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Attributable risk for diet, alcohol, and family history in the Melbourne colorectal cancer study Gabriel A. Kune a
a b
a
, Susan Bannerman & Lyndsey F. Watson
a
University of Melbourne , Melbourne, Australia
b
61 Erin St., Richmond, Victoria, 3121, Australia Published online: 04 Aug 2009.
To cite this article: Gabriel A. Kune , Susan Bannerman & Lyndsey F. Watson (1992) Attributable risk for diet, alcohol, and family history in the Melbourne colorectal cancer study, Nutrition and Cancer, 18:3, 231-235, DOI: 10.1080/01635589209514223 To link to this article: http://dx.doi.org/10.1080/01635589209514223
PLEASE SCROLL DOWN FOR ARTICLE Taylor & Francis makes every effort to ensure the accuracy of all the information (the “Content”) contained in the publications on our platform. However, Taylor & Francis, our agents, and our licensors make no representations or warranties whatsoever as to the accuracy, completeness, or suitability for any purpose of the Content. Any opinions and views expressed in this publication are the opinions and views of the authors, and are not the views of or endorsed by Taylor & Francis. The accuracy of the Content should not be relied upon and should be independently verified with primary sources of information. Taylor and Francis shall not be liable for any losses, actions, claims, proceedings, demands, costs, expenses, damages, and other liabilities whatsoever or howsoever caused arising directly or indirectly in connection with, in relation to or arising out of the use of the Content. This article may be used for research, teaching, and private study purposes. Any substantial or systematic reproduction, redistribution, reselling, loan, sub-licensing, systematic supply, or distribution in any form to anyone is expressly forbidden. Terms & Conditions of access and use can be found at http://www.tandfonline.com/page/termsand-conditions
Attributable Risk for Diet, Alcohol, and Family History in the Melbourne Colorectal Cancer Study Gabriel A. Kune, Susan Bannerman, and Lyndsey F. Watson
Downloaded by [University of Cambridge] at 09:26 18 December 2014
Abstract From the data obtained in a large comprehensive population-based case-control study of colorectal cancer (The Melbourne Colorectal Cancer Study), attributable risk was calculated for a family history of colorectal cancer in near relatives for diet (when >5 of the 11 previously determined dietary risk factors were present) and for beer consumption (for rectal cancer only). The attributable risk was 11% in the presence of a family history of colorectal cancer and 46% in the presence of five or more dietary risk factors. The attributable risk for rectal cancer in the presence of beer consumption was 31% in males and 11% in females. These data are relevant in the consideration of primary prevention of colorectal cancer in Australia, but their general application needs to be approached with caution in view of major differences in the genetic background and the dietary practices in various regions of the world and in view of the uncertainty of what is achievable change, especially for dietary practices. (Nutr Cancer 18, 231-235, 1992)
Introduction
Previous diet, alcohol consumption, and a family history of colorectal cancer have been the three most studied etiologic factors for large bowel cancer. The Melbourne Colorectal Cancer Study is a large comprehensive population-based investigation of colorectal cancer incidence, etiology, and survival conducted in Melbourne, Australia, and its dietary, alcohol, and family history findings have been published in detail (1-6). The purpose of this communication is to describe the risk attributable to each of these likely etiologic factors from the findings of the case-control part of the Melbourne study. Methods The proportion of cases attributed to the risk factor among all members of the target population has been known as population attributable risk (7) and also as attributable risk percent (8), etiologic fraction (9), attributable fraction (10), and excess fraction (11). We use the term attributable risk (AR) calculated by the formula from Levin (7): AR = P e (RRl)/[Pe(RR-l)f 1], where Pe is the proportion exposed in the target population and RR is the relative risk of the factor of interest. We use the relative risk estimate obtained from unconditional logistic regression (12), where it is a summary measure of risk, having adjusted for age and sex, the study design constraints. The 95% confidence intervals (13) are computed to be: l-(l-AR)exp(+1.96SE) and l-(l-AR)exp(-1.96SE), where SE is the standard error of the attributable risk calculated The authors are affiliated with the University of Melbourne, Melbourne, Australia.
Copyright © 1992, Lawrence Erlbaum Associates, Inc.
