US Male Health Research Articles

Abstract 4203: A prospective study of birth weight and prostate cancer risk: extended analysis in the Health Professionals Follow-up Study

Abstract Introduction: Birth weight, a potential marker of the in utero hormonal and growth factor milieu, has been associated with an increased risk of prostate cancer (PCa) in some, but not all, previous studies. It was also associated with a non-significantly greater risk of advanced stage PCa (relative risk [RR] = 1.37, 95% confidence interval [CI]: 0.61-3.05 for ≥10 lbs compared to 7.0-8.4 lbs, p-trend = 0.087) in our previous analysis in the Health Professionals Follow-up Study (HPFS). However, these suggestive findings were based on a relatively small number of advanced stage cases and short follow-up. We have now updated our previous analysis of birthweight and PCa risk in the HPFS with an additional 14 years of follow-up. Method: Birth weight was assessed by self-report on the 1994 follow-up questionnaire using pre-specified categories. PCa diagnoses were ascertained on each biennial follow-up questionnaire and confirmed by medical record review. Cox proportional hazards regression was used to evaluate the association between birth weight and PCa risk through 2016. Result: Of the 17,949 eligible men who reported their birth weight in 1994, 3,167 were subsequently diagnosed with PCa. With the exception of a suggestive positive trend between increasing birth weight and high-grade PCa (RRadj per pound: 1.06; 95% CI: 0.98-1.16; p-trend=0.15), no associations were observed between birth weight and risk of total, organ-confined, low-grade, advanced stage, lethal, or fatal PCa. Conclusion: Overall, no association was observed between birth weight and PCa risk and mortality in this large prospective cohort study of US male health professionals. Table 1. Associations between self-reported birth weight and prostate cancer in the Health Professionals Follow-up Study, 1994-2016 Birth weight (lbs) <5.5(<2,495 g) 5.5-6.9(2,495-3,174 g) 7.0-8.4(3,175-3,855 g) 8.5-9.9(3,856-4,535 g) ≥10.0(≥4,536 g) Per 1 lb (454g) increase Total prostate cancer Cases/person-years 125/17,019 518/80,053 1,931/297,495 396/60,445 197/22,993 HRa (95% CI) 0.98 (0.81-1.18) 0.86 (0.78-0.95) 1.00 0.85 (0.76-0.95) 0.98 (0.84-1.13) 1.01 (0.96-1.05) High-grade prostate cancer (Score 4+3 and higher) Cases/person-years 23/17,117 119/80,434 453/299,015 105/60,741 52/23,148 HRa (95% CI) 0.76 (0.50-1.16) 0.83 (0.68-1.03) 1.00 0.93 (0.75-1.16) 1.03 (0.76-1.39) 1.06 (0.98-1.16) Advanced stage prostate cancer (T3b+) at diagnosis Cases/person-years 4/17,135 29/80,516 109/299,370 25/60,811 12/23,195 HRa (95% CI) 0.53 (0.19-1.46) 0.91 (0.60-1.40) 1.00 0.98 (0.62-1.54) 1.02 (0.54-1.92) 1.08 (0.91-1.29) Lethal prostate cancer Cases/person-years 11/17,127 70/80,491 225/299,247 51/60,791 27/23,178 HRa (95% CI) 0.81 (0.43-1.50) 1.15 (0.86-1.52) 1.00 1.07 (0.78-1.47) 1.01 (0.66-1.54) 1.00 (0.89-1.13) Fatal prostate cancer Cases/person-years 10/17,551 59/82,316 197/307,363 43/62,246 23/23,996 HRa (95% CI) 0.88 (0.45-1.67) 1.17 (0.86-1.60) 1.00 1.11 (0.78-1.56) 1.03 (0.65-1.63) 1.00 (0.87-1.14) RR=relative risk; CI = confidence interval a Adjusted for age, calendar time, race, smoking status, family history of prostate cancer (yes or no), PSA testing in >50% of previous cycles (yes or no), physical activity, diabetes, diet (tomato sauce intake, coffee, and energy intake), alcohol intake, multivitamin use, vitamin E supplement use, and aspirin use. Citation Format: Qinran Liu, Yiwen Zhang, Jane B. Vaselkiv, Lorelei A. Mucci, Edward L. Giovannucci, Elizabeth A. Platz, Siobhan Sutcliffe. A prospective study of birth weight and prostate cancer risk: extended analysis in the Health Professionals Follow-up Study. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 4203.

