intact men, the penile frenulum is a male “G-spot” that is highly pleasurable when repeatedly stretched and relaxed during sexual activity [13]. Depending on the surgical method used, the frenulum is partially to completely destroyed by circumcision.

7. Proper blood flow. The foreskin contains several feet of blood vessels, including the frenular artery and branches of the dorsal artery. The loss of this rich vascularization interrupts normal blood flow to the shaft and glans of the penis, damaging the natural function of the penis and altering its development [1].

8. Immunological defense. The soft mucosa of the inner foreskin produces plasma cells, which secrete immunoglobulin antibodies, and antibacterial and antiviral proteins [7, 14], such as the pathogen-killing enzyme called lysozyme [15 and see explanation]. All of the human mucosa (the linings of the mouth, eyelids, vagina, foreskin and anus) are the body’s first line of defense against disease. This benefit of the foreskin could be one possible explanation why intact men are at lower risk of chlamydia and other sexually transmitted diseases[16-21].

9.  Langerhans cells. These specialized epithelial cells are a component of the immune system and may play a role in protecting the penis from sexually transmitted infections such as HIV (AIDS) [see explanation and 14-16, 18].

10. Proper lymph flow. The foreskin contains lymphatic vessels, which are necessary for proper lymph flow and immunological functioning.

11. Estrogen receptors. The foreskin contains estrogen receptors, whose purpose is not yet fully understood and needs further study [22].

12. Apocrine glands. These glands produce pheromones, nature’s invisible yet compelling signals to potential sexual partners. The effect of their absence on human sexual behavior has never been studied [23].

13. Sebaceous glands. The oils produced by these glands lubricate and moisturize the foreskin and glans, so that the two structures function together smoothly.

14. Dartos fascia. This is a smooth muscle sheath that underlies the scrotum, the entire penis and the tip of the foreskin. It is necessary for proper temperature regulation of the genitals (causing these structures to elongate in the heat and shrink in the cold). Approximately half of the Dartos fascia is destroyed by circumcision [7].

15. Natural texture and coloration of the glans. In the intact penis, the glans normally appears moist, shiney, and pinkish-red to dark purple. These visual cues often attract and excite a sexual partner. The glans of a circumcised penis is dry, rough and often light pink to bluish-gray in color [see photos].

16. Zero risk of serious infection or surgical injury.  Unfortunate boys who suffer botched circumcisions lose part or all of their penis from surgical mishap or subsequent infection. They are often “sexually reassigned” by castration and “transgender surgery.” They are relegated to a life of hormone therapy and are compelled to live their lives as pseudo-females, the success of which has never been fully assessed [24-46].

17. Zero risk of death from surgery. Every year boy die from the complications of circumcision, a fact that the American circumcision industry ignores, obscures, or downplays [29-31].

18. Zero risk of delayed or diminished maternal bonding. Circumcision, even if anesthesia is used, causes unavoidable operative trauma and post-operative pain that has been shown to disrupt bonding with the mother, which in turn interferes with the first developmental task of every human, that of trust (trust in human contact, in personal safety, etc) [47-51].

19.  Electromagnetic “cross-communication.” Anecdotal reports suggest that, without the mucosa of its foreskin, the penis lacks the capacity for the subtle electromagentic energy transfer that occurs during contact between two mucous membranes (the vaginal walls and the exposed inner lining of the foreskin). Such contact contributes to the full experience of sexual pleasure. These reports deserve further scientific study.

20. The foreskin is necessary for optimal health and well-being of the male, as well as contributing to fulfillment
in his sexual relationships.

Adapted for use by NOHARMM from a list compiled by
Gary L. Harryman (NORM/Southern California)


1. Taylor, J. R. et al., “The Prepuce: Specialized Mucosa of the Penis and Its Loss to Circumcision,” British Journal of Urology 77 (1996): 291-295.

2.  Werker, P, Terng, A, Kon, M, “The Prepuce Free Flap: Dissection Feasibility Study and Clinical Application of a Super-Thin New Flap,” Plastic & Reconstructive Surgery 102 (1998): 1075-1082.

3. Money, J. and Davison J., “Adult penile circumcision: erotosexual and cosmetic sequelae,” The Journal of Sex Research, Vol 19 No. 3, Aug 1983.

4. Hammond, T. “A Preliminary Poll of Men Circumcised in Infancy or Childhood,” BJU International 83, Suppl. 1 (1999): 85-92.

