Relation between Psychosocial Risk Factors and Incident Erectile Dysfunction: Prospective Results from the Massachusetts Male Aging Study

Andre B. Araujo, Catherine B. Johannes, Henry A. Feldman, Carol A. Derby and John B. McKinlay

From the New England Research Institutes, Watertown, MA.


    ABSTRACT
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Erectile dysfunction (ED) is recognized as a major public health problem. ED may be due to a wide range of factors, but recent work has focused on the medical and physical etiology of ED. The importance of psychosocial risk factors should not be dismissed, however, and several cross-sectional studies have reported associations between ED and depression, anger, and dominance. Whether these factors are prospectively associated with the risk of ED has yet to be established. Longitudinal data obtained from 776 respondents in the Massachusetts Male Aging Study (1987–1997) were used to examine whether the presence of depressive symptoms, the way in which anger was expressed, or the trait of dominance independently contributed to the risk of ED 8.8 years later. The results suggest that new cases of ED are much more likely to occur among men who exhibit a submissive personality. The implications of these findings are discussed. Am J Epidemiol 2000;152:533–41.

aging; anger; depression; dominance-subordination; impotence; incidence; longitudinal studies; psychology

Abbreviations: CES-D, Center for Epidemiologic Studies Depression [Scale]; ED, erectile dysfunction


    INTRODUCTION
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Erectile dysfunction (ED) is the consistent inability to attain and maintain a penile erection sufficient for satisfactory sexual performance (1Go). ED is widespread and was recently recognized as a major public health problem by a National Institutes of Health consensus development panel (1Go). Results from the National Health and Social Life Survey indicate that 10.4 percent of men aged 18–59 years report having had trouble achieving or maintaining an erection over the past 12 months (2Go). Nationwide projections from the Massachusetts Male Aging Study suggest that ED could affect up to 18 million men (3Go). Data from the National Ambulatory Medical Care Survey indicate that there were 1.3 million office visits for ED in the United States in 1996 (4Go). Worldwide projections from the Massachusetts Male Aging Study suggest that there will be 170 million more men aged 40–79 years with ED in 2025 than there were in 1995, assuming that the natural history of the condition does not change (5Go).

Although ED was once thought to be primarily a condition of psychogenic origin, recent work suggests that medical or physical influences may be of greater import. ED may be related to a wide range of factors, including age (6Go), smoking (7Go, 8Go), side effects of therapeutic agents (especially antihypertensive and antidepressant medications) (9Go, 10Go), atherogenesis (11GoGoGo–14Go), or neuropathy of diabetic (15Go, 16Go), surgical (17Go), or other origin (e.g., bicycling) (18Go). However, the importance of psychosocial risk factors for ED should not be dismissed. Several cross-sectional studies have reported an association between ED and depression (19GoGo–21Go), anger (3Go, 22Go), and the personality trait of dominance (3Go). Whether these factors are prospectively associated with the risk of ED has yet to be established. Thus, the purpose of this investigation was to use longitudinal data from the Massachusetts Male Aging Study to examine whether depressive symptoms, anger expression, or dominance independently contribute to the risk of ED after other established ED risk factors are taken into account.


    MATERIALS AND METHODS
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Study sample
The Massachusetts Male Aging Study is a prospective observational study of health in randomly selected men. The study design has been well described elsewhere (23Go, 24Go). Of 3,258 eligible respondents, 1,709 completed the baseline in-home protocol. The low response rate (52 percent) reflected in part the requirements for early morning phlebotomy and an intensive in-person interview in a population-based sample.

The follow-up phase of the Massachusetts Male Aging Study was conducted from 1995 to 1997 (average follow-up interval = 8.8 years). During this phase, men who were alive, had not moved out of the country, and were not seriously ill were eligible for interview. Of the original 1,709 respondents to the baseline survey, 180 were confirmed to be deceased, five were residing outside of the United States, and 28 were seriously ill, which left 1,496 men eligible for the follow-up interview. Of these 1,496 eligible men, 1,156 completed a follow-up interview (a follow-up response rate of 77 percent).