Association Between the Sulfur Microbial Diet and Risk of Colorectal Cancer

Sulfur-metabolizing bacteria that reduce dietary sulfur to hydrogen sulfide have been associated with colorectal cancer (CRC). However, there are limited studies investigating the association between diet and sulfur-metabolizing bacteria in the development of CRC. To develop a dietary score that correlates with gut sulfur-metabolizing bacteria and to examine its association with CRC risk. This prospective cohort study included data from the Health Professionals Follow-up Study (1986-2014), Nurses' Health Study (1984-2016), and Nurses' Health Study II (1991-2017). Participants were US male health professionals and female registered nurses who were free of inflammatory bowel disease and cancer at baseline, with a subsample of participants who provided stool samples from 2012 to 2014. Statistical analysis was conducted from September 1, 2020, to June 1, 2021. A dietary pattern, assessed by a food-frequency questionnaire, that most correlated with 43 sulfur-metabolizing bacteria identified through taxonomic and functional profiling of gut metagenome data. Incident CRC. Among 214 797 participants comprising 46 550 men (mean [SD] age at baseline, 54.3 [9.7] years) and 168 247 women (mean [SD] age at baseline, 43.0 [9.2] years), 3217 incident cases of CRC (1.5%) were documented during 5 278 048 person-years of follow-up. The sulfur microbial diet, developed in a subsample of 307 men (mean [SD] age, 70.5 [4.3] years) and 212 women (mean [SD] age, 61.0 [3.8] years), was characterized by high intakes of low-calorie beverages, french fries, red meats, and processed meats and low intakes of fruits, yellow vegetables, whole grains, legumes, leafy vegetables, and cruciferous vegetables. After adjustment for other risk factors, greater adherence to the sulfur microbial diet was associated with an increased risk of CRC, with a hazard ratio (HR) of 1.27 (95% CI, 1.12-1.44) comparing the highest vs the lowest quintile of the diet score (linear trend of diet score quintiles; P < .001 for trend). When assessed by anatomical subsites, greater adherence to the sulfur microbial diet was positively associated with distal CRC (HR, 1.25; 95% CI, 1.05-1.50; P = .02 for trend) but not proximal colon cancer (HR, 1.13; 95% CI, 0.93-1.39; P = .19 for trend). Adherence to the sulfur microbial diet was associated with an increased risk of CRC, suggesting a potential mediating role of sulfur-metabolizing bacteria in the associaton between diet and CRC. Further research is needed to confirm these findings and to determine the underlying mechanisms.

Association of Diet With Erectile Dysfunction Among Men in the Health Professionals Follow-up Study

Erectile dysfunction, especially in younger men, is an early sign of cardiovascular disease and may decrease quality of life. Men may be motivated to adopt a healthy dietary pattern if it lowers their risk of erectile dysfunction. To assess the association between adherence to a diet quality index based on healthy dietary patterns and erectile dysfunction in men. This population-based prospective cohort study included men from the Health Professionals Follow-up Study with follow-up from January 1, 1998, through January 1, 2014. Participants included US male health professionals aged 40 to 75 years at enrollment. Men with erectile dysfunction or a diagnosis of myocardial infarction, diabetes, stroke, or genitourinary cancer at baseline were excluded. Analyses were completed in February 2020. A food frequency questionnaire was used to determine nutrient and food intake every 4 years. Diet quality was assessed by Mediterranean Diet score and the Alternative Healthy Eating Index 2010 score, with higher scores indicating healthier diet. Dietary index scores were cumulatively updated from 1986 until men developed erectile dysfunction, cardiovascular disease, died, or were lost to follow-up. Incident erectile dysfunction was assessed with questionnaires in 2000, 2004, 2008, and 2012. Hazard ratios (HRs) by prespecified categories or quintiles of dietary index scores were estimated using Cox proportional hazards regression analyses stratified by age. Among 21 469 men included in analysis, mean (SD) age at baseline was 62 (8.4) years. During a mean (SD) follow-up of 10.8 (5.4) years and 232 522 person-years, there were 968 incident erectile dysfunction cases among men younger than 60 years, 3703 cases among men aged 60 to less than 70 years, and 4793 cases among men aged 70 years or older. Men younger than 60 years and in the highest category of the Mediterranean Diet score had the lowest relative risk of incident erectile dysfunction compared with men in the lowest category (HR, 0.78; 95% CI, 0.66-0.92). Higher Mediterranean diet scores were also inversely associated with incident erectile dysfunction among older men (age 60 to <70 years: HR, 0.82; 95% CI, 0.76-0.89; age ≥70 years: HR, 0.93; 95% CI, 0.86-1.00). Men scoring in the highest quintile of the Alternative Healthy Eating Index 2010 also had a lower risk of incident erectile dysfunction, particularly among men age younger than 60 years (quintile 5 vs quintile 1: HR, 0.78; 95% CI, 0.63-0.97). This cohort study found that adherence to healthy dietary patterns was associated with a lower risk for erectile dysfunction, suggesting that a healthy dietary pattern may play a role in maintaining erectile health.