5. Bullough, V. L. and Bullough, B. ed., “Circumcision: Male-Effects Upon Human Sexuality,” Human Sexuality Encyclopedia,Garland, 1994.

6. O’Hara, K. and O’Hara, J., “The effect of male circumcision on the sexual enjoyment of the female partner,” British Journal of Urology, 83, Supplement 1, (1999): 79-84.

7. Cold, C, Taylor, J, “The Prepuce,” BJU International 83, Suppl. 1, (1999): 34-44.

8. Bazett, H. C. et al., “Depth, Distribution and Probable Identification in the Prepuce of Sensory End-Organs Concerned in Sensations of Temperature and Touch; Thermometric Conductivity,” Archives of Neurology and Psychiatry 27 (1932): 489-517.

9. Dogiel, A. S., “Die Nervenendigungen in der Haut der äusseren Genitalorgane des Menschen,” [Nerve endings in human genital mucosa] Archiv fur Mikroskopische Anatomie 41 (1893): 585-612.

10. Winkelmann, R. K., “The Cutaneous Innervation of Human Newborn Prepuce,” Journal of Investigative Dermatology 26 (1956): 53-67.

11. Winkelmann, R. K., “The Erogenous Zones: Their Nerve Supply and Its Significance,” Proceedings of the Staff Meetings of the Mayo Clinic, 1959.

12. Erickson, J. A., “Three Zones of Penile Skin,” Blue_ArrowD096.gif (140 bytes)five photographs in Lander M. M., “The Human Prepuce,” in Denniston, G. C. and Milos, M. F., eds., Sexual Mutilations: A Human Tragedy, Plenum Press (1997): 79-81.

13. Seifer, Judith, R.N. (President, American Assn. of Sex Educators, Counselors and Therapists) “Ask men’s health.” Men’s Health (October 1994): 133

14. Fleiss, P., Hodges, F. M., and Van Howe, R. S., “Immunological Functions of the Human Prepuce,” Sexually Transmitted Infections, 1998.

15. Lee-Huang, S, Huang P.L., Sun Y., et al “Lysozyme and RNases as anti-HIV components in beta-core preparations of human chorionic gonadotropin,” Proc Natl Acad Sci (U S A) 1999 (Mar 16);96(6):2678-2681.

16. Van Howe, R.S., “Does Circumcision Influence Sexually Transmitted Diseases?” BJU International 83, Suppl. 1 (1999): 52-62.

17. Laumann, E.O. et al., “Circumcision in the United States: Prevalence, Prophylactic Effects, and Sexual Practice,” JAMA 277, 1997.

18. Nicoll, A. “Routine male neonatal circumcision and risk of infection with HIV-1 and other sexually transmitted diseases,” Archives of Disease in Childhood (London) 1997;77(3):194-195.

19. Smith, G. L. et al., “Circumcision as a Risk Factor for Urethritis in Racial Groups,” American Journal of Public Health 77, 1987.

20. Cook, L. S. et al., “Clinical Presentation of Genital Warts among Circumcised and Uncircumcised Heterosexual Men Attending an Urban STD Clinic,” Genitourinary Medicine 69 (1993): 262-264.

21. Tanne, J.H., “U.S. has epidemic of sexually transmitted disease,” BMJ 1998;317:1616.

22. Hausmann, R. et al., “The Forensic Value of the Immunohistochemical Detection of Oestrogen Receptors in Vaginal Epithelium,” International Journal of Legal Medicine 109 (1996): 10-30.

23. Ahmed, A. and Jones, A. W., “Apocrin Cystadenoma: A Report of Two Cases Occurring on the Prepuce,” British Journal of Dermatology, 1969.

24. Cleary, D. G. and Kohl, S., “Overwhelming infection with group B beta-hemolytic streptococcus associated with circumcision,” Pediatrics, Vol 64, no 3, (September 1979), pp. 301-303.

25. Williams and Kapila, “Complications of Circumcision,” British Journal of Surgery, Oct 1993.

26. Diamond, M. and Sigmundson, H. K., “Sex Reassignment at Birth,” Archives of Pediatrics and Adolescent Medicine, 1997.

27. Money, J., “Ablatio Penis: Normal Male Infant Sex-Reassigned as a Girl,” Archives of Sexual Behavior, 1975.

28. Bradley, S. J. et al, “Experiment of Nurture: Ablatio Penis at 2 Months, Sex Reassignment at 7 months, and a Psychosexual Follow-up in Young Adulthood,” Pediatrics 1998.

