Populations at high risk for prostate cancer

Hsieh, Kisseng; Albertsen, Peter C.

doi:10.1016/s0094-0143(03)00058-2

Cited by 24 publications

(12 citation statements)

References 86 publications

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“…Because clinical prostate tumors appear to have less 1α-OHase than noncancerous prostates, men with clinical cancer are less likely to benefit from prohormonal forms of vitamin D. (However, the recent findings of Woo et al (98), in which men with recurrent prostate cancer appeared to benefit from 2000 IU vitamin D 3 , suggest that there may be a role for vitamin D even in later disease.) Men without clinical disease, but who are at increased risk for prostate cancer, such as men with histologic evidence of prostate intraepithelial neoplasia (PIN), a possible precursor of prostate cancer (123), or men with a positive family history, may consider supplementation with 25(OH)D or vitamin D, as these drugs should be converted to 1,25(OH) 2 D intraprostatically. Finally, for virtually all other men, especially men who live at extreme geographic latitudes and/ or who receive little effective exposure to sunlight, prophylactic supplementation with vitamin D may be prudent.…”

Section: Resultsmentioning

confidence: 99%

VITAMIN D IN HEALTH AND DISEASE: Vitamin D and the Epidemiology of Prostate Cancer

Schwartz

2005

Seminars in Dialysis

102

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Mortality rates from prostate cancer are significantly higher among African Americans than Caucasian Americans and are inversely related to the availability of ultraviolet (UV) radiation. These findings support the hypothesis, originally proposed in 1990, that prostate cancer may be caused by vitamin D deficiency. In 1992, specific receptors for 1,25-dihydroxyvitamin D [1,25(OH)2D] were demonstrated in human prostate cells. We and others have shown that 1,25(OH)2D exerts prodifferentiating, antiproliferative, and antimetastatic effects on these cells. In 1998 we demonstrated that normal prostate cells express 1alpha-hydroxylase and synthesize their own 1,25(OH)2D. Thus, 1,25(OH)2D is an autocrine hormone in the prostate. The consensus emerging from analytic epidemiologic studies is that low levels of UV radiation/vitamin D are indeed associated with an increased risk of prostate cancer in individual men. The evolution of our understanding of the role of vitamin D in the epidemiology of prostate cancer parallels our understanding of the role of vitamin D in the epidemiology of rickets. In both diseases, ecologic observations about UV radiation preceded experimental observations and were subsequently validated by them.

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Section: Resultsmentioning

confidence: 99%

VITAMIN D IN HEALTH AND DISEASE: Vitamin D and the Epidemiology of Prostate Cancer

Schwartz

2005

Seminars in Dialysis

102

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“…Because of their increased risk of PCa [16] and high-grade disease [18] as well as PCa-specific death [10,19], more intensive screening of African Americans is likely warranted.…”

Section: Evidence Synthesismentioning

confidence: 99%

Risk-Based Prostate Cancer Screening

et al. 2012

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Context Widespread mass screening of prostate cancer (PCa) is not recommended because the balance between benefits and harms is still not well established. The achieved mortality reduction comes with considerable harm such as unnecessary biopsies, overdiagnoses, and overtreatment. Therefore, patient stratification with regard to PCa risk and aggressiveness is necessary to identify those men who are at risk and may actually benefit from early detection. Objective This review critically examines the current evidence regarding risk-based PCa screening. Evidence acquisition A search of the literature was performed using the Medline database. Further studies were selected based on manual searches of reference lists and review articles. Evidence synthesis Prostate-specific antigen (PSA) has been shown to be the single most significant predictive factor for identifying men at increased risk of developing PCa. Especially in men with no additional risk factors, PSA alone provides an appropriate marker up to 30 yr into the future. After assessment of an early PSA test, the screening frequency may be determined based on individualized risk. A limited list of additional factors such as age, comorbidity, prostate volume, family history, ethnicity, and previous biopsy status have been identified to modify risk and are important for consideration in routine practice. In men with a known PSA, risk calculators may hold the promise of identifying those who are at increased risk of having PCa and are therefore candidates for biopsy. Conclusions PSA testing may serve as the foundation for a more risk-based assessment. However, the decision to undergo early PSA testing should be a shared one between the patient and his physician based on information balancing its advantages and disadvantages.

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“…Studies have found intergenerational and familial associations for cardiovascular disease (Greenlund et al 1997, Parikh et al 2007, Rose 1967, Sesso et al 2001), non-insulin-dependent diabetes mellitus (Dallo & Weller 2003, Meigs et al 2000, Newman et al 1987, Srinivasan et al 2003), metabolic syndrome (Lascaux-Lefebvre et al 2001), cancer (Hsieh & Albertsen 2003, Jonsson et al 2004, Pharoah et al 1997), asthma (Arshad et al 2005), obesity (Reilly et al 2005, Whitaker et al 1997), health-related behaviours, including smoking, drug and alcohol use (Chassin et al 1998, Hill et al 2005, Merikangas et al 1998, Shenassa et al 2003), diet and exercise (Hood et al 2000, Mattocks et al 2008), and other health-related influences such as socio-economic status (Corcoran 1995, Zimmerman 1992). …”

Section: Introductionmentioning

confidence: 99%

Inter-generational continuity in periodontal health: findings from the Dunedin Family History Study

Shearer

Thomson

Caspi

et al. 2011

Journal of Clinical Periodontology

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Objective To determine whether parental periodontal disease history is a risk factor for periodontal disease in adult offspring. Methods Proband periodontal examination (combined attachment loss (CAL) at age 32, and incidence of CAL from ages 26–32) and interview data were collected during the age-32 assessments in the Dunedin Study. Parental data were also collected. The sample was divided into two familial-risk groups for periodontal disease (high- and low-risk) based on parents’ self-reported periodontal disease. Results Periodontal risk analysis involved 625 proband-parent(s) groups. After controlling for confounding factors, the high-familial-risk periodontal group was more likely to have 1+ sites with 4+mm CAL (RR 1.45; 95% CI 1.11–1.88), 2+ sites with 4+mm CAL (RR 1.45; 95% CI 1.03–2.05), 1+ sites with 5+mm CAL (RR 1.60; 95% CI 1.02–2.50) and 1+ sites with 3+mm incident CAL (RR 1.64; 95% CI 1.01–2.66) than the low-familial-risk group. Predictive validity was enhanced when information was available from both parents. Conclusions Parents with poor periodontal health tend to have offspring with poor periodontal health. Family/parental history of oral health is a valid representation of the shared genetic and environmental factors that contribute to an individual’s periodontal status, and may help predict patient prognosis and preventive treatment need.

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Populations at high risk for prostate cancer

Cited by 24 publications

References 86 publications

VITAMIN D IN HEALTH AND DISEASE: Vitamin D and the Epidemiology of Prostate Cancer

VITAMIN D IN HEALTH AND DISEASE: Vitamin D and the Epidemiology of Prostate Cancer

Risk-Based Prostate Cancer Screening

Inter-generational continuity in periodontal health: findings from the Dunedin Family History Study

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