LETTERS TO THE EDITOR
15 Mickulecky’ M, Tuomilehto J. The worldwide incidence rates of
childhood IDDM in WHO Diamond project related to the geographic latitude? Chronobiology & its roots in the cosmos. In: Mickulecky’ M Sr (ed.). Proceedings 3rd International Workshop 2–6 September 1979. Bratislava, pp. 1–3. 16 Jongbloet PH. The effects of preovulatory overripeness of human eggs on development. In: Blandau RJ (ed.). Aging Gametes. Their Biology and Pathology. International Symposium, Seattle 1973. Basel: Karger, 1975, pp. 300–29. 17 Jongbloet PH. Seasonal fluctuation of pathological and optimum conceptions, maternal subfecundity, gender dimorphism and survival. Coll Anthropol 1992;16:99–107. 18 Hurni H. Daylength and breeding in the domestic cat. Labor Anim 1981;15:229–33.
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19 Van Horn RN. Seasonal reproductive patterns in primates. Prog Reprod
Biol 1980;5:181–221. 20 Roenneberg T, Aschoff J. Annual rhythm of human reproduction: II
Environmental correlations. J Biol Rhythms 1990;5:271–39. 21 James WH. Seasonal variation in human births. J Biosoc 1990;22:
113–19. 22 Butcher RL. Experimentally induced gametopathies. In: Iffy L,
Kaminetzky HA (eds). Principles and Practice of Obstetrics and Perinatology. New York: J Wiley & Sons 1981, pp. 339–49. 23 Mikamo K. Intrafollicular overripeness and teratologic development. Cytogenetics 1968;7:223–31. 24 Bomsel-Helmreich O, Papiernik-Berkhauer E. Delayed ovulation and monozygotic twinning. Acta Genet Med Gemellol 1976;25:73–76. DOI: 10.1093/ije/dyg242
Can dietary fatty acids affect colon cancer risk? Reply to Leitzmann and Giovannucci From ANDRE NKONDJOCK,1,4 BRYNA SHATENSTEIN,2 PATRICK MAISONNEUVE3 and PARVIZ GHADIRIAN4 Sirs—In their commentary entitled ‘Can dietary fatty acids affect colon cancer risk?’1 Drs Leitzmann and Giovannucci have critically evaluated our recently published paper on the association between specific fatty acids and the risk of colorectal cancer,2 and raised some important points. They have clearly justified that diet is not the only source of many fatty acids, so that isolating diet-related fatty acid effects on colon cancer is complex. We agree. In fact, very few nutrients are provided exclusively by diet. Some essential nutrients are synthesized endogenously to a certain extent, in addition to being consumed in foods or supplements. Drs Leitzmann and Giovannucci have suggested that other factors in dairy products, such as calcium, rather than medium chain fatty acids may have accounted for the inverse associations observed between these fatty acids and colorectal cancer risk. Based on our study, the main sources of medium chain fatty acids among French-Canadians were dairy products, and there is evidence that dietary calcium intake is associated with reduced colorectal cancer risk. It has been hypothesized that the protective effect of calcium could be due to the formation of calcium soaps in the colon, which neutralize the bowelirritating effect of bile acids and fatty acids.3 It is indeed possible that calcium may have contributed to this effect since a significant inverse association of dietary calcium with colon carcinoma, with approximately 30% risk reduction, was found in this population.4 Another point made by Drs Leitzmann and Giovannucci was that the increased colorectal cancer risk associated with arachidonic acid, which we observed in our study, may have reflected a correlated component of meat intake. There is strong evidence that high consumption of red meat, especially when well
done and highly cooked, increases the risk of colorectal cancer, particularly in individuals who also smoke and are genetically susceptible.5 We disagree with their hypothesis, however, since in our study we found that the main arachidonic acid sources were poultry products (white meat), which have not been consistently associated with an increase in colorectal cancer risk. Drs Leitzmann and Giovannucci have also suggested an alternative explanation for the gender-specific variations observed in our study. Since a higher proportion of ever smokers were likely to be male, they proposed that smoking-related colon cancers among men might have diluted the relative risks associated with specific fatty acid intakes—if these cancers develop through a pathway different from that of fatty acid intake. We addressed this point by adjusting for smoking, which did not substantially change our findings. In addition, we investigated the effect modification by smoking status in both genders. We noted important changes in females, while our findings were unaltered in males, ruling out their proposition. For example, alpha-linolenic acid was associated with a 22% reduction in colorectal cancer risk. Among women who never smoked, this inverse association became stronger and the trend was highly significant (OR = 0.31; 95% CI: 0.13, 0.77; P = 0.002), while no association was observed among those who ever smoked (OR = 1.45; 95% CI: 0.69, 3.04; P = 0.486). Finally, underlying mechanisms regarding the possible role of specific fatty acids in the aetiology of colorectal cancer have been proposed,6 so that the hypothesis generated by our data, and stressed by Drs Leitzmann and Giovannucci, that dietrelated individual fatty acids could affect colorectal cancer is promising and deserves further evaluation.
1 McLaughlin Centre for Population Health Risk Assessment, Institute of
References
Population Health, University of Ottawa, Ottawa, ON, Canada. 2 Centre de Recherche, Institut Universitaire de Gériatrie de Montréal,
Montreal, QC, Canada. 3 Division of Epidemiology and Biostatistics, European Institute of Oncology,
Milan, Italy. 4 Epidemiology Research Unit, Research Centre, CHUM-Hôtel-Dieu,
Montreal, QC, Canada. E-mail:
[email protected]
1 Leitzmann MF, Giovannucci EL. Commentary: can dietary fatty acids
affect colon cancer risk? Int J Epidemiol 2003;32:209–10. 2 Nkondjock A, Shatenstein B, Maisonneuve P, Ghadirian P. Assessment
of risk associated with specific fatty acids and colorectal cancer among French-Canadians in Montreal: a case-control study. Int J Epidemiol 2003;32:200–09.