Downloaded by [University of Cambridge] at 09:26 18 December 2014
from the estimated standard errors of the proportion exposed in the population and the relative risk (or, more correctly, from the log relative risk estimated by logistic regression analysis) by use of variance transformation formulas. The proportion exposed is obtained from the control group, which is regarded to be a reasonable estimate of the target population, inasmuch as the Melbourne study was population based (1,14,15). The case-control part of The Melbourne Colorectal Cancer Study compared 715 histologically confirmed cases of colorectal adenocarcinoma with 727 age- and sex-matched community-based controls. All the respondents were residents of metropolitan Melbourne, which at the time of the study had a population of 2.81 million. Of the 1,150 cases in the population-based incidence study, 715 (62%) were included in the case-control study, and of the 1,024 eligible controls, 727 (71%) participated. The selection and exclusion criteria for both cases and controls, as well as the demographic characteristics of age, sex, country of birth, and religion of those excluded from the study compared with those included in the study, have been described in detail (1,6,14,15). However, on the basis of the analyses of the demographic characteristics of those selected versus those excluded, neither selection bias nor exclusion bias was significant in the Melbourne study (14). In the consideration of the causal pathway for colorectal carcinogenesis, it was assumed that a hereditary predisposition, as indicated by a family history of colorectal cancer in near relatives and previously found to be a highly statistically significant risk factor (p < 0.001) in the Melbourne study (6), needs to be considered first. Thus the attributable risk for a family history of colorectal cancer was calculated first. The family history' effect was previously found to be independent of the dietary and alcohol risk (6). Dietary factors in the Melbourne study were also found to be highly statistically significantly (p < 0.001) associated with colorectal cancer risk (1,5). These risk factors were a low intake of dietary fiber/vegetables, cruciferous vegetables, dietary vitamin C, pork, fish, "other meats" (as defined in the study), and vitamin supplements, low or high intake of milk drinks, and high intake of fat and beef (xj\ = 212, p < 0.001). For these dietary factors, a "risk score" had also been previously calculated (1), and in this score each dietary risk factor was arbitrarily given an equal weight. For the purpose of calculating the attributable risk, an arbitrary dichotomization of the cases and controls was made at the median score for controls. Thus a risk score >5 constituted a diet risk. The attributable risk for diet was calculated next, first individually and then also stratified by family history of colorectal cancer status. Beer drinking was found to be a statistically significant risk factor for rectal cancer in males (p = 0.01) and marginally significant in females (p = 0.06) in the Melbourne study (2). The attributable risk was calculated for rectal cancer, stratified by males and females and independently of the attributable risk for family history and diet. Results The data for calculating the attributable risk, expressed as a percentage of 1.00, is shown in Table 1. This indicates that, in The Melbourne Colorectal Cancer Study and as calculated by the method described above, the attributable risk is 11% in the presence of a family history of colorectal cancer in near relatives and 46% in the presence of any five or more of the previously described dietary risk factors; the attributable risk for rectal cancer with beer consumption is 31% in males and 11% in females (Table 1). The data also show that the attributable risk of diet is 51% in the presence of a positive family history of colorectal cancer in near relatives and 45% in the absence of a family history of colorectal cancer (Table 1). The dietary risk factors were also dichotomized at four or more dietary factors, and the attributable risk for diet was estimated at 68%. For brevity, these data are not shown in detail.
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Table 1. Attributable Risk of Diet, Alcohol, and Family History in The Melbourne Colorectal Cancer Study
Family history of colorectal cancer in near relatives Exposed Not exposed Diet* Exposed Not exposed Diet and family history Exposed Not exposed Diet and no family history Exposed Not exposed Beer consumption and rectal cancer in males Exposed Not exposed Beer consumption and rectal cancer in females Exposed Not exposed
Proportion Exposed in Target Population
Relative Risk
Attributable Risk as Fraction of 1.00"
Confidence Interval
95%
No. of Cases
No. of Controls
114 507
68 602
0.10
2.15
0.11 (11%)
0.03-0.18
462 253
265 462
0.36
3.35
0.46 (46%)
0.24-0.62
78 36
26 42
0.38
3.69
0.51 (51%)
0.00-0.85
320 187
216 386
0.36
3.24
0.45 (45%)
0.18-0.63
122 59
220 176
0.56
1.81
0.31 (31%)
0.00-0.54
28 107
52 276
0.16
1.74
0.11(11%)
0.00-0.25
a: Values in parentheses are percent. b: tS dietary risk factors.