Physical activity across adulthood and subjective cognitive function in older men

Low subjective cognitive function (SCF), which is associated with APOE4 genotype, adversely impacts quality of life and has predicted clinical dementia. We examined whether physical activity during early adulthood or mid-to-late life is associated with late-life SCF. We followed 28,481 US male health professionals aged 40-75years who reported their physical activity in 1986 and biennially thereafter. SCF was reported in 2008 and 2012. The SCF score was averaged for the 2008 and 2012 assessments and categorized as "good", "moderate", and "poor". Men in the highest versus lowest quintile of mid-to-late life physical activity in 1986 had 38% lower odds of poor versus good SCF score (multivariable-adjusted odds ratio (OR) 0.62; 95% CI 0.53, 0.72; P for trend<0.0001). Being physically active in early adulthood was also associated with a 23% lower odds of poor SCF, independent of later activity, and being active both in early and mid-to-late adulthood was associated with a 48% lower odds of poor SCF score compared with those who were always sedentary (OR 0.52; 95% CI 0.38, 0.71). Our results suggest that being physically active during early adulthood and mid-to-late life independently contribute to prevention of poor subjective cognitive function in late-life.

The effects of stress at work and at home on inflammation and endothelial dysfunction.

This study examined whether stress at work and at home may be related to dysregulation of inflammation and endothelial function, two important contributors to the development of cardiovascular disease. In order to explore potential biological mechanisms linking stress with cardiovascular health, we investigated cross-sectional associations between stress at work and at home with an inflammation score (n's range from 406–433) and with two endothelial biomarkers (intercellular and vascular adhesion molecules, sICAM-1 and sVCAM-1; n's range from 205–235) in a cohort of healthy US male health professionals. No associations were found between stress at work or at home and inflammation. Men with high or medium levels of stress at work had significantly higher levels of sVCAM-1 (13% increase) and marginally higher levels of sICAM-1 (9% increase), relative to those reporting low stress at work, independent of health behaviors. Men with high levels of stress at home had marginally higher levels of both sVCAM-1 and sICAM-1 than those with low stress at home. While lack of findings related to inflammation are somewhat surprising, if replicated in future studies, these findings may suggest that endothelial dysfunction is an important biological mechanism linking stress at work with cardiovascular health outcomes in men.

Restless Legs Syndrome: An Early Clinical Feature of Parkinson Disease in Men

The association between restless legs syndrome (RLS) and Parkinson disease has been extensively studied, but the temporal relationship between the two remains unclear. We thus conduct the first prospective study to examine the risk of developing Parkinson disease in RLS. Prospective study from 2002-2010. United States. There were 22,999 US male health professionals age 40-75 y enrolled in the Health Professionals Follow-up Study without Parkinson disease, arthritis, or diabetes mellitus at baseline. RLS was assessed in 2002 using a set of standardized questions recommended by the International RLS Study Group. Incident Parkinson disease was identified by biennial questionnaires and then confirmed by review of participants' medical records by a movement disorder specialist. We documented 200 incident Parkinson disease cases during 8 y of follow-up. Compared to men without RLS, men with RLS symptoms who had symptoms greater than 15 times/mo had higher risk of Parkinson disease development (adjusted relative risk = 1.47; 95% confidence interval: 0.59, 3.65; P = 0.41). This was statistically significant only for cases diagnosed within 4 y of follow-up (adjusted relative risk = 2.77; 95% confidence interval: 1.08, 7.11; P = 0.03). Severe restless legs syndrome may be an early feature of Parkinson disease.

Long-term alcohol consumption in relation to all-cause and cardiovascular mortality among survivors of myocardial infarction: the Health Professionals Follow-up Study.