Measures used
The field protocol for the Massachusetts Male Aging Study has been previously described (23Go, 24Go). Briefly, a trained field technician/phlebotomist visited each subject in his home, administered a health questionnaire and psychological assessment instruments, and obtained two nonfasting blood samples. Height, weight, and blood pressure (two measurements) were measured according to standard research protocols developed for large scale fieldwork (25Go). Age, education, income level, and marital and employment status were noted. This study received institutional review board approval, and written informed consent was given by all study participants.

The presence of medical conditions, including heart disease, diabetes mellitus, and hypertension, was ascertained through self-report. The field technician inventoried all current prescription and nonprescription medications, noting the subject's stated reason for use of each. Medications were then coded according to the American Hospital Formulary Service classification (26Go).

Main outcome variable: incident ED.
A self-administered questionnaire on sexual activity was given to each subject for completion in private. The questionnaire was then returned to the interviewer in a sealed envelope. The baseline sexual activity questionnaire included questions related to erectile function, but it concentrated on specific items (e.g., frequency and quality of erections) rather than on the global subjective self-assessment which later became the method of choice in this field of research (1Go). The follow-up questionnaire included the specific items related to erectile function plus an additional single-question global subjective self-assessment whereby men classified themselves into one of four levels of ED: none, minimal, moderate, or complete.

To maintain a consistent definition of ED status at baseline and follow-up, discriminant analysis was applied to the follow-up data to assess the relation between the specific responses and the global self-assessment (27Go). This resulted in functions that determined the probability that an individual with a given set of responses would fall into a particular ED category. Once the functions were constructed, they were applied to both baseline and follow-up questionnaires, and subjects were then assigned to the category of ED for which they had the greatest probability of membership. The four-category ED status variable was dichotomized into absence or presence of ED, the latter defined as moderate or complete ED. New cases of ED were those identified as cases of moderate or complete ED at follow-up among men who were free of ED at baseline.

Baseline psychosocial risk factors for incident ED.
Baseline depressive symptomatology was measured using the Center for Epidemiologic Studies Depression (CES-D) Scale (28Go). This instrument measures current levels of depressive symptomatology in community populations and does not indicate a diagnosis of clinical depression. Scores can range from 0 to 60, with higher scores indicating more depressive symptomatology. For the present analysis, the presence of depressive symptomatology was indicated by a score greater than or equal to 16 on the CES-D Scale (29Go).

Dominance was measured using the Jackson dominance scale, a subscale of the Jackson Personality Research Form E (30Go). This scale consists of 16 items regarding the frequency of attempts to control one's environment, influence others, and express opinions forcefully. The response set for this scale includes "false," "true," and "don't know," coded as 0, 1, and 0.5, respectively. Scores can range from 0 to 16, with higher scores indicating a higher degree of dominance. For the present analysis, dominance was measured at baseline and was categorized into tertiles (low dominance (a score of 0–9), moderate dominance (9.5–12.5), and high dominance (13–16)).

The Anger-In and Anger-Out subscales of the Spielberger Anger Expression Scale (31Go) were used to measure the frequency with which anger was experienced but not expressed (Anger-In) and expressed (Anger-Out). Each subscale consists of eight questions pertaining to feelings of anger, addressing how often the subject generally reacts or behaves in the manner described. Each item is scored from 1 ("almost never") to 4 ("almost always"). Scores for each subscale can range from 8 to 32, with higher scores indicating a tendency to experience but not express anger (Anger-In) and a tendency to express oneself when angry (Anger-Out). For the present analysis, each subscale was administered at baseline, and scores were then categorized into tertiles (low Anger-In (a score of 7–13), moderate Anger-In (14–16), and high Anger-In (17–29) and low Anger-Out (8–12), moderate Anger-Out (13–14), and high Anger-Out (15–25)).