Discussion
The concept that hereditary susceptibility, previous diet, and previous alcohol consumption are important predisposing causal factors in colorectal cancer is currently subject to considerable scientific debate regarding both the nature and the extent to which these factors play a role in the etiology of large bowel cancer. If the assumption is made for the purpose of this discussion that heredity, diet, and alcohol are etiologic factors, then the calculation of attributable risks is relevant in any considerations concerning the prevention of colorectal cancer, particularly for factors amenable to change, such as diet and alcohol consumption. The extent to which one can generalize from the data presented here is probably limited because of the several assumptions that have been made in arriving at the calculation of attributable risk. First, it was assumed that a family history of colorectal cancer in near relatives is an accurate index of a genetically determined predisposition to colorectal cancer, an assumption based on the finding that the family history effect in the Melbourne study was independent of both the dietary and alcohol risk (6). The attributable risk of 11% in the Melbourne study for the genetically determined component is similar to the 10% attributable risk for the North American populations estimated by Lynch and Lynch (16), but this value may be very different if applied to a region with a genetic pool that is substantially different from that of the United States or Australia, such as Japan or Africa. Second, giving an equal weighting to each dietary factor may not be valid, and for example, the risk associated with a low vegetable/fruit/fiber diet may be more important than that associated with a high fat/meat diet. In this regard also, certain dietary factors may be more generally applicable to one region of the world than to another. Furthermore the dichotomi-
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zation of the dietary risk factors at the median score for controls (at a risk score >5 dietary risk factors) may not be valid or, at least, may be too arbitrary. For example, when the dietary risk factors were dichotomized at four or more factors, the attributable risk rose to 68%. Third, there is some evidence from the Melbourne study and from other studies that the beer risk may not be universally applicable and that it may, in part, be dependent on certain as yet not clearly identified aspects of beer manufacture itself (2,17-19). Finally, age distribution of colorectal cancer in other populations may be different from that of the Melbourne study. Given the above reservations, it is clear that although the present attributable risks are likely to apply to Melbourne and the rest of Australia and possibly also to other cultures dominated by a European genetic pool and with so-called Western dietary and alcohol habits, such as the United States, the United Kingdom, and Europe, they may not be applicable to regions with vastly different genetic pools and dietary habits, such as Africa, Asia, or Japan. In countries such as Australia, New Zealand, the United Kingdom, or the United States, the risk attributable to genetic factors is likely to be in the vicinity of 10%, but because at present this risk is not modifiable, this value is of academic rather than practical interest. Although difficult to quantify precisely and with previous estimates of up to 70% (20), the attributable dietary risk for colorectal cancer in so-called Western countries is likely to be in the region of 50%. Thus, if previous diet is a causal predisposition for colorectal cancer, then large-scale dietary modification is likely to lead to a decrease in its incidence. At present, the extent of dietary modifications that may be achievable in Western cultures is not known. However, in the Melbourne study, the difference in attributable risk by modifying just one of the risk factors, such as fat or vegetable/fiber consumption, was 18% (from 68% to 46%). In this regard, the work of Wahrendorf (20) is of special interest, because he developed a measure of preventable proportions as an adjunct to the concept of attributable risk, particularly for exposures such as diet that occur on a continuous scale and are unlikely to disappear completely. Using this measure, he showed that with modest changes in diet, which are probably achievable, 15-20% of the excess incidence of colorectal cancer can be eliminated (20). This estimate is similar to the 18% arrived at in the Melbourne study for changes in just one dietary risk factor. Acknowledgements and Notes This work was generously supported by The Nicholas and Elizabeth Slezak Cancer Research Fund of the University of Melbourne (Melbourne, Australia). Address reprint requests to Dr. Gabriel A. Kune, 61 Erin St., Richmond, Victoria 3121, Australia. Submitted 3 November 1991; accepted in final form 26 May 1992.