The aim of this study was to examine the association between long-term alcohol consumption, alcohol consumption before and after myocardial infarction (MI), and all-cause and cardiovascular mortality among survivors of MI. The Health Professionals Follow-up Study (HPFS) is a prospective cohort study of 51 529 US male health professionals. From 1986 to 2006, 1818 men were confirmed with incident non-fatal MI. Among MI survivors, 468 deaths were documented during up to 20 years of follow-up. Long-term average alcohol consumption was calculated beginning from the time period immediately before the first MI and updated every 4 years afterward. Cox proportional hazards were used to estimate the multivariable-adjusted hazard ratios (HR) and 95% confidence intervals (CI). Compared with non-drinkers, the multivariable-adjusted HRs for all-cause mortality were 0.78 (95% CI: 0.62-0.97) for 0.1-9.9 g/day, 0.66 (95% CI: 0.51-0.86) for 10.0-29.9 g/day, and 0.87 (95% CI: 0.61-1.25) for ≥30 g/day (P(quadratic)= 0.006). For cardiovascular mortality, the corresponding HRs were 0.74 (95% CI: 0.54-1.02), 0.58 (95% CI: 0.39-0.84), and 0.98 (95% CI: 0.60-1.60), P(quadratic)= 0.003. These findings were consistent when restricted to pre- and post-MI alcohol assessments. In subgroup analyses, moderate alcohol consumption was inversely associated with mortality among men with non-anterior infarcts, and among men with mildly diminished left ventricular function. Long-term moderate alcohol consumption is inversely associated with all-cause and cardiovascular mortality among men who survived a first MI. This U-shaped association may be strongest among individuals with less impaired cardiac function after MI and should be examined further.

Abstract P064: Dietary Glycemic Index and Glycemic Load and Risk of Coronary Heart Disease in a Prospective Study Among US Male Health Professionals

Introduction: The associations between dietary glycemic index (GI) and glycemic load (GL) with subsequent risk of coronary heart disease (CHD) are inconclusive among men. The association is further complicated by the potential biological interactions between the carbohydrate quality of the diet and factors that may influence underlying insulin resistance. Hypothesis: We hypothesized that long-term exposure to a diet with high GI and GL would be associated with increased CHD risk in a cohort of US men, and the association would be further modified by fiber intake, alcohol consumption and BMI. Methods: We included 37,736 men aged 40–75 years from the Health Professional Follow-up Study, with no previous diagnosis of CHD, cancer, or type 2 diabetes. We confirmed 3,121 total incident CHD cases during 22 years of follow-up. Cox proportional hazard models were used to adjust for covariates. Results: After adjusting for lifestyle and dietary covariates, the hazard ratio (RR) and 95% confidence intervals comparing men in the highest vs. the lowest quintile was 1.16 (1.04, 1.31; p for trend=0.03) for dietary GI, and 1.09 (0.94, 1.27; p for trend =0.16) for GL. We found a significant effect modification by fiber intake (p=0.02); The associations between GL and CHD risk were strongest among participants in the lowest tertile of fiber intake (RR= 1.00, 1.00, 0.93, 1.11 and 1.16 with increasing quintiles of GL; RR=1.00, 0.68, 0.79, 0.73 and 0.76 for participants in the highest tertile of fiber intake). The association between GL and CHD was stronger among men with body mass index (BMI) greater than 25 kg/m2 than normal weight men, even though the test for interaction was only marginally significant (RR=1.00, 1.03, 1.05, 1.10, and 1.16 for increasing quintles of GL among men with BMI≥25 kg/m2 and RR= 1.00, 0.92, 0.96, 1.09 and 1.04 for men with BMI&lt;25 kg/m2, p for interaction=0.09). Alcohol intake did not modify the association of GL with CHD (p for interaction=0.44). Conclusion: We observed a significantly increased risk of CHD with high GI diet and a modestly elevated association between GL and CHD among men with low fiber intakes or who were overweight or obese. No effect modification by alcohol was observed, but we did find that the association between GL and CHD was more pronounced among those with lower fiber intake or higher BMI.