Other baseline risk factors for incident ED.
ED classification at baseline was categorized as none or minimal. Overweight was defined as a body mass index (weight (kg)/height (m)2) of 27.8 or more (32Go). Physical activity was estimated from recall of the past 7 days' activities (both work-related and leisure), including frequency and duration. Sedentary behavior was indicated when a subject's energy expenditure was less than 200 kcal/day, aligning with the recent recommendation from the Centers for Disease Control and Prevention and the American College of Sports Medicine that individuals accumulate at least 30 minutes of moderate-intensity physical activity per day (33Go). Subjects' customary alcohol intake was estimated by self-report of beer, wine, and liquor consumption, accounting for frequency, quantity, and binge drinking using the formula of Khavari and Farber (34Go).

Exposure to cigarette smoke was ascertained through self-report. Subjects were classified as unexposed, passively exposed to smoke in the home, and actively exposed (35Go). Nutritional intake was measured using the semiquantitative 1-year food frequency questionnaire of Willett et al. (36Go). A high fat diet was indicated when a subject obtained more than 30 percent of his calories from fat (37Go). Hypertension at baseline was indicated if one or more of the following four conditions were met: 1) the subject reported being treated for high blood pressure; 2) an inventory of medications revealed use of antihypertensive medication; 3) the subject's systolic blood pressure (second reading) was greater than or equal to 140 mmHg (38Go); or 4) the subject's diastolic blood pressure (second reading) was greater than or equal to 90 mmHg (38Go).

Nonfasting blood samples were drawn from the antecubital space within 4 hours of the subject's awakening, to control for diurnal variation in hormone levels (Go). Blood was kept in an ice-cooled container for transport and was centrifuged within 6 hours. Serum was stored in 5-ml scintillation vials at -20°C, shipped to the laboratory within 1 week by same-day courier, and stored at -70°C until the time of assay. One tube of blood was taken for lipid assays (conducted at Miriam Hospital in Providence, Rhode Island). Total cholesterol was measured by standard techniques (40Go). High blood cholesterol in this analysis was defined as a blood cholesterol level greater than or equal to 200 mg/dl (37Go). Two additional tubes of blood were drawn for hormone assays (conducted at the University of Massachusetts in Worcester, Massachusetts). These tubes of blood were drawn 30 minutes apart, and serum was pooled for analysis in equal aliquots in order to smooth out episodic secretion (41Go). Total testosterone level was measured by radioimmunoassay (42Go).

Follow-up characteristics.
Age at follow-up was treated as a three-category variable (<60, 60–69, and >=70 years). Follow-up total testosterone level (ng/dl) and antihypertensive medication use were tested as mediators of the relation between psychosocial risk factors and ED, based on their potential concurrent influence on ED.

Statistical analysis
The relation of psychosocial and other risk factors and follow-up characteristics to risk of ED was evaluated using simple and multiple logistic regression.

Analysis sample
Of the 1,156 men interviewed at follow-up, 125 failed to provide sufficient sexual activity data and were not assigned an ED scoring. To determine the sample at risk for developing ED, we excluded 184 men who either were missing information on baseline ED status or had moderate or complete ED at baseline. This left 847 men at risk of developing ED. Thirteen men who had undergone radical prostatectomy between the baseline and follow-up phases of the Massachusetts Male Aging Study were excluded, because of the strong association of this procedure with ED. In addition, we excluded 21 men who reported having diabetes or using related medications at baseline and 35 men who reported having heart disease or using related medications at baseline. After these exclusions, 778 men remained eligible for the analysis sample. Two men who were missing data on smoking status were excluded from the final regression model.

The exclusion of men with diabetes or heart disease at baseline was based on results indicating potential effect modification of the ED-dominance relation in these groups. In men with diabetes or use of related medications at baseline (n = 21), the percentage of men with ED increased with increasing dominance scores. By contrast, in men without diabetes, the percentage of men with ED decreased as dominance scores increased. In men with heart disease or use of related medications (n = 37; two of the 21 men with diabetes also had heart disease), an identical pattern emerged. Thus, including these groups in the analysis sample could have distorted the relation between ED and dominance. Stratification according to heart disease and diabetes was not possible because of small sample sizes in both groups; thus, men with heart disease or diabetes at baseline were excluded from the analysis sample.