References 1. Kune, S, Kune, GA, and Watson, LF. "Case-Control Study of Dietary Etiological Factors: The Melbourne Colorectal Cancer Study." Nutr Cancer 9, 21-42, 1987. 2. Kune, S, Kune, GA, and Watson, LF: "Case-Control Study of Alcoholic Beverages as Etiological Factors: The Melbourne Colorectal Cancer Study." Nutr Cancer 7, 43-56, 1987. 3. Kune, GA, Kune, S, and Watson, LF: "Dietary Sodium and Potassium Intake and Colorectal Cancer Risk." Nutr Cancer 12, 351-359, 1989. 4. Kune, GA, Kune, S, and Watson, LF: "Body Weight and Physical Activity as Predictors of Colorectal Cancer Risk." Nutr Cancer 13, 9-17, 1990. 5. Kune, G, Kune, S, Field, B, and Watson, LF: "The Nutritional Causes of Large Bowel Cancer. Data from the Melbourne Colorectal Cancer Study and a 25 Year World Literature Overview 1965-1989." In Nutrients and Cancer Prevention, KN Prasad and FL Myskens, Jr (eds). Clifton, NJ: Humana, 1990, pp 241-259. 6. Kune, GA, Kune, S, and Watson, LF: "The Role of Heredity in the Etiology of Large Bowel Cancer: Data From the Melbourne Colorectal Cancer Study." World J Surg 13, 124-131, 1989.
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7. Levin, ML: "The Occurrence of Lung Cancer in Man." Acta Union Int Contr Cancer 9, 531-541, 1953. 8. Cole, P, and MacMahon, B: "Attributable Risk Percent in Case-Control Studies." Br J Prev Soc Med 25, 242-244, 1971. 9. Miettinen, OS: "Proportion of Disease Caused or Prevented by a Given Exposure, Trait or Intervention." Am J Epidemiol 99, 325-332, 1974. 10. Greenland, S: "Bias in Methods for Deriving Standardised Morbidity Ratio and Attributable Fraction Estimates." Stat Med 3, 131-141, 1984. 11. Greenland, S, and Robins, JM: "Conceptual Problems in the Definition and Interpretation of Attributable Fractions." Am J Epidemiol 128, 1185-1197, 1988. 12. Baker, RJ, and Nelder, JA: The GLIM System. Release 3. Oxford, UK: Numerical Algorithm Group, 1978. 13. Walter, SD: "Distribution of Levin's Measure of Attributable Risk." Biometrika 62, 171-374, 1975. 14. Kune, GA, Kune, S, and Watson, LF: "Children, Age at First Birth and Colorectal Cancer Risk. Data From the Melbourne Colorectal Cancer Study." Am J Epidemiol 129, 533-542, 1989. 15. Kune, S: An Epidemiological Study of Colorectal Cancer. Ann Arbor, MI: University Microfilms, 1986, pp 1-407. 16. Lynch, PM, and Lynch, HT: Colon Cancer Genetics. New York: Van Nostrand, 1985. 17. Dean, G, MacLennan, R, McLaughlin, H, and Shelley, E: "The Causes of Death of Blue Collar Workers at a Dublin Brewery 1954-1974." Br J Cancer 40, 581-589, 1979. 18. Jensen, OM: "Cancer Morbidity and Causes of Death Among Danish Brewing Workers." Int J Cancer 23, 454-463, 1979. 19. Kune, GA, and Vitetta, L: "Alcohol Consumption and the Etiology of Colorectal Cancer. A Review of the Scientific Evidence for the 35 Years 1957-1991." Nutr Cancer 18, 97-111, 1992. 20. Wahrendorf, J: "An Estimate of the Proportion of Colorectal and Stomach Cancers Which Might Be Prevented by Certain Changes in Dietary Habits." Int J Cancer 40, 625-628, 1987.
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235
Nutrition and Cancer Publication details, including instructions for authors and subscription information: http://www.tandfonline.com/loi/hnuc20
Attributable risk for diet, alcohol, and family history in the Melbourne colorectal cancer study Gabriel A. Kune a