Abstract P106: Dietary Patterns and Incidence of Atrial Fibrillation: the Health Professionals Follow-up Study (HPFS)

Introduction: Atrial fibrillation (AF) is a growing public health problem. Overall diet quality has proven informative for studying chronic diseases, but potential relations with AF risk are unknown. Methods: We followed 39,840 US male health professionals free from AF at baseline (age 70.5±9.8 y) for incidence of AF from 2002 to 2010. Diet was assessed every 4 ys by validated questionnaires, with cumulative updating of past diet. We also performed analyses evaluating only more recent diet. A diet pattern was characterized based on biologic considerations using 8 dietary factors that might influence risk factors for AF: higher fruits, vegetables, whole grain, seafood, nuts, and polyunsaturated to saturated fat ratio, and lower glycemic load and trans-fat. Each factor was scored in quintiles (1- 5), in ascending order for more healthful factors and descending order for less healthful factors. These scores were summed to quantify the diet pattern score (range 8-40). Incident AF was identified from initial self-report that was also subsequently confirmed by detailed supplementary questionnaire; these methods were validated against medical records in a subset (positive predictive value=95%). We estimated risk using Cox models adjusting for age, prevalent diseases, lifestyle habits, and health-seeking behaviors (greater multivitamin use; more routine physical, sigmoidoscopy, and rectal exams). Results: During 308,144 person-years follow-up, 879 incident AF cases occurred. Men with higher diet scores were older, less likely to smoke, more likely to be physically active and be on aspirin, and more likely to have health seeking behaviors. The multivariable-adjusted HR (95%CI) for quintiles 2 to5 vs. quintile 1 were 1.06 (0.84, 1.33), 1.04 (0.82, 1.32), 1.15 (0.92, 1.45), and 1.26 (0.98, 1.60), respectively (p trend=0.04). Exploring each of the 8 dietary factors individually, none were significantly associated with incident AF, except seafood which was inversely associated (HR for quintile 5 vs. 1=0.79; 95%CI=0.63, 1.00). Health-seeking behaviors were associated with trend toward AF risk (extreme quartile HR 1.21, 95% CI 0.92-1.59). Stratified by health seeking behavior, the diet score showed positive association with AF only in men with greatest health seeking behaviors (p trend 0.01), but not in the other groups (p&gt;0.8). Sensitivity analyses using only more recent diet, stratifying by aspirin use, or limiting to symptomatic AF cases did not appreciably alter results. Conclusions: Contrary to our hypothesis, a more healthful diet pattern was linked to higher AF risk. This association might partly relate to unmeasured or residual confounding due to greater health seeking behaviors that could increase AF diagnosis. Overall, our novel findings suggest no major benefits of a generally healthy diet on AF incidence, except perhaps for seafood consumption.

A Prospective Study of Magnesium and Iron Intake and Pancreatic Cancer in Men

Many studies have investigated the relation between magnesium and iron intake and diabetes and, separately, between diabetes and pancreatic cancer. However, no known study has examined the direct association of magnesium and iron intake with pancreatic cancer risk. The authors obtained magnesium and iron intake data using food frequency questionnaires from the US male Health Professionals Follow-up Study, which began in 1986. During 851,476 person-years and 20 years of follow-up, 300 pancreatic cancer cases were documented. Cox proportional hazards models were used to estimate relative risks, adjusting for age, smoking, and body mass index. No associations were observed between magnesium or iron intake and pancreatic cancer (highest vs. lowest quintile: relative risk (RR) = 0.94, 95% confidence interval (CI): 0.66, 1.32 and RR = 0.93, 95% CI: 0.65, 1.34, respectively). Similarly, iron or magnesium supplement use was not related to pancreatic cancer. A statistically significant inverse relation was noted between magnesium and pancreatic cancer for subjects with a body mass index of > or =25 kg/m(2) (RR = 0.67, 95% CI: 0.46, 0.99; P-trend = 0.04). Although, overall, no relation between magnesium or iron intake and pancreatic cancer was observed in this cohort of men, an inverse association with magnesium was suggested among overweight individuals, which should be examined in other studies.