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3 Newmark HL, Wargowich MJ, Bruce WR. Colon cancer and dietary
6 Nkondjock A, Shatenstein B, Maisonneuve P, Ghadirian P. Specific
fat, phosphate, and calcium: a hypothesis. J Natl Cancer Inst 1984;74: 1323–25.
fatty acid and human colorectal cancer: an overview. Cancer Detect Prev 2003;27:55–66.
4 Ghadirian P, Lacroix A, Maisonneuve P et al. Nutritional factors and
DOI: 10.1093/ije/dyg268
colon carcinoma. A case control study involving French Canadians in Montreal, Quebec, Canada. Cancer 1997;80:858–64. 5 Le Marchand L, Hankin JH, Pierce LM et al. Well-done red meat,
metabolic phenotypes and colorectal cancer in Hawaii. Mut Res 2002; 506–507:205–14.
Epidemiologists: clinging to coat-tails or donning them? From BEN A LOPMAN1 and CLARENCE C TAM1,2 Sirs—In 2002, the US Department of Health and Human Services and the National Institutes of Health disbursed a combined $2.75 billion for biopreparedness and biodefence research.1,2 Investments in epidemiology, particularly for improving pathogen detection and incident response, are already underway. This recent focus on biodefence, however, is not universally welcome. According to Ezra and Mervyn Susser,3 a three-way division is emerging among epidemiologists: those favouring prioritization of biodefence, those who feel that it will divert attention, resources, and expertise from immediate public health problems, and those who suggest pragmatically that such investment can create a ‘coat-tail effect’, eventually benefiting all through improvement of disease surveillance infrastructures. Taking the latter view, the Sussers argue that epidemiologists can contribute to defence against terrorism and call for an open discussion on the role of epidemiologists in the aftermath of 11 September 2001. Their question, ‘what’s an epidemiologist to do?’ is well-pointed, since it implies that epidemiologists themselves can, or at least should, steer the discourse about their collective future. In the short term, epidemiologists may have a limited say in the matter. Prioritization of biopreparedness is, after all, what the public and politicians want. We should, however, consider what this could mean, both now and in the future. And to do this, where better to start from than the past. The uneasy alliance between public health and national defence stems from the state’s need to protect its population, trade, and colonial interests from infectious disease. In this sense, the current situation is not unique. Public health campaigns were crucial in establishing European colonial power in Africa and Asia, Japanese occupation in Taiwan, and American supremacy in Central America,4–6 while governments’ ability during the mid-20th century to simultaneously slash local public health budgets and fund research into potentially weaponizable agents has been linked to a national security-public health alliance that exploited irrational Cold War fears.7 Such activities have left indelible marks in geopolitical and cultural terms, yet
1 Gastrointestinal Diseases Division, Health Protection Agency Communic-
able Disease Surveillance Centre, London, UK. 2 Infectious Disease Epidemiology Unit, Department of Infectious & Tropical
Diseases, London School of Hygiene & Tropical Medicine, London, UK. Correspondence: Ben A Lopman, Gastrointestinal Diseases Division, Health Protection Agency Communicable Disease Surveillance Centre, London NW9 5EQ, UK. E-mail:
[email protected]
their adverse effects remain largely unspoken and are limited primarily to their justification in terms of successful reductions in disease incidence. The argument for the coat-tail effect is based on the premise that the ends justify the means. The real questions, however, are what are the ends and who defines them. Claiming immediate public health successes while ignoring long-term societal impacts is short-sighted and naïve. Returning to the present, the threat of terrorism, although not new, has not previously received much attention from epidemiologists. Franklin White’s call for an epidemiology of terrorism8 is thus interesting and worth exploring. However, a number of problems would confront an epidemiological approach to terrorism including, most basically, its definition. The US Army definition: ‘violence and the threat of violence exercised for political effect’,9 is valid yet very broad. Studying the causes and health impacts of all such violence would be a massive undertaking for epidemiologists, requiring the development of methods and causal frameworks deeply rooted in social theory and the expansion of epidemiology into political analysis. Epidemiology currently lacks such expertise. Furthermore, epidemiologists would have to accept responsibility for what to do with the findings of such enquiry, particularly when it becomes uncomfortable for the national security complex to which we are drawing ever closer. Most crucially, if we truly believe that the threat from terrorism is greater now than previously, and that we as epidemiologists can contribute towards its prevention, then our response must be global and multilateral. Anything else risks further dividing epidemiology along political lines that run counter to our public health interests. In an age of increasingly global health initiatives, our state-centred view of biodefence is incompatible with the ideal of ‘health for all’.10,11 The billions being spent by industrialized nations on national defence will not directly benefit those in other countries whose individuals experience the threat of infectious disease and violence on a daily basis, many of whom are at no lesser risk of terrorist acts. And now to the future. The Global Fund to fight AIDS, tuberculosis, and malaria is widely regarded as the most significant international health collaboration to date. It also provides a prime example of the national security–public health nexus. The resulting surge in human immunodeficiency virus (HIV)/ AIDS funding is unarguably a good thing for those affected by the pandemic and the motives behind the fund are now largely moot. Their consequences for epidemiologists, however, are