a b
a
, Susan Bannerman & Lyndsey F. Watson
a
University of Melbourne , Melbourne, Australia
b
61 Erin St., Richmond, Victoria, 3121, Australia Published online: 04 Aug 2009.
To cite this article: Gabriel A. Kune , Susan Bannerman & Lyndsey F. Watson (1992) Attributable risk for diet, alcohol, and family history in the Melbourne colorectal cancer study, Nutrition and Cancer, 18:3, 231-235, DOI: 10.1080/01635589209514223 To link to this article: http://dx.doi.org/10.1080/01635589209514223
PLEASE SCROLL DOWN FOR ARTICLE Taylor & Francis makes every effort to ensure the accuracy of all the information (the “Content”) contained in the publications on our platform. However, Taylor & Francis, our agents, and our licensors make no representations or warranties whatsoever as to the accuracy, completeness, or suitability for any purpose of the Content. Any opinions and views expressed in this publication are the opinions and views of the authors, and are not the views of or endorsed by Taylor & Francis. The accuracy of the Content should not be relied upon and should be independently verified with primary sources of information. Taylor and Francis shall not be liable for any losses, actions, claims, proceedings, demands, costs, expenses, damages, and other liabilities whatsoever or howsoever caused arising directly or indirectly in connection with, in relation to or arising out of the use of the Content. This article may be used for research, teaching, and private study purposes. Any substantial or systematic reproduction, redistribution, reselling, loan, sub-licensing, systematic supply, or distribution in any form to anyone is expressly forbidden. Terms & Conditions of access and use can be found at http://www.tandfonline.com/page/termsand-conditions
Attributable Risk for Diet, Alcohol, and Family History in the Melbourne Colorectal Cancer Study Gabriel A. Kune, Susan Bannerman, and Lyndsey F. Watson
Downloaded by [University of Cambridge] at 09:26 18 December 2014
Abstract From the data obtained in a large comprehensive population-based case-control study of colorectal cancer (The Melbourne Colorectal Cancer Study), attributable risk was calculated for a family history of colorectal cancer in near relatives for diet (when >5 of the 11 previously determined dietary risk factors were present) and for beer consumption (for rectal cancer only). The attributable risk was 11% in the presence of a family history of colorectal cancer and 46% in the presence of five or more dietary risk factors. The attributable risk for rectal cancer in the presence of beer consumption was 31% in males and 11% in females. These data are relevant in the consideration of primary prevention of colorectal cancer in Australia, but their general application needs to be approached with caution in view of major differences in the genetic background and the dietary practices in various regions of the world and in view of the uncertainty of what is achievable change, especially for dietary practices. (Nutr Cancer 18, 231-235, 1992)
Introduction
Previous diet, alcohol consumption, and a family history of colorectal cancer have been the three most studied etiologic factors for large bowel cancer. The Melbourne Colorectal Cancer Study is a large comprehensive population-based investigation of colorectal cancer incidence, etiology, and survival conducted in Melbourne, Australia, and its dietary, alcohol, and family history findings have been published in detail (1-6). The purpose of this communication is to describe the risk attributable to each of these likely etiologic factors from the findings of the case-control part of the Melbourne study. Methods The proportion of cases attributed to the risk factor among all members of the target population has been known as population attributable risk (7) and also as attributable risk percent (8), etiologic fraction (9), attributable fraction (10), and excess fraction (11). We use the term attributable risk (AR) calculated by the formula from Levin (7): AR = P e (RRl)/[Pe(RR-l)f 1], where Pe is the proportion exposed in the target population and RR is the relative risk of the factor of interest. We use the relative risk estimate obtained from unconditional logistic regression (12), where it is a summary measure of risk, having adjusted for age and sex, the study design constraints. The 95% confidence intervals (13) are computed to be: l-(l-AR)exp(+1.96SE) and l-(l-AR)exp(-1.96SE), where SE is the standard error of the attributable risk calculated The authors are affiliated with the University of Melbourne, Melbourne, Australia.
Copyright © 1992, Lawrence Erlbaum Associates, Inc.
