Incidence rates for pancreatic cancer are consistently lower in women than in men. Previous studies suggest that reproductive factors, particularly parity, may reduce pancreatic cancer risk in women. We examined parity, breast feeding history, age at first birth, menstrual factors, and exogenous hormone use in relation to pancreatic cancer risk in a prospective cohort study of women. Information on parity and other reproductive factors was assessed by questionnaires in 1976 and updated biennially. Multivariate relative risks were adjusted for cigarette smoking, body mass index, diabetes, and height. During 22 years of follow-up (1976-1998), 115,474 women contributed 2.4 million years of person time, and 243 cases of pancreatic cancer were identified. Compared with nulliparous women, the relative risk of pancreatic cancer was 0.86 [95% confidence interval (CI), 0.55-1.36] for women with 1-2 births, 0.75 (95% CI, 0.48-1.17) for 3-4 births, and 0.58 (95% CI, 0.34-0.98) for those with >/=5 births after adjusting for other factors. An analysis for linear trend indicates a 10% reduction in risk for each birth (P(trend) = 0.008). Other reproductive factors and exogenous hormone use were not significantly related to pancreatic cancer risk. In this large prospective cohort of women, parity was associated significantly with a reduced risk of pancreatic cancer. Additional studies should examine the physiological or hormonal changes underlying pregnancy or childbirth that may explain this finding.
"Characteristics of the 20 included studies are shown in Table 1. Among these studies, seven were conducted in USA15183032333540, two in Canada2039, seven in Europe16172627343638, one in Japan31, and two in China1937, one in Egypt14. The average of following- up duration of cohort studies was 18.65 years, ranged from 7.1 to 38 years. "
[Show abstract][Hide abstract] ABSTRACT: Multiple studies have hypothesized parity is associated with pancreatic cancer risk but obtained conflicting results. We conducted a meta-analysis (including a dose-response approach) of current available epidemiologic studies to investigate the association between parity and risk of pancreatic cancer. Ten cohort studies and ten case-control studies including 8205 cases were eligible for inclusion. The combined RR (relative risk) of pancreatic cancer for the parous vs. nulliparous was 0.91 (95% CI, confidence interval = 0.85-0.97, I(2) = 39.0%, Ph = 0.01). We observed an inverse association between giving birth to two children pancreatic cancer risk with RR of 0.86 (95% CI = 0.80-0.93, I(2) = 8.7%, Ph = 0.36). And no evidence supported there was non-linear (P = 0.33) or linear relationship (P = 0.14) between number of parity and risk of pancreatic cancer. Findings from this meta-analysis indicate that giving birth to two children has the lowest pancreatic cancer risk, mechanism of this protective effect needs further investigation.
[Show abstract][Hide abstract] ABSTRACT: Life-history theory predicts a tradeoff between reproductive effort and lifespan. It has been suggested that this tradeoff is a result of reproductive costs accelerating senescence of the immune system, leading to earlier death. Longevity costs of reproduction are suggested for some human populations, but whether high reproductive effort leads to impaired immune function is unknown. We examined how reproductive effort affected postreproductive survival and the probability of dying of an infectious disease in women born in preindustrial Finland between 1702 and 1859. We found that mothers delivering twins had reduced postreproductive survival after age 65. This effect arose because mothers of twins had a higher probability of succumbing to an infectious disease (mainly tuberculosis) than mothers delivering singletons. The risk among mothers of twins of dying of an infectious disease was further elevated if mothers had started reproducing early. In contrast, neither female postreproductive survival nor the risk of succumbing to an infectious disease was influenced by the total number of offspring produced. Our results provide evidence of a long-term survival cost of twinning in humans and indicate that the mechanism mediating this cost might have been accelerated immunosenescence.
Proceedings of the National Academy of Sciences 09/2004; 101(33):12391-6. DOI:10.1073/pnas.0402215101 · 9.67 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: There is little doubt that cigarette smoking remains a major environmental health risk that humans are facing in the twenty-first century. Cigarette smokers are more likely to develop many forms of diseases than nonsmokers, including cancers and vascular diseases. With the availability of the human genome sequence, we become more aware of the genetic contributions to these common diseases, especially the interactive relations between environmental factors (e.g., smoking) and genes on disease susceptibility, development, and prognosis. Although smoking is responsible for up to 30% of pancreatic cancers and about 10% of cases are ascribed to genetic reasons, some genetic variants do not predispose carriers to disease development unless they are exposed to a specific adverse environment such as smoking. This smoke-gene interaction could potentially be responsible for most of the cases. Certain polymorphisms in genes such as CYP1A1 have been shown particularly sensitive to smoking-induced pathogenesis, including pancreatic cancer and atherosclerosis. We found that individuals with CYP1A1 CC genotype had a more than three fold increase in risk for severe coronary atherosclerosis when they smoked. Patients with endothelial nitric oxide synthase (eNOS) intron 4 27 repeat homozygotes were more likely to develop severe coronary stenosis when they smoked. On the other hand, DNA variants at the eNOS gene also dictate how smoking affects the expression of eNOS. We showed that GSTM1 deficiency was not involved in smoking-induced vascular diseases, but p53 polymorphisms tended to modify the disease severity in smokers. We are still at an early stage of defining the pairs and mechanisms of smoke-gene interaction, and this etiologic mechanism may hold great potential for risk assessment, treatment strategy, and prognostic predictions.
World Journal of Surgery 04/2005; 29(3):344-53. DOI:10.1007/s00268-004-7819-0 · 2.64 Impact Factor
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.