29. “Baby bleeds to death after circumcision,” Miami Herald, June 21, 1993.

30. “Boy in coma most of his 6 years dies,” Associated Press, July 10, 1992.

31. “Circumcision that didn’t heal kills boy,” NewsNet5 – Cleveland, Ohio, October 20, 1998.

32. “Permanent foreshortening and disfigurement of the penis,” Associated Press, November 30, 1995.

33. Palmer, J. M. and Link, D., “Impotence following anesthesia for elective circumcision,” JAMA 1979; 241:2635-6.

34. Pearlman, C. K., “Reconstruction Following Iatrogenic Burn of the Penis,” Journal of Pediatric Surgery 11 (1976): 121-122.

35. Persad, R. et al., “Clinical Presentation and Pathophysiology of Meatal Stenosis Following Circumcision,” Brit Journal of Urology 75, 1995.

36. Lerner, B. L., “Amputation of the penis as a complication of circumcision,” Med Rec Ann 1952; 46: 229-31.

37. Levitt, S. B., Smith R. B., Ship A.G,. “Iatrogenic microphallus secondary to circumcision,” Urology 1976; 8: 472-4.

38. Gearhart, J. P. and Rock, J. A., “Total Ablation of the Penis after Circumcision with Electrocautery: A Method of Management and Long-Term Followup,” Journal of Urology 142 (1989): 799-801.

39. Gluckman, G. R. et al., “Newborn Penile Glans Amputation during Circumcision and Successful Reattachment,” Journal of Urology 153 (1995): 778.

40. Kaplan, G. W., “Complications of Circumcision,” Urologic Clinics of North America 10, 1983.

41. Stefan, H., “Reconstruction of the Penis Following Necrosis from Circumcision Used High Frequency Cutting Current,” Sbornik Vedeckych Praci Lekarske Fakulty Karlovy Univerzity (Hradci Kralove) vol. 35, no. 5 (Suppl) 1992, pp. 449-454.

42. Strimling, B. S., “Partial Amputation of Glans Penis during Mogen Clamp Circumcision,” Pediatrics 87 (1996): 906-907.

43. Taddio, A. et al., “Effect of Neonatal Circumcision on Pain Response during Subsequent Routine Vaccination,” Lancet 349 (1997): 599-603.

44. Talarico, R. D. and Jasaitis, J. E., “Concealed Penis: A Complication of Neonatal Circumcision,” Journal of Urology 110 (1973): 732-733.

45. Kirkpatrick, B. V. and Eitzman, D. V., “Neonatal Septicemia after Circumcision,” Clinical Pediatrics 13 (1974): 767-768.

46. Lee L.D., and Millar A.J.W. “Ruptured bladder following circumcision using Plastibell device,” British Journal of Urology 1990; 65: 216-17.

47. Cansever, G., “Psychological effects of circumcision,” Br J Med Psychol 1965; 38: 321-31.

48. Marshall, R. E. et al., “Circumcision: II. Effects upon Mother-Infant Interaction,” Early Human Development , 1982.

49. Goldman, R., “Circumcision: The Hidden Trauma,” Vanguard Publications, 1997.

50. Prescott, J. W., “Genital Pain vs. Genital Pleasure: Why the One and Not the Other?” Truth Seeker 1 (1989): 14-21.

51. Immerman, R. S. and Mackey, W.C., “A Proposed Relationship Between Circumcision and Neural Reorganization,” Journal of Genetic Psychology, 1998.




Circumcision and AIDS in Africa

By Roberto Giraldo, June 2000

The idea that HIV, the virus that supposedly causes AIDS, is “heterosexually transmitted” in African countries and mostly “homosexually transmitted” in Western countries cannot be explained by known epidemiological rules.

This is why, since the beginning of AIDS in Africa, when reports showed that the syndrome was equally distributed in men and women, researchers have been speculating about explanations for what they call “An Epidemiologic Paradigm” (1).

The difficulty is that the belief that HIV is the cause of AIDS prevents health care professionals, researchers, journalists, and lay people from perceiving genuine explanations for the ways in which the AIDS epidemic is manifesting itself within different communities, countries, and continents. HIV is an obstacle to discovering the objective causes of AIDS. Nor does the HIV theory permit proper measures to be taken to stop the spread of the epidemic. This is the true danger of HIV!