Downloaded by [University of Cambridge] at 09:26 18 December 2014
from the estimated standard errors of the proportion exposed in the population and the relative risk (or, more correctly, from the log relative risk estimated by logistic regression analysis) by use of variance transformation formulas. The proportion exposed is obtained from the control group, which is regarded to be a reasonable estimate of the target population, inasmuch as the Melbourne study was population based (1,14,15). The case-control part of The Melbourne Colorectal Cancer Study compared 715 histologically confirmed cases of colorectal adenocarcinoma with 727 age- and sex-matched community-based controls. All the respondents were residents of metropolitan Melbourne, which at the time of the study had a population of 2.81 million. Of the 1,150 cases in the population-based incidence study, 715 (62%) were included in the case-control study, and of the 1,024 eligible controls, 727 (71%) participated. The selection and exclusion criteria for both cases and controls, as well as the demographic characteristics of age, sex, country of birth, and religion of those excluded from the study compared with those included in the study, have been described in detail (1,6,14,15). However, on the basis of the analyses of the demographic characteristics of those selected versus those excluded, neither selection bias nor exclusion bias was significant in the Melbourne study (14). In the consideration of the causal pathway for colorectal carcinogenesis, it was assumed that a hereditary predisposition, as indicated by a family history of colorectal cancer in near relatives and previously found to be a highly statistically significant risk factor (p < 0.001) in the Melbourne study (6), needs to be considered first. Thus the attributable risk for a family history of colorectal cancer was calculated first. The family history' effect was previously found to be independent of the dietary and alcohol risk (6). Dietary factors in the Melbourne study were also found to be highly statistically significantly (p < 0.001) associated with colorectal cancer risk (1,5). These risk factors were a low intake of dietary fiber/vegetables, cruciferous vegetables, dietary vitamin C, pork, fish, "other meats" (as defined in the study), and vitamin supplements, low or high intake of milk drinks, and high intake of fat and beef (xj\ = 212, p < 0.001). For these dietary factors, a "risk score" had also been previously calculated (1), and in this score each dietary risk factor was arbitrarily given an equal weight. For the purpose of calculating the attributable risk, an arbitrary dichotomization of the cases and controls was made at the median score for controls. Thus a risk score >5 constituted a diet risk. The attributable risk for diet was calculated next, first individually and then also stratified by family history of colorectal cancer status. Beer drinking was found to be a statistically significant risk factor for rectal cancer in males (p = 0.01) and marginally significant in females (p = 0.06) in the Melbourne study (2). The attributable risk was calculated for rectal cancer, stratified by males and females and independently of the attributable risk for family history and diet. Results The data for calculating the attributable risk, expressed as a percentage of 1.00, is shown in Table 1. This indicates that, in The Melbourne Colorectal Cancer Study and as calculated by the method described above, the attributable risk is 11% in the presence of a family history of colorectal cancer in near relatives and 46% in the presence of any five or more of the previously described dietary risk factors; the attributable risk for rectal cancer with beer consumption is 31% in males and 11% in females (Table 1). The data also show that the attributable risk of diet is 51% in the presence of a positive family history of colorectal cancer in near relatives and 45% in the absence of a family history of colorectal cancer (Table 1). The dietary risk factors were also dichotomized at four or more dietary factors, and the attributable risk for diet was estimated at 68%. For brevity, these data are not shown in detail.
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Table 1. Attributable Risk of Diet, Alcohol, and Family History in The Melbourne Colorectal Cancer Study
Family history of colorectal cancer in near relatives Exposed Not exposed Diet* Exposed Not exposed Diet and family history Exposed Not exposed Diet and no family history Exposed Not exposed Beer consumption and rectal cancer in males Exposed Not exposed Beer consumption and rectal cancer in females Exposed Not exposed
Proportion Exposed in Target Population
Relative Risk
Attributable Risk as Fraction of 1.00"
Confidence Interval
95%
No. of Cases
No. of Controls
114 507
68 602
0.10
2.15
0.11 (11%)
0.03-0.18
462 253
265 462
0.36
3.35
0.46 (46%)
0.24-0.62
78 36
26 42
0.38
3.69
0.51 (51%)
0.00-0.85
320 187
216 386
0.36
3.24
0.45 (45%)
0.18-0.63
122 59
220 176
0.56
1.81
0.31 (31%)
0.00-0.54
28 107
52 276
0.16
1.74
0.11(11%)
0.00-0.25
a: Values in parentheses are percent. b: tS dietary risk factors.