Mortality, Health Outcomes, and Body Mass Index in the Overweight Range

Health hazards of obesity have been recognized for centuries, appearing, for example, in writings attributed to Hippocrates. From the later decades of the 20th century through the present, there have been numerous epidemiological studies of the relationship between excess weight and the total, or all-cause, mortality rate,1 a critical cumulative measure of the public health impact of any health condition. Using body mass index (BMI), an indicator of relative weight for height (weight [kg]/height [m]2) and a frequently used surrogate for assessment of excess body fat, these studies have found linear, U-shaped, or J-shaped relationships between total mortality and BMI. That is, in some studies, both the thin and the obese were more likely to die than those in between. There is, however, always a point at which increasing BMI is associated with increasing mortality risk, but the BMI at which this occurs varies across studies and populations.2 Currently,3 overweight in adults is defined as a BMI of 25.0 to <30.0 kg/m2 and obesity as a BMI of ≥30.0 kg/m2 (Table 1). A number of studies have found no significant relationship between BMI in the overweight range and mortality rate4 and have shown the nadir of mortality risk to be in the overweight range. In particular, commentaries in both the lay press5–7 and scientific literature2,8,9 subsequent to recent reports from National Health and Nutrition Examination Surveys (NHANES)10,11 have highlighted the confusion and controversy regarding this issue. Some have interpreted the recent data to mean that overweight is not detrimental to health and is not in itself a public health concern and that drawing attention to the need for weight loss in this range will have negative effects on the health and well-being of the general population.8 Others have argued …

Fish consumption and risk of major chronic disease in men

Background:Although fish consumption may reduce specific disease endpoints, such as sudden cardiac death and prostate cancer, the effects of major chronic disease on total burden, reflecting sums of effects on a variety of endpoints and risk pathways, are not well established. Higher n−6 fatty acid consumption has also been hypothesized to reduce the health benefits of n−3 fatty acids in fish. Objective:The aim was to study the associations of fish and n−3 fatty acid consumption with risk of total major chronic disease (cardiovascular disease, cancer, and death) and to determine whether a high n−6 intake modifies the associations. Design:Lifestyle and other risk factors were assessed every 2 y and diet every 4 y in 40,230 US male health professionals aged 40–75 y and free of major chronic disease at baseline in 1986. During 18 y of follow-up, 9715 major chronic disease events occurred, including 3639 cardiovascular disease events, 4690 cancers, and 1386 deaths from other causes. Results:After multivariable adjustment, neither fish nor dietary n−3 fatty acid consumption was significantly associated with risk of total major chronic disease. Compared with fish consumption of <1 serving/mo, consumption of 1 serving/wk and of 2–4 servings/wk was associated with a lower risk of total cardiovascular disease of ≈15%. No significant associations were seen with cancer risk. Higher or lower n−6 fatty acid intake did not significantly modify the results (P for interaction > 0.10). Conclusions:Modest fish consumption was associated with a lower risk of total cardiovascular disease, consistent with cardiac mortality benefits but not with total cancer or overall major chronic disease; n−6 fatty acid consumption did not influence these relations.

