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Re: Insulin Resistance and Prostate Cancer Risk

Re: Insulin Resistance and Prostate Cancer Risk In three papers from the same case–control series recruited from Shanghai, China, Hsing et al. (1–3) have reported statistically significant associations between prostate cancer risk and aspects of insulin resistance syndrome. First, they observed an increase in prostate cancer risk associated with abdominal obesity, measured by waist-to-hip ratio (odds ratio [OR] = 2.71 for highest versus lowest quartile) (1). Subsequently, they reported an OR of 2.80 for highest versus lowest tertile of insulin (2), and they reported an OR of 2.78 for highest versus lowest tertile of an index of insulin resistance, calculated from fasting insulin and blood glucose levels in a homeostasis model (HOMA IR) (3). Equivalent results, but in the opposite direction, were found for an index of insulin sensitivity, instead of insulin resistance, calculated as “QUICKI.” Hsing et al. pointed out the need for prospective studies on insulin resistance syndrome and prostate cancer risk. Prompted by the work of Hsing et al. (1–3), we re-analyzed our data from The Northern Sweden Health and Disease Cohort, in which prostate cancer risk was not associated with body mass index (BMI) or insulin in blood samples collected, on average, 4 years before cancer diagnosis (4). We then calculated the ORs for indices of insulin resistance (HOMA IR) and insulin sensitivity (QUICKI), and we found no association between these indices or insulin levels and prostate cancer risk (Table 1). Given the strong correlation between insulin and HOMA IR (Spearman coefficient of correlation, r = .95) and between insulin and QUICKI (r = −.95) in our study, it is not surprising that all three measures resulted in very similar risk estimates. The Chinese study subjects in the studies by Hsing et al. (1–3) had a substantially lower mean BMI than the Swedish study subjects (21 kg/m2 versus 26 kg/m2), were older at recruitment (71 years versus 59 years), and were more frequently smokers (60% versus 20%). The Chinese case subjects had a much higher percentage of nonlocalized disease (64% versus 11%) and high-grade tumors (37% versus 13%) than the Swedish case subjects. The distribution of BMI and tumor stage and grade in the Swedish study group was similar to that in cohorts from Europe and the United States (5,6). Possibly, prostate cancer risk is associated with insulin only at the lower end of the scale of insulin resistance and BMI, but not at levels common in subjects from Europe and the United States. BMI, a strong determinant of insulin resistance, has not been strongly associated with prostate cancer risk in Western populations (7). Alternatively, aggressive disease, which was more common in the Chinese study, may have a stronger association with hormonal changes than less aggressive disease. To what extent the results from the Chinese study subjects can be extrapolated to men in Western countries, or may explain the higher incidence rates in the West, remains to be elucidated. Table 1. Associations between prostate cancer risk and plasma insulin, indices of insulin resistance (HOMA IR), and insulin sensitivity (QUICKI) in a case–control study of 135 Swedish men   Tertile*  Ptrend    1  2  3  Categories  Continuous  *Odds ratios and 95% confidence intervals in an analysis of 135 matched case–control subjects were determined by conditional logistic regression with available measurements of insulin and glucose (4).  †HOMA-IR index = homeostasis assessment model of insulin resistance; (I0 [μU/mL] × G0 [mmol/L])/22.5, where I0 = fasting insulin measured in plasma by an immunoradiometric assay (Immunotech, Marseille, France) and G0 = fasting glucose by the hexokinase method (Boehringer Mannheim, Mannheim, Germany) (3,4).  ‡QUICKI = quantitative insulin sensitivity check index: 1/(log I0 [μU/mL] + log G0 [mmol/L]). Adjustment for fasting, body mass index, and smoking did not essentially alter the odds ratios. Fasting times were greater than 8 hours for 63% of the subjects and 4–8 hours for 37%; smoking was coded as current smoker, past smoker, and never smoker.  Insulin  1.00 (referent)  1.12 (0.67 to 1.88)  0.91 (0.55 to 1.50)  .59  .71      No. of case patients/No. of control subjects  46/82  46/85  43/92          Mean (μU/mL)  3.28  5.76  13.49      HOMA IR†  1.00 (referent)  1.26 (0.74 to 2.13)  0.81 (0.49 to 1.34)  .22  .38      No. of case patients/No. of control subjects  46/89  49/85  40/100          Mean  0.748  1.39  3.59      QUICKI‡  1.00 (referent)  1.46 (0.86 to 2.47)  1.12 (0.68 to 1.86)  .75  .62      No. of case patients/No. of control subjects  40/94  49/86  46/94          Mean  0.24  0.29  0.37        Tertile*  Ptrend    1  2  3  Categories  Continuous  *Odds ratios and 95% confidence intervals in an analysis of 135 matched case–control subjects were determined by conditional logistic regression with available measurements of insulin and glucose (4).  †HOMA-IR index = homeostasis assessment model of insulin resistance; (I0 [μU/mL] × G0 [mmol/L])/22.5, where I0 = fasting insulin measured in plasma by an immunoradiometric assay (Immunotech, Marseille, France) and G0 = fasting glucose by the hexokinase method (Boehringer Mannheim, Mannheim, Germany) (3,4).  ‡QUICKI = quantitative insulin sensitivity check index: 1/(log I0 [μU/mL] + log G0 [mmol/L]). Adjustment for fasting, body mass index, and smoking did not essentially alter the odds ratios. Fasting times were greater than 8 hours for 63% of the subjects and 4–8 hours for 37%; smoking was coded as current smoker, past smoker, and never smoker.  Insulin  1.00 (referent)  1.12 (0.67 to 1.88)  0.91 (0.55 to 1.50)  .59  .71      No. of case patients/No. of control subjects  46/82  46/85  43/92          Mean (μU/mL)  3.28  5.76  13.49      HOMA IR†  1.00 (referent)  1.26 (0.74 to 2.13)  0.81 (0.49 to 1.34)  .22  .38      No. of case patients/No. of control subjects  46/89  49/85  40/100          Mean  0.748  1.39  3.59      QUICKI‡  1.00 (referent)  1.46 (0.86 to 2.47)  1.12 (0.68 to 1.86)  .75  .62      No. of case patients/No. of control subjects  40/94  49/86  46/94          Mean  0.24  0.29  0.37      View Large References 1 Hsing AW, Deng J, Sesterhenn IA, Mostofi FK, Stanczyk FZ, Benichou J, et al. Body size and prostate cancer: a population-based case-control study in China. Cancer Epidemiol Biomarkers Prev  2000; 9: 1335–41. Google Scholar 2 Hsing AW, Chua S Jr, Gao YT, Gentzschein E, Chang L, Deng J, et al. Prostate cancer risk and serum levels of insulin and leptin: a population-based study. J Natl Cancer Inst  2001; 93: 783–9. Google Scholar 3 Hsing AW, Gao YT, Chua S Jr, Deng J, Stanczyk FZ. Insulin resistance and prostate cancer risk. J Natl Cancer Inst  2003; 95: 67–71. Google Scholar 4 Stattin P, Bylund A, Rinaldi S, Biessy C, Dechaud H, Stenman UH, et al. Plasma insulin-like growth factor-I, insulin-like growth factor-binding proteins, and prostate cancer risk: a prospective study. J Natl Cancer Inst  2000; 92: 1910–7. Google Scholar 5 Dennis LK, Resnick MI. Analysis of recent trends in prostate cancer incidence and mortality. Prostate  2000; 42: 247–52. Google Scholar 6 Online data for BMI in populations in the World Health Organization’s Monitoring Trends in Cardiovascular Diseases (MONICA) Project. Available at: www.ktl.fi/publications/monica. [Last accessed May 27, 2003.] Google Scholar 7 Kaaks R, Lukanova A, Sommersberg B. Plasma androgens, IGF-I, body size and prostate cancer risk: a synthetic review. Prostate Cancer Prostatic Dis  2000; 3: 157–72. Google Scholar © Oxford University Press http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png JNCI: Journal of the National Cancer Institute Oxford University Press