    RESULTS
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Selected characteristics of the baseline, follow-up, and analysis samples of the Massachusetts Male Aging Study are displayed in table 1. This allows for inspection of how the distribution of variables might have changed from baseline to follow-up to analysis sample, such that assessment of the effects of attrition and exclusion of select groups becomes possible. Equal percentages of respondents in their 40s, 50s, and 60s were interviewed. The cohort was predominantly White, married, and employed and had engaged in study beyond high school. Twenty percent reported a household income greater than $80,000 per year.


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TABLE 1. Selected characteristics of respondents in the Massachusetts Male Aging Study, Boston, Massachusetts, 1987–1997

 
Also presented in table 1 are the distributions of ED risk factors measured at baseline. In the analysis sample, 71 percent of the men had no baseline ED, while 30 percent had minimal ED. Twenty-eight percent were hypertensive. Twenty-six percent were active cigarette smokers, and 14 percent reported passive exposure to cigarette smoke at home. Thirty-five percent of the men were overweight (body mass index >=27.8), and 30 percent exhibited sedentary behavior. Half of the sample consumed less than one alcoholic beverage per day. Over half of the sample had a diet high in fat (62 percent) and high blood cholesterol (54 percent). At follow-up, the mean age was 61 years (not shown) and the mean serum testosterone level was 461.1 ng/dl; 22 percent of the men were using antihypertensive medication.

Overall, 163 of the 778 men in the analysis sample (21 percent) were classified as having moderate or complete ED at follow-up. The distributions of the main psychosocial risk factors and outcome are presented in table 1. The prevalence of depressive symptoms (CES-D score >=16) in the analysis sample was 9 percent at baseline; the mean baseline CES-D score was 5.81 (not shown). Mean baseline scores for dominance, Anger-In, and Anger-Out were 10.51, 14.81, and 13.73, respectively (not shown).

The analysis sample was similar to the baseline and follow-up samples with regard to most study variables presented, most notably with respect to the main predictors of interest. Small differences between samples were observed with respect to ED, age, education, income, high blood pressure, and cigarette smoke exposure.

The occurrence of ED at follow-up according to the baseline psychosocial risk factors is presented in table 2. The presence of depressive symptoms at baseline was not a significant predictor of incident ED (p = 0.12). The percentage of persons developing ED was actually lower in men with baseline depressive symptoms than in those without them (13.2 percent vs. 21.3 percent). The percentage of men with new ED tended to decrease as baseline dominance score increased (p < 0.001), falling from 30.1 percent among those with low dominance scores to 16.4 percent and 15.4 percent among those with moderate and high scores, respectively. Neither baseline Anger-In nor baseline Anger-Out was a significant predictor of ED at the bivariate level (p > 0.50).


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TABLE 2. Bivariate (or unadjusted) association of baseline psychosocial risk factors with erectile dysfunction during the follow-up phase (n = 778*) of the Massachusetts Male Aging Study, Boston, Massachusetts, 1987–1997

 
Table 3 summarizes how baseline ED risk factors and follow-up characteristics related to ED. Baseline ED (none or minimal) (p < 0.001), hypertension (p < 0.001), cigarette smoke exposure (p = 0.01), overweight (p = 0.01), and a high fat diet (p = 0.03) were associated with incident ED, as were follow-up age (p < 0.001), serum testosterone level (p = 0.001), and antihypertensive medication use (p < 0.001).


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TABLE 3. Bivariate (or unadjusted) association of baseline cardiovascular risk factors with erectile dysfunction (ED), controlled for baseline ED risk factors, during the follow-up phase (n = 778*) of the Massachusetts Male Aging Study, Boston, Massachusetts, 1987–1997

 
Results of the multiple regression analysis are shown in table 4. Depressive symptoms, Anger-In, and Anger-Out failed to attain statistical significance at the bivariate level and thus were omitted from the final logistic regression model. High fat diet was not included in the final model, since it failed to attain statistical significance in multivariate models and data were missing for numerous (n = 71) subjects. Neither follow-up antihypertensive medication use nor testosterone level emerged as a mediator of the relation between dominance and ED; thus, both factors were removed from the final model. Dominance remained strongly predictive of incident ED (p = 0.002) after data were controlled for baseline ED, hypertension, exposure to cigarette smoke, overweight, and follow-up age. A twofold reduction in risk of ED was noted among men with moderate or high levels of dominance relative to those with low levels of dominance (for moderate levels, odds ratio = 0.47 (95 percent confidence interval: 0.29, 0.76); for high levels, odds ratio = 0.53 (95 percent confidence interval: 0.34, 0.82)).