Periodontal diseases and cancer

Chronic periodontitis and aggressive periodontitis are inflammatory forms of periodontal disease (figure) caused by microorganisms from plaque biofilm that forms around the teeth. Chronic inflammation of the periodontium results in continuous release of cytokines, prostaglandins, bacterial toxins, and many other destructive enzymes from cells in the area. This chronic process leads to formation of periodontal pockets and progressive destruction of connective tissue and alveolar bone. 1 Pihlstrom B Michalowicz B Johnson N Periodontal diseases. Lancet. 2005; 366: 1809-1820 Summary Full Text Full Text PDF PubMed Scopus (2535) Google Scholar Chronic periodontitis and aggressive periodontitis are the most common causes of tooth loss in adults. Many studies have shown an association between periodontal diseases and systemic manifestations of cardiovascular disease, diabetes, and premature low-weight birth. 1 Pihlstrom B Michalowicz B Johnson N Periodontal diseases. Lancet. 2005; 366: 1809-1820 Summary Full Text Full Text PDF PubMed Scopus (2535) Google Scholar However, there is no evidence for a causal effect. A recent study assessed periodontitis and premature death in young adults in urban regions of Sweden. 2 Söder B Jin L Klinge B Söder P Periodontitis and premature death: a 16-year longitudinal study in a Swedish urban population. J Periodontal Res. 2007; 42: 361-366 Crossref PubMed Scopus (49) Google Scholar The findings showed that young individuals with periodontitis and missing molar teeth, compared with those with no periodontitis, had increased risk of premature death because of cancer, circulatory, and digestive diseases. In this issue of The Lancet Oncology, Michaud and colleagues 3 Michaud DS Liu Y Meyer M Giovannucci E Joshipura K Periodontal disease, tooth loss, and cancer risk in male health professionals: a prospective cohort study. Lancet Oncol. 2008; 9: 550-558 Summary Full Text Full Text PDF PubMed Scopus (261) Google Scholar present important data from a prospective study that shows an increase in cancer risk in a large population of well-characterised US male health professionals who self-reported having periodontal disease with alveolar bone loss. Their findings showed a significant association between periodontal disease and haematological, kidney, and pancreatic cancer. The cancer risk persisted in individuals who never smoked. In a previous study, 4 Michaud D Joshipura K Giovannucci E Fuchs C A prospective study of periodontal disease and pancreatic cancer in US male health professionals. J Natl Cancer Inst. 2007; 99: 171-175 Crossref PubMed Scopus (205) Google Scholar Michaud and co-workers suggested an association between periodontal disease and pancreatic cancer in the same population of health professionals. They concluded that plausible biological mechanisms, such as systemic inflammation or increased concentrations of carcinogenic compounds (or both) as a result of bacteria in the oral cavity of those with periodontal disease, could be involved in the development of cancer. Furthermore, a recent case–control study suggested that chronic periodontitis is associated with increased risk of developing tongue cancer. 5 Tezal M Sullivan M Reid M et al. Chronic periodontitis and the risk of tongue cancer. Arch Otolaryngol Head Neck Surg. 2007; 133: 450-454 Crossref PubMed Scopus (130) Google Scholar However, other researchers believe that the association between periodontal disease and cancer might be spurious. 6 Hujoel P Drangsholt M Spiekerman C Weiss N An exploration of the periodontitis-cancer association. Ann Epidemiol. 2003; 13: 312-316 Summary Full Text Full Text PDF PubMed Scopus (192) Google Scholar Therefore, future studies that assess in more detail potential mechanisms for the association between periodontal diseases and cancer are warranted. (A) Diagnosis should include clinical presentation, periodontal pocket probings, and radiographical assessment of bone levels. Note that the gingival tissues are red and swollen, and the level of the gingival margins is irregular. (B) Radiograph of top teeth shows only the tips of the roots inserted in alveolar bone (arrow). Periodontal disease, tooth loss, and cancer risk in male health professionals: a prospective cohort studyPeriodontal disease was associated with a small, but significant, increase in overall cancer risk, which persisted in never-smokers. The associations recorded for lung cancer are probably because of residual confounding by smoking. The increased risks noted for haematological, kidney, and pancreatic cancers need confirmation, but suggest that periodontal disease might be a marker of a susceptible immune system or might directly affect cancer risk. Full-Text PDF

Smoking Increases the Incidence of Tooth Loss and Smoking Cessation Reduces it

Tobacco use and incidence of tooth loss among US male health professionals Dietrich T, Maserejian NN, Joshipura KJ, Krall EA, Garcia RI. J Dent Res 2007;86(4):373-7 B The authors evaluated the associations between the use of various tobacco products (cigarettes, pipes, cigars, or chewing tobacco) and the incidence of tooth loss. The study also investigated the association between cessation of cigarette smoking and the incidence of tooth loss. Government Prospective Cohort Study

Periodontal disease, tooth loss, and cancer risk in male health professionals: a prospective cohort study