Discussion
The concept that hereditary susceptibility, previous diet, and previous alcohol consumption are important predisposing causal factors in colorectal cancer is currently subject to considerable scientific debate regarding both the nature and the extent to which these factors play a role in the etiology of large bowel cancer. If the assumption is made for the purpose of this discussion that heredity, diet, and alcohol are etiologic factors, then the calculation of attributable risks is relevant in any considerations concerning the prevention of colorectal cancer, particularly for factors amenable to change, such as diet and alcohol consumption. The extent to which one can generalize from the data presented here is probably limited because of the several assumptions that have been made in arriving at the calculation of attributable risk. First, it was assumed that a family history of colorectal cancer in near relatives is an accurate index of a genetically determined predisposition to colorectal cancer, an assumption based on the finding that the family history effect in the Melbourne study was independent of both the dietary and alcohol risk (6). The attributable risk of 11% in the Melbourne study for the genetically determined component is similar to the 10% attributable risk for the North American populations estimated by Lynch and Lynch (16), but this value may be very different if applied to a region with a genetic pool that is substantially different from that of the United States or Australia, such as Japan or Africa. Second, giving an equal weighting to each dietary factor may not be valid, and for example, the risk associated with a low vegetable/fruit/fiber diet may be more important than that associated with a high fat/meat diet. In this regard also, certain dietary factors may be more generally applicable to one region of the world than to another. Furthermore the dichotomi-
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zation of the dietary risk factors at the median score for controls (at a risk score >5 dietary risk factors) may not be valid or, at least, may be too arbitrary. For example, when the dietary risk factors were dichotomized at four or more factors, the attributable risk rose to 68%. Third, there is some evidence from the Melbourne study and from other studies that the beer risk may not be universally applicable and that it may, in part, be dependent on certain as yet not clearly identified aspects of beer manufacture itself (2,17-19). Finally, age distribution of colorectal cancer in other populations may be different from that of the Melbourne study. Given the above reservations, it is clear that although the present attributable risks are likely to apply to Melbourne and the rest of Australia and possibly also to other cultures dominated by a European genetic pool and with so-called Western dietary and alcohol habits, such as the United States, the United Kingdom, and Europe, they may not be applicable to regions with vastly different genetic pools and dietary habits, such as Africa, Asia, or Japan. In countries such as Australia, New Zealand, the United Kingdom, or the United States, the risk attributable to genetic factors is likely to be in the vicinity of 10%, but because at present this risk is not modifiable, this value is of academic rather than practical interest. Although difficult to quantify precisely and with previous estimates of up to 70% (20), the attributable dietary risk for colorectal cancer in so-called Western countries is likely to be in the region of 50%. Thus, if previous diet is a causal predisposition for colorectal cancer, then large-scale dietary modification is likely to lead to a decrease in its incidence. At present, the extent of dietary modifications that may be achievable in Western cultures is not known. However, in the Melbourne study, the difference in attributable risk by modifying just one of the risk factors, such as fat or vegetable/fiber consumption, was 18% (from 68% to 46%). In this regard, the work of Wahrendorf (20) is of special interest, because he developed a measure of preventable proportions as an adjunct to the concept of attributable risk, particularly for exposures such as diet that occur on a continuous scale and are unlikely to disappear completely. Using this measure, he showed that with modest changes in diet, which are probably achievable, 15-20% of the excess incidence of colorectal cancer can be eliminated (20). This estimate is similar to the 18% arrived at in the Melbourne study for changes in just one dietary risk factor. Acknowledgements and Notes This work was generously supported by The Nicholas and Elizabeth Slezak Cancer Research Fund of the University of Melbourne (Melbourne, Australia). Address reprint requests to Dr. Gabriel A. Kune, 61 Erin St., Richmond, Victoria 3121, Australia. Submitted 3 November 1991; accepted in final form 26 May 1992.
References 1. Kune, S, Kune, GA, and Watson, LF. "Case-Control Study of Dietary Etiological Factors: The Melbourne Colorectal Cancer Study." Nutr Cancer 9, 21-42, 1987. 2. Kune, S, Kune, GA, and Watson, LF: "Case-Control Study of Alcoholic Beverages as Etiological Factors: The Melbourne Colorectal Cancer Study." Nutr Cancer 7, 43-56, 1987. 3. Kune, GA, Kune, S, and Watson, LF: "Dietary Sodium and Potassium Intake and Colorectal Cancer Risk." Nutr Cancer 12, 351-359, 1989. 4. Kune, GA, Kune, S, and Watson, LF: "Body Weight and Physical Activity as Predictors of Colorectal Cancer Risk." Nutr Cancer 13, 9-17, 1990. 5. Kune, G, Kune, S, Field, B, and Watson, LF: "The Nutritional Causes of Large Bowel Cancer. Data from the Melbourne Colorectal Cancer Study and a 25 Year World Literature Overview 1965-1989." In Nutrients and Cancer Prevention, KN Prasad and FL Myskens, Jr (eds). Clifton, NJ: Humana, 1990, pp 241-259. 6. Kune, GA, Kune, S, and Watson, LF: "The Role of Heredity in the Etiology of Large Bowel Cancer: Data From the Melbourne Colorectal Cancer Study." World J Surg 13, 124-131, 1989.
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