Re: Insulin Resistance and Prostate Cancer Risk

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Publisher
Oxford University Press
Copyright
© Oxford University Press
ISSN
0027-8874
eISSN
1460-2105
DOI
10.1093/jnci/95.14.1086
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Abstract

In three papers from the same case–control series recruited from Shanghai, China, Hsing et al. (1–3) have reported statistically significant associations between prostate cancer risk and aspects of insulin resistance syndrome. First, they observed an increase in prostate cancer risk associated with abdominal obesity, measured by waist-to-hip ratio (odds ratio [OR] = 2.71 for highest versus lowest quartile) (1). Subsequently, they reported an OR of 2.80 for highest versus lowest tertile of insulin (2), and they reported an OR of 2.78 for highest versus lowest tertile of an index of insulin resistance, calculated from fasting insulin and blood glucose levels in a homeostasis model (HOMA IR) (3). Equivalent results, but in the opposite direction, were found for an index of insulin sensitivity, instead of insulin resistance, calculated as “QUICKI.” Hsing et al. pointed out the need for prospective studies on insulin resistance syndrome and prostate cancer risk. Prompted by the work of Hsing et al. (1–3), we re-analyzed our data from The Northern Sweden Health and Disease Cohort, in which prostate cancer risk was not associated with body mass index (BMI) or insulin in blood samples collected, on average, 4 years before cancer diagnosis (4). We then calculated the ORs for indices of insulin resistance (HOMA IR) and insulin sensitivity (QUICKI), and we found no association between these indices or insulin levels and prostate cancer risk (Table 1). Given the strong correlation between insulin and HOMA IR (Spearman coefficient of correlation, r = .95) and between insulin and QUICKI (r = −.95) in our study, it is not surprising that all three measures resulted in very similar risk estimates. The Chinese study subjects in the studies by Hsing et al. (1–3) had a substantially lower mean BMI than the Swedish study subjects (21 kg/m2 versus 26 kg/m2), were older at recruitment (71 years versus 59 years), and were more frequently smokers (60% versus 20%). The Chinese case subjects had a much higher percentage of nonlocalized disease (64% versus 11%) and high-grade tumors (37% versus 13%) than the Swedish case subjects. The distribution of BMI and tumor stage and grade in the Swedish study group was similar to that in cohorts from Europe and the United States (5,6). Possibly, prostate cancer risk is associated with insulin only at the lower end of the scale of insulin resistance and BMI, but not at levels common in subjects from Europe and the United States. BMI, a strong determinant of insulin resistance, has not been strongly associated with prostate cancer risk in Western populations (7). Alternatively, aggressive disease, which was more common in the Chinese study, may have a stronger association with hormonal changes than less aggressive disease. To what extent the results from the Chinese study subjects can be extrapolated to men in Western countries, or may explain the higher incidence rates in the West, remains to be elucidated. Table 1. Associations between prostate cancer risk and plasma insulin, indices of insulin resistance (HOMA IR), and insulin sensitivity (QUICKI) in a case–control study of 135 Swedish men   Tertile*  Ptrend    1  2  3  Categories  Continuous  *Odds ratios and 95% confidence intervals in an analysis of 135 matched case–control subjects were determined by conditional logistic regression with available measurements of insulin and glucose (4).  †HOMA-IR index = homeostasis assessment model of insulin resistance; (I0 [μU/mL] × G0 [mmol/L])/22.5, where I0 = fasting insulin measured in plasma by an immunoradiometric assay (Immunotech, Marseille, France) and G0 = fasting glucose by the hexokinase method (Boehringer Mannheim, Mannheim, Germany) (3,4).  ‡QUICKI = quantitative insulin sensitivity check index: 1/(log I0 [μU/mL] + log G0 [mmol/L]). Adjustment for fasting, body mass index, and smoking did not essentially alter the odds ratios. Fasting times were greater than 8 hours for 63% of the subjects and 4–8 hours for 37%; smoking was coded as current smoker, past smoker, and never smoker.  Insulin  1.00 (referent)  1.12 (0.67 to 1.88)  0.91 (0.55 to 1.50)  .59  .71      No. of case patients/No. of control subjects  46/82  46/85  43/92          Mean (μU/mL)  3.28  5.76  13.49      HOMA IR†  1.00 (referent)  1.26 (0.74 to 2.13)  0.81 (0.49 to 1.34)  .22  .38      No. of case patients/No. of control subjects  46/89  49/85  40/100          Mean  0.748  1.39  3.59      QUICKI‡  1.00 (referent)  1.46 (0.86 to 2.47)  1.12 (0.68 to 1.86)  .75  .62      No. of case patients/No. of control subjects  40/94  49/86  46/94          Mean  0.24  0.29  0.37        Tertile*  Ptrend    1  2  3  Categories  Continuous  *Odds ratios and 95% confidence intervals in an analysis of 135 matched case–control subjects were determined by conditional logistic regression with available measurements of insulin and glucose (4).  †HOMA-IR index = homeostasis assessment model of insulin resistance; (I0 [μU/mL] × G0 [mmol/L])/22.5, where I0 = fasting insulin measured in plasma by an immunoradiometric assay (Immunotech, Marseille, France) and G0 = fasting glucose by the hexokinase method (Boehringer Mannheim, Mannheim, Germany) (3,4).  ‡QUICKI = quantitative insulin sensitivity check index: 1/(log I0 [μU/mL] + log G0 [mmol/L]). Adjustment for fasting, body mass index, and smoking did not essentially alter the odds ratios. Fasting times were greater than 8 hours for 63% of the subjects and 4–8 hours for 37%; smoking was coded as current smoker, past smoker, and never smoker.  Insulin  1.00 (referent)  1.12 (0.67 to 1.88)  0.91 (0.55 to 1.50)  .59  .71      No. of case patients/No. of control subjects  46/82  46/85  43/92          Mean (μU/mL)  3.28  5.76  13.49      HOMA IR†  1.00 (referent)  1.26 (0.74 to 2.13)  0.81 (0.49 to 1.34)  .22  .38      No. of case patients/No. of control subjects  46/89  49/85  40/100          Mean  0.748  1.39  3.59      QUICKI‡  1.00 (referent)  1.46 (0.86 to 2.47)  1.12 (0.68 to 1.86)  .75  .62      No. of case patients/No. of control subjects  40/94  49/86  46/94          Mean  0.24  0.29  0.37      View Large References 1 Hsing AW, Deng J, Sesterhenn IA, Mostofi FK, Stanczyk FZ, Benichou J, et al. Body size and prostate cancer: a population-based case-control study in China. Cancer Epidemiol Biomarkers Prev  2000; 9: 1335–41. Google Scholar 2 Hsing AW, Chua S Jr, Gao YT, Gentzschein E, Chang L, Deng J, et al. Prostate cancer risk and serum levels of insulin and leptin: a population-based study. J Natl Cancer Inst  2001; 93: 783–9. Google Scholar 3 Hsing AW, Gao YT, Chua S Jr, Deng J, Stanczyk FZ. Insulin resistance and prostate cancer risk. J Natl Cancer Inst  2003; 95: 67–71. Google Scholar 4 Stattin P, Bylund A, Rinaldi S, Biessy C, Dechaud H, Stenman UH, et al. Plasma insulin-like growth factor-I, insulin-like growth factor-binding proteins, and prostate cancer risk: a prospective study. J Natl Cancer Inst  2000; 92: 1910–7. Google Scholar 5 Dennis LK, Resnick MI. Analysis of recent trends in prostate cancer incidence and mortality. Prostate  2000; 42: 247–52. Google Scholar 6 Online data for BMI in populations in the World Health Organization’s Monitoring Trends in Cardiovascular Diseases (MONICA) Project. Available at: www.ktl.fi/publications/monica. [Last accessed May 27, 2003.] Google Scholar 7 Kaaks R, Lukanova A, Sommersberg B. Plasma androgens, IGF-I, body size and prostate cancer risk: a synthetic review. Prostate Cancer Prostatic Dis  2000; 3: 157–72. Google Scholar © Oxford University Press

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JNCI: Journal of the National Cancer Institute – Oxford University Press

Published: Jul 16, 2003

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