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TABLE 4. Multivariate (or adjusted) association of baseline dominance with erectile dysfunction (ED), controlled for baseline ED risk factors, during the follow-up phase (n = 776*) of the Massachusetts Male Aging Study, Boston, Massachusetts, 1987–1997

 

    DISCUSSION
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Although most of the current epidemiologic and clinical work in the area of ED concentrates on the effects of medical or physical variables, psychosocial factors have been shown to be strongly correlated with ED in numerous cross-sectional studies. This investigation sought to determine whether baseline psychosocial risk factors could predict new cases of ED 8.8 years later. The results suggest that subjects' level of dominance plays an important role in the 8.8-year incidence of ED, independent of other important ED risk factors. New cases of ED were much more likely to appear in men who exhibited a submissive personality.

In interpreting these findings, some limitations of the study should be noted. It is possible that dominant men respond differently to questions about sexual function, and thus the findings could be partly due to self-reporting bias. Another limitation is the extent to which the analysis sample differed from the original baseline sample, restricting the generalizability of the results. Furthermore, a number of subjects with baseline diabetes or heart disease were excluded from the analysis sample on the basis of results indicating possible effect modification of the ED-dominance relation in these groups. However, these exclusions were not related to the main predictors of interest (see table 1), and thus the chance that bias was introduced by these exclusions is minimal. Despite these limitations, we believe that the results of this study are important in that no other studies (to our knowledge) have examined the prospective relation between psychosocial risk factors and ED.

The risk of ED in this sample was inversely related to subjects' level of dominance. Men scoring moderate or high in dominance were approximately two times less likely to develop ED at follow-up than men with low dominance scores; this finding is in line with previous cross-sectional findings from the Massachusetts Male Aging Study in terms of magnitude, strength, and direction (3Go). We know of no other study that has examined dominance in relation to ED. However, dominance has been studied in relation to various other health outcomes. Contrary to the findings presented herein, dominance has been positively related to such outcomes as peripheral atherosclerotic disease (43Go), coronary artery disease (44Go), cardiovascular reactivity (45Go), and mortality (46Go). On the other hand, research has also shown dominant individuals to be at lower risk for poor health outcomes (47Go, 48Go).

Hamm et al. (48Go) suggested that the mechanism for dominance may be a function of the long term stress experienced by submissive individuals in response to stressful circumstances; dominant individuals presumably respond better. This stress may lead to neurocardiovascular changes (e.g., transient increases in cardiac output, damaging cardiac arteries directly or indirectly via the release of catecholamines into the bloodstream, and chronic activation of the autonomic nervous system) which may increase susceptibility to coronary artery atherosclerosis (49Go). Given that some have heralded ED as a possible sentinel for subclinical cardiovascular disease (13Go, 14Go, 50Go), a similar physiologic mechanism may explain the prospective relation between ED and dominance. That is, this association may be due to submissive individuals' inability to cope with stress, resulting in neurocardiovascular changes that could play a role in their subsequent development of ED. If a submissive behavioral tendency is a contributing factor in the etiology of ED, psychosocial or behavioral counseling addressing this issue might be useful, especially in men for whom treatment with Viagra (Pfizer, Inc., New York, New York) (51Go) is contraindicated, such as those taking cardiac drugs (52Go).

Neither Anger-In nor Anger-Out predicted incident ED in this sample. In previous studies, the prevalence of ED has been shown to be associated with anger. Bozman and Beck (22Go) found that penile tumescence was lower when a man was in an angry condition than when he was in a controlled condition. In the baseline phase of the Massachusetts Male Aging Study, anger suppression and anger expression were both positively correlated with ED (3Go). Given the lack of a prospective relation between ED and anger, it is possible that the effects of anger are more short-lived. The literature on the relation between anger and cardiovascular disease supports this possibility, since anger may be associated only with transient risk of myocardial infarction (53Go).