The following are some of the reasons that researchers who believe that HIV is the cause of AIDS have given to explain why, in Africa, AIDS affects both sexes equally: late age at marriage; sexual cravings and excesses; gross heterosexual promiscuity; high levels of polygyny; the rubbing of monkey’s blood into cuts as an aphrodisiac; truck drivers who get HIV from prostitutes and then infect their wives; duration of postpartum abstinence; women being allowed to participate in commerce and maintain separate budgets from husbands; high levels of sterility caused by widespread sexually transmitted diseases; unusual sexual practices that facilitate transmission; the practice of female circumcision; the lack of male circumcision; etc. (2-6).

Western health experts and journalists accuse Africans of gross heterosexual promiscuity. Do they have proof for it? Recently, Nobel Prize winner Nadine Gordiner wrote in the New York Times that African promiscuity “is difficult to condemn when sex is the cheapest or only available satisfaction for people society leaves to live on the street” (7).

Regarding male circumcision, the following are among the arguments that defenders of HIV as the cause of AIDS provide to promote male genital mutilation in Africa (2,8-12):

“A joint Canadian-Kenyan medical research team working in Kenyatta Medical School in Nairobi, where the epidemic is intense, had reported a year earlier that AIDS rates were higher among Luo migrants from western Kenya than among the Kikuyu from central Kenya.” Later the authors “surmised that the Luo were at greater risk because, unlike the Kukuyu, they were not circumcised” (2,10).

“An American team led by John Bongaarts of the Population Council published a paper showing that the regions across sub-Saharan Africa with high levels of HIV infection among local peoples corresponded well with the areas where men were typically uncircumcised” (9).

“Most of the ideas we investigated failed to explain the extraordinarily high rate of infection in the AIDS belt. One factor did stand out, however: lack of male circumcision. In the area where men are typically uncircumcised, HIV rates are among the highest in the AIDS belt” (2).

“We noted that the areas of Africa with large numbers of uncircumcised men were almost exactly the same as the regions suffering from the severe AIDS epidemic,” and “The link between lack of circumcision and elevated levels of HIV infection appears robust” (2).

“For uncircumcised men, thorough cleaning of the genitals can be particularly challenging” (2).

“Outside the AIDS belt, in the city of Abidjan, the capital of Ivory Cost, levels of HIV infection are as high as they are in some cities of the AIDS belt; we believe the epidemic in Abidjan is very likely sustained by immigrants who come from a surrounding area where the majority of men are uncircumcised” (2).

“Thus, we concluded that in the AIDS belt, lack of male circumcision in combination with risky sexual behavior, such as having multiple sex partners, engaging in sex with prostitutes and leaving chancroid untreated, has led to rampant HIV transmission. Unsafe sexual practices have certainly contributed to the spread of AIDS across Africa and indeed around the world” (2).

HIV researchers have gone further: “In sub-Saharan Africa, circumcision could be offered as a reinforcement of other protective measures” (2).

“These men are appearing at hospitals in sharply increasing numbers, requesting circumcision for themselves and often for their sons. Clinics that offer adult male circumcision as a protection against AIDS now advertise in Tanzanian newspapers” (2).

However, HIV researchers knew in advance that such measures would not be sufficient: “Although the epidemic in sub-Saharan Africa may subside somewhat, because of greater use of condoms and probably increased incidence of circumcision, Africans in the AIDS belt remain at extremely high risk of HIV infection” (2). These researchers are opening doors to pharmaceutical companies to bring to Africa the expensive “help” of the World Bank, to medicate with immunotoxic antiretrovirals HIV-positive Africans and those who are merely presumed to be positive (13).

The words of a professor of African History speak for themselves: “Racist assumptions about African sexuality merit scrutiny. Generalizations about African sexual practices are analytically useless but perpetuate racist stereotypes about insatiable sexual appetites and carnal exotica. Media misinterpretations of African sexuality and its alleged link to AIDS have spawned inordinate anxieties and pervasive despair in regions already afflicted with extreme poverty, ravaged by war, and deprived of primary health care delivery systems” and, he continues, “the political economy of underdevelopment and environmentally caused endemic sickness, not extraordinary sexual behavior or a sexually transmitted virus, are what’s killing Africans. The so-called AIDS epidemic has become the medicalization of poverty to justify Western medical intervention in the form of vaccine trials, drug testing, and evangelistic demands for behavior modification. AIDS scientists and public health planners must reconsider the role of malnutrition, poor sanitation, anemia, and parasitic and endemic infections for producing the clinical AIDS symptoms that are manifestations of non-HIV insults” (5).