Studies suggest that tooth loss and periodontal disease might increase the risk of developing various cancers; however, smoking might have confounded the reported associations. We aimed to assess whether periodontal disease or tooth loss is associated with cancer risk. The analysis was done in a prospective study (the Health Professionals Follow-Up Study [HPFS]), which was initiated in 1986 when US male health professionals aged 40-75 years responded to questionnaires posted by the Department of Nutrition, Harvard University School of Public Health, Boston, MA, USA. In addition to the baseline questionnaires, follow-up questionnaires were posted to all living participants every 2 years and dietary questionnaires every 4 years. At baseline, participants were asked whether they had a history of periodontal disease with bone loss. Participants also reported number of natural teeth at baseline and any tooth loss during the previous 2 years was reported on the follow-up questionnaires. Smoking status and history of smoking were obtained at baseline and in all subsequent questionnaires. Additionally at baseline, participants reported their mean frequency of food intake over the previous year on a 131-item semiquantitative food-frequency questionnaire. Participants reported any new cancer diagnosis on the follow-up questionnaires. Endpoints for this study were risk of total cancer and individual cancers with more than 100 cases. Multivariate hazard ratios (HRs) and 95% CIs were calculated by use of Cox proportional hazard models according to periodontal disease status and number of teeth at baseline. In the main analyses, 48 375 men with median follow-up of 17.7 years (1986 to Jan 31, 2004) were eligible after excluding participants diagnosed with cancer before 1986 (other than non-melanoma skin cancer, n=2076) and those with missing data on periodontal disease (n=1078). 5720 incident cancer cases were documented (excluding non-melanoma skin cancer and non-aggressive prostate cancer). The five most common cancers were colorectal (n=1043), melanoma of the skin (n=698), lung (n=678), bladder (n=543), and advanced prostate (n=541). After adjusting for known risk factors, including detailed smoking history and dietary factors, participants with a history of periodontal disease had an increased risk of total cancer (HR 1.14 [95% CI 1.07-1.22]) compared with those with no history of periodontal disease. By cancer site, significant associations for those with a history of periodontal disease were noted for lung (1.36 [1.15-1.60]), kidney (1.49 [1.12-1.97]), pancreas (1.54 [1.16-2.04]; findings previously published), and haematological cancers (1.30 [1.11-1.53]). Fewer teeth at baseline (0-16) was associated with an increase in risk of lung cancer (1.70 [1.37-2.11]) for those with 0-16 teeth versus those with 25-32 teeth. In never-smokers, periodontal disease was associated with significant increases in total (1.21 [1.06-1.39]) and haematological cancers (1.35 [1.01-1.81]). By contrast, no association was noted for lung cancer (0.96 [0.46-1.98]). Periodontal disease was associated with a small, but significant, increase in overall cancer risk, which persisted in never-smokers. The associations recorded for lung cancer are probably because of residual confounding by smoking. The increased risks noted for haematological, kidney, and pancreatic cancers need confirmation, but suggest that periodontal disease might be a marker of a susceptible immune system or might directly affect cancer risk.

Tobacco use and incidence of tooth loss among US male health professionals

Tobacco use and incidence of tooth loss among US male health professionals

Complement factor H (Y402H) polymorphism and risk of coronary heart disease in US men and women

Complement factor H (CFH) Y402H polymorphism is located in a region that binds C-reactive protein and may affect inflammatory processes and risk of coronary heart disease (CHD). We assessed the association between Y402H and risk of CHD in nested case-control studies among two large prospective cohorts of US male health professionals and female nurses. Among participants who were disease-free at baseline, we confirmed 266 (men) and 249 (women) incident CHD deaths and non-fatal myocardial infarctions (MIs) over 6 and 8 years of follow-up, respectively. Using risk-set sampling, controls were matched 2:1 on the basis of age, smoking, and date of blood draw. Comparing homozygous HH with YY, the relative risk (RR) of CHD was 0.94 [95% confidence interval (CI) 0.59-1.49] among men and 0.51 (95% CI 0.29-0.89) among women (pooled RR 0.73, 95% CI 0.51-1.04). The HH genotype was inversely associated with CHD among those <65 years at onset (men: RR 0.39, 95% CI 0.16-0.95; women: 0.21, 95% CI 0.07-0.65; pooled: 0.30, 95% CI 0.15-0.61), but not among those > or =65 years (pooled RR 1.09, 95% CI 0.71-1.68). CFH Y402H was inversely associated with CHD among women, but not men. This inverse association was observed in both populations with earlier age of CHD.

Re: A Prospective Study of Periodontal Disease and Pancreatic Cancer in US Male Health Professionals

Re: A Prospective Study of Periodontal Disease and Pancreatic Cancer in US Male Health Professionals

Response: Re: A Prospective Study of Periodontal Disease and Pancreatic Cancer in US Male Health Professionals

Response: Re: A Prospective Study of Periodontal Disease and Pancreatic Cancer in US Male Health Professionals

Tobacco Use and Incidence of Tooth Loss among US Male Health Professionals

Data on the dose-dependent effects of smoking and smoking cessation on tooth loss are scarce. We hypothesized that smoking has both dose- and time-dependent effects on tooth loss incidence. We used longitudinal data on tobacco use and incident tooth loss in 43,112 male health professionals, between 1986 and 2002. In multivariate Cox models, current smokers of 5 to 14 and 45+ cigarettes daily had a two-fold (HR, 1.94; 95% CI, 1.72, 2.18) and three-fold (HR, 3.05; 95% CI, 2.38, 3.90) higher risk of tooth loss, respectively, compared with never-smokers. Risk decreased with increasing time since cessation, but remained elevated by 20% (95% CI, 16%, 25%) for men who had quit 10+ years before. Current pipe/cigar smokers had a 20% (95% CI, 1.11, 1.30) increased risk of tooth loss compared with never- and former smokers of pipes/cigars.