The presence of depressive symptoms was not associated with new cases of ED in this study sample. This finding could be explained in three different ways. First, depression may not be a cause of ED. If this were true, the previously demonstrated cross-sectional association of ED with depression might indicate either that ED causes depression or that the two conditions coexist simultaneously. Second, it may not be a preponderance of depressive symptoms that leads to ED but rather the more endogenous and severe forms of depression. If this were so, the measure of depressive symptoms in this study would be inadequate to detect an association with ED. Third, it could be that the presence of depressive symptoms is not a long term risk factor for ED. In other words, the effect that depressive symptoms have on ED may be transient, lasting only while someone is in the depressed state. This would have been undetectable in the current study, given the length of follow-up. Conversely, major depression may be more longstanding, affecting the autonomic nervous system, increasing vagal and sympathetic tone and platelet aggregability, and leading to poor adherence to medical regimens (31Go, 54Go). Thus, it is possible that only these chronic effects of major depression are associated with ED over the long term.

The question of whether ED leads to depression, depression leads to ED, or each affects the other is of great interest to the urologic community and remains unresolved. Despite the longitudinal nature of these data, we were unable to clarify this issue. A study including both clinical measures of depression and epidemiologic measures of depressive symptoms evaluated at repeated, regular intervals would be able to address the question more rigorously.


    ACKNOWLEDGMENTS
 
This work was supported by grant AG 04673 from the National Institute on Aging and by grants DK 44995 and DK 51345 from the National Institute of Diabetes and Digestive and Kidney Diseases.


    NOTES
 
Reprint requests to Andre B. Araujo, New England Research Institutes, 9 Galen Street, Watertown, MA 02472 (e-mail: AndreA{at}neri.org).