Belief in HIV prevents the understanding that AIDS in Africa is occurring now because never before has poverty been so prevalent and intense as it is now in the African areas where AIDS is epidemic. The only rational way to stop the spread of the AIDS epidemic in the African continent is by finding solutions for the economic disparities that are rampant in Africa (14,15).

AIDS in Africa is not an epidemiologic paradigm. There exists a serious crisis in the scientific methodology; currently, the problem is that epidemiologic ignorance is pandemic. Let us go back to the teaching of epidemiology to find a solution to AIDS in Africa and elsewhere (16-41).

President Thabo Mbeki is absolutely correct when he demands a scientific answer to the question: “Why is HIV/AIDS in sub-Saharan Africa heterosexually transmitted while in the Western world it is said to be largely homosexually transmitted?”

I am certain that Africans will continue questioning and rejecting the ethnic fictions and racial slanders described here. They are already standing up to defend their integrity.


  1. Quinn TC, Mann JM, Curran JW, Piot P. AIDS in Africa: An Epidemiologic Paradigm. Science 1986; 234: 956-963.
  2. Caldwell JC, Caldwell P. The African AIDS Epidemic. In parts of sub-Saharan Africa, nearly 25 percent of the population is HIV-positive as a result of heterosexual transmission of the virus. Could lack of circumcision make men in this region particularly susceptible? Scientific American 1996; 274(3): 62-68.
  3. Geshekter CL. Rethinking AIDS in Africa. Reappraising AIDS 1995; 3(2): 1-4
  4. Geshekter CL. Outbreak? AIDS, Africa, and the Medicalization of Poverty. Is Africa facing a lethal pandemic? Transition 1995; 5(3): 5-14.
  5. Geshekter CL. AIDS, Underdevelopment, and Sexual Stereotypes: Rethinking AIDS in Africa. 39th Annual Meeting of the African Studies Association. San Francisco, California. November 23-26, 1996.
  6. Bethell T. Mbeki takes on the AIDS Industry. South African President queries epidemic, AZT. Reappraising AIDS 2000; 8(3): 1-4.
  7. Gordimer N. Africa’s Plague, and Everyone’s” The New York Times. April 11, 2000.
  8. Ankomah B. Are 26 millions Africans Dying of AIDS? “The biggest lie of the century” under fire. New African 1998; No. 369: 34-42.
  9. Bongaarts J, Reining P, Way P, Conant F. The Relationship Between Male Circumcision and HIV Infection in African Populations. AIDS 1989; 3(6): 373-377.
  10. Moses S et al. Geographical Patterns of Male Circumcision Practices in Africa: Association with HIV Seroprevalence. Internat J Epidemiol 1990; 19(3): 693-697.
  11. Orubuloye IO, Caldwell JC, Caldwell P, Santow G Editors. Sexual Networking and AIDS in Sub-Saharan Africa: Behavioural Research and the Social Context. Australian National University. 1994.
  12. Forum: The East African AIDS Epidemic and the Absence of Male Circumcision: What is the Link? Health Transition Review 1995; 5(1): 97-117.
  13. World Bank. Confronting AIDS: Public Priorities in a Global Epidemic. A World Bank Policy Research Report. New York: Oxford University Press; 1999: 365.
  14. Giraldo R. AIDS and Stressors: AIDS is not an infectious disease nor is sexually transmitted. It is a toxic-nutritional syndrome caused by the alarming worldwide increment of immunological stressor agents. Medellin, Colombia: Impresos Begon, 1997: 205.
  15. Giraldo R et al. Is it rational to treat or prevent AIDS with toxic antiretroviral drugs in pregnant women, infants, children, and anybody else? The answer is negative. Continuum (London) 1999; 5(6): 38-52.
  16. Abramson JH. Making Sense of Associations. Factors and Risk Markers. Causes and Effects. In: Making Sense of Data; A Self- Instruction Manual on the Interpretation of Epidemiological DATA. New York: Oxford University Press, 1988: 193-264, 219-228 and 265-316.
  17. Buck C, Llopis A, Najera E, et al. Etiologic Investigations. Studies in Epidemics. In: The Challenge of Epidemiology, Issues and Selected Readings. Pan American Health Organization, Scientific Publication No. 505. PAHO, Pan American Sanitary Bureau, Regional Office of the WHO. Washington DC, 1988: 147-166 and 415-482.
  18. Elwood JM. The Diagnosis of Causation. In: Causal Relationships in Medicine. A Practical System for Critical Appraisal. New York: Oxford University Press, 1988: 163-182.
  19. Elwood JM. The Importance of Causal Relationships in Medicine and Health Care. What is Causation? A Direct Test of Causation. In: Critical Appraisal of Epidemiological Studies and Clinical Trials. Oxford: Oxford University Press, 1998: 3-13.
  20. Fletcher RH, Fletcher SW, Wagner EH. Risk. Cause. In: Clinical Epidemiology: the Essentials. Baltimore: Williams and Wilkins, 1996: 94-110 and 228-248.
  21. Friedman GD. Making Sence out of Statistical Associations. In: Primer of Epidemiology. New York: McGraw-Hill, Inc., 1994: 194-224.
  22. Garb JL. Understanding Medical Research. A Practitioner’s Guide. Boston: Little, Brown and Company, 1996: 256.
  23. Gordis L. Estimating Risk: Is There an Association? From Association to Causation: Deriving Inferences From Epidemiologic Studies. More on Causal Inferences: Bias, Confounding, and Interactions. In: Epidemiology. Philadelphia: W.B. Saunders Company, 1996: 141-154, 167-182 and 183-195.
  24. Hutt MSR, Burkitt DP. Environment and the causes of disease. In: The Geography of Non-Infectious Disease. Oxford: Oxford University Press, 1986: 1-6.
  25. Jekel JF, Elmore JG, Katz DL. The Study of Causation in Epidemiologic Investigations and Reasearch. Assessment of Risk in Epidemiologic Studies. In: Epidemiology, Biostatistics and Preventive Medicine. Philadelphia: W.B. Saunders Company, 1996: 54-64 and 74-84.
  26. MacMahon B, Trichopoulos D. Concepts of Cause. In: Epidemiology Principles and Methods. Boston: Little Brown and Company, 1996: 19-30.
  27. Malenka DJ, Baron JA, Jhonson S, et al. The Framing Effect of Relative and Absolute Risk. J Gen Intern Med 1993; 8:543-548.
  28. McMaster University Health Services Centre, Department of Clinical Epidemiology and Biostatistics. How to Read Clinical Journals IV: To Determine Etiology or Causation. Can Med Assoc J 1981; 124:985-990.
  29. Rothman KJ. Causal Inference in Epidemiology. Multiple Analysis. Interactions Between Causes. Analysis with Multiple Levels of Exposure. In: Modern Epidemiology. Boston: Little Brown, 1986: 7-22, 285-310, 311-326 and 327-350.
  30. Rothman KJ, Greenland S. Causation and Causal Inference. In: Detels R et al. Oxford Textbook of Public Health. Third Edition. Volume 2; The Methods of Public Health. New York: Oxford University Press, 1997: 617-630.
  31. Rothman KJ, Greenland S. Causation and Causal Inference. In: Modern Epidemiology. Lippincott — Raven, 1998: 7-28.
  32. Schlesselman JJ. “Proof” of Cause and effect in Epidemiologic Studies: Criteria for Judments. Prev Med 1987; 16:195-210.
  33. Sheldon H. Causes of Disease. In: Boyd’s Introduction to the Study of Disease. Philadelphia: Lea & Febiger, 1992: 49-82.
  34. Soskolne CL, MacFarlane DK. Scientific Misconduct in Epidemiologic Research. In: Coughlin SS, Beauchamp TL. Ethics in Epidemiology. New York: Oxford University Press, 1996: 274-289.
  35. Stolley Pd, Lasky T. Epidemics and Science. In: Investigating Disease Patterns. The Science of Epidemiology. New York: Scientific American Library, 1995: 1-22.
  36. Streiner DL, Norman GR. Assessing Causation. In: PDQ Epidemiology. St. Louis: Mosby, 1996: 121-134.
  37. Susser M. Causal Thinking in the Health Sciences: Concepts and Strategies of Epidemiology. Oxford: Oxford University Pres, 1973: 181.
  38. Susser M. What is a Cause and How Do We Know One? A Grammar for Pragmatic Epidemiology. Amer J Epidemiol 1991; 133:635-648.
  39. Torrence ME. Causality. In: Understanding Epidemiology. St. Louis: Mosby, 1997: 133-151.
  40. Weed DL. On the Logic of Causal Inference. Am J Epidemiol 1986; 123: 965-979.
  41. Weiss NS. Natural History of Illness. In: Clinical Epidemiology: The Study of the Outcome of Illness.

Leave a Reply

Your email address will not be published. Required fields are marked *