    REFERENCES
 TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

  1. NIH Consensus Panel on Impotence. Impotence. JAMA 1993;270:83–90.
  2. Laumann EO, Gagnon JH, Michael RT, et al. The social organization of sexuality: sexual practices in the United States. Chicago, IL: University of Chicago Press, 1994.
  3. Feldman HA, Goldstein I, Hatzichristou DG, et al. Impotence and its medical and psychosocial correlates: results of the Massachusetts Male Aging Study. J Urol 1994;151:54–61.[ISI][Medline]
  4. National Center for Health Statistics. 1996 National Ambulatory Medical Care Survey. (CD-ROM series 13, no. 14, SETS version 2.0 (beta)). Hyattsville, MD: National Center for Health Statistics, 1998.
  5. Aytaç IA, McKinlay JB, Krane RJ. The likely worldwide increase in erectile dysfunction between 1995 and 2025 and some possible policy consequences. Br J Urol 1999;84:50–6.
  6. Jønler M, Moon T, Brannan W, et al. The effect of age, ethnicity and geographical location on impotence and quality of life. Br J Urol 1995;75:651–5.[ISI][Medline]
  7. Mannino DM, Klevens RM, Flanders WD. Cigarette smoking: an independent risk factor for impotence? Am J Epidemiol 1994;140:1003–8.[Abstract]
  8. Rosen MP, Greenfield AJ, Walker TG, et al. Cigarette smoking: an independent risk factor for atherosclerosis in the hypogastric-cavernous arterial bed of men with arteriogenic impotence. J Urol 1991;145:759–63.[ISI][Medline]
  9. Wein AJ, Van Arsdalen KN. Drug-induced male sexual dysfunction. Urol Clin North Am 1988;15:23–31.[ISI][Medline]
  10. Weiss RJ. Effects of antihypertensive agents on sexual function. Am Fam Physician 1991;44:2075–82.[ISI][Medline]
  11. Rosen MP, Greenfield AJ, Walker TG, et al. Arteriogenic impotence: findings in 195 impotent men examined with selective internal pudendal angiography. Radiology 1990;174:1043–8.[Abstract]
  12. Greenstein A, Chen J, Miller H, et al. Does severity of ischemic coronary disease correlate with erectile function? Int J Impot Res 1997;9:123–6.[ISI][Medline]
  13. Michal V. Arterial disease as a cause of impotence. Clin Endocrinol Metab 1982;11:725–48.[ISI][Medline]
  14. Morley JE, Korenman SG, Kaiser FE, et al. Relationship of penile brachial pressure index to myocardial infarction and cerebrovascular accidents in older men. Am J Med 1988;84:445–8.[ISI][Medline]
  15. Klein R, Klein BE, Lee KE, et al. Prevalence of self-reported erectile dysfunction in people with long-term IDDM. Diabetes Care 1996;19:135–41.[Abstract]
  16. Shabsigh R, Fishman IJ, Schum C, et al. Cigarette smoking and other vascular risk factors in vasculogenic impotence. Urology 1991;38:227–31.[ISI][Medline]
  17. Benet AE, Melman A. The epidemiology of erectile dysfunction. Urol Clin North Am 1995;22:699–709.[ISI][Medline]
  18. Salimpour P, Doursounian M, Cantey-Kier J, et al. Sexual and urinary tract dysfunctions in bicyclists. (Abstract). J Urol 1998;159S:30.
  19. Araujo AB, Durante R, Feldman HA, et al. The relationship between depressive symptoms and male erectile dysfunction: cross-sectional results from the Massachusetts Male Aging Study. Psychosom Med 1998;60:458–65.[Abstract]
  20. Laumann EO, Paik A, Rosen RC. Sexual dysfunction in the United States: prevalence and predictors. JAMA 1999;281:537–44.[Abstract/Free Full Text]
  21. Shabsigh R, Klein LT, Seidman S, et al. Increased incidence of depressive symptoms in men with erectile dysfunction. Urology 1998;52:848–52.[ISI][Medline]
  22. Bozman AW, Beck JG. Covariation of sexual desire and sexual arousal: the effects of anger and anxiety. Arch Sex Behav 1991;20:47–60.[ISI][Medline]
  23. McKinlay JB, Feldman HA. Age-related variation in sexual activity and interest in normal men: results from the Massachusetts Male Aging Study. In: Rossi AS ed. Sexuality across the life course: proceedings of the MacArthur Foundation Research Network on Successful Mid-Life Development, 1992. New York, NY: University of Chicago Press, 1994:261–85.
  24. McKinlay JB, Longcope C, Gray A. The questionable physiologic and epidemiologic basis for a male climacteric syndrome: preliminary analysis from the Massachusetts Male Aging Study. Maturitas 1989;11:103–15.[ISI][Medline]
  25. McKinlay SM, Kipp DM, Johnson P, et al. A field approach for obtaining physiological measures in surveys of general populations: response rates, reliability, and costs. In: Proceedings of the fourth conference on health survey research methods. Washington, DC: US Public Health Service, 1984:195–204. (DHHS publication no. (PHS) 84-3346).
  26. McEvoy GK. American Hospital Formulary Service drug information. Bethesda, MD: American Society of Hospital Pharmacists, 1989.
  27. Kleinman KP, Feldman HA, Johannes CB, et al. A new surrogate variable for erectile dysfunction status in the Massachusetts Male Aging Study. J Clin Epidemiol 2000;53:71–8.[ISI][Medline]
  28. Radloff LS. The CES-D Scale: a self-report depression scale for research in the general population. Appl Psychol Meas 1977;1:385–401.
  29. Comstock GW, Helsing KJ. Symptoms of depression in two communities. Psychol Med 1976;6:551–64.[ISI][Medline]
  30. Jackson DN. Personality Research Form manual. Post Huron, MI: Sigma Assessment Systems, Inc., 1989.
  31. Spielberger CD, Johnson EH, Russell SF, et al. The experience and expression of anger: construction and validation of an anger expression scale. In: Chesney MA, Rosenman RH, eds. Anger and hostility in cardiovascular and behavioral disorders. New York, NY: McGraw-Hill Publishing Corporation, 1985:5–30.
  32. National Center for Health Statistics. Health, United States, 1998—with socioeconomic status and health chartbook. Hyattsville, MD: National Center for Health Statistics, 1998.
  33. Pate RR, Pratt M, Blair SN, et al. Physical activity and public health: a recommendation from the Centers for Disease Control and Prevention and the American College of Sports Medicine. JAMA 1995;273:402–7.[Abstract]
  34. Khavari KA, Farber PD. A profile instrument for the quantification and assessment of alcohol consumption. J Stud Alc 1978;39:1525–39.[ISI][Medline]
  35. Howard G, Wagneknecht LE, Burke GL, et al. Cigarette smoking and progression of atherosclerosis: The Atherosclerosis Risk in Communities (ARIC) Study. JAMA 1998;279:119–24.[Abstract/Free Full Text]
  36. Willett WC, Reynolds RO, Cottrell-Hoehner S, et al. Validation of a semi-quantitative food frequency questionnaire: comparison with a 1-year diet record. J Am Diet Assoc 1987;87:43–7.[ISI][Medline]
  37. National Cholesterol Education Program. Report of the Expert Panel on Population Strategies for Blood Cholesterol Reduction. Bethesda, MD: National Heart, Lung and Blood Institute, 1990. (NIH publication no. 90-3046).
  38. National High Blood Pressure Program. The sixth report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure. Bethesda, MD: National Heart, Lung and Blood Institute, 1997. (NIH publication no. 98-4080).
  39. Krieger DT. Rhythms of ACTH and corticosteroid secretion in health and disease, and their experimental modification. J Steroid Biochem 1975;6:785–91.[ISI][Medline]
  40. Sady SP, Thompson PD, Cullinance EM, et al. Prolonged exercise augments plasma triglyceride clearance. JAMA 1986;256:2552–5.[Abstract]
  41. Brambilla DJ, McKinlay SM, McKinlay JB, et al. Does collecting repeated blood samples from each subject improve the precision of estimated steroid hormone levels? J Clin Epidemiol 1996;49:345–50.[ISI][Medline]
  42. Longcope C, Franz C, Morello C, et al. Steroid and gonadotropin levels in women during the perimenopausal years. Maturitas 1986;8:189–96.[ISI][Medline]
  43. Dreary UJ, Fowkes FG, Donnan PT, et al. Hostile personality and peripheral arterial disease in the general population. Psychosom Med 1994;56:197–202.[Abstract]
  44. Hayano J, Kimura K, Hosaka T, et al. Coronary disease-prone behavior among Japanese men: job-centered lifestyle and social dominance. Am Heart J 1997;134:1029–36.[ISI][Medline]
  45. Smith TW, Allred KD, Morrison CA, et al. Cardiovascular reactivity and interpersonal influence: active coping in a social context. J Pers Soc Psychol 1989;56:209–18.[ISI][Medline]
  46. Houston BK, Babyak MA, Chesney MA, et al. Social dominance and 22-year all-cause mortality. Psychosom Med 1997;59:5–12.[Abstract]
  47. Harburg E, Julis S, McGinn NF, et al. Personality traits and behavioral patterns associated with systolic blood pressure levels in college males. J Chronic Dis 1964;17:405–14.[ISI]
  48. Hamm TE, Kaplan JR, Clarkson TB, et al. Effects of gender and social behavior on the development of coronary artery atherosclerosis in cynomolgus macaques. Atherosclerosis 1983;48:221–33.[ISI][Medline]
  49. Pandya D. Psychological stress, emotional behavior, and coronary heart disease. Compr Ther 1998;24:265–70.[Medline]
  50. Sullivan ME, Miller MA, Bell CR, et al. Does severity of ischaemic coronary disease correlate with erectile function? (Letter). Int J Impot Res 1998;10:75.[ISI][Medline]
  51. Goldstein I, Lue TF, Padma-Nathan H, et al. Oral sildenafil in the treatment of erectile dysfunction. N Engl J Med 1998;338:1397–404.[Abstract/Free Full Text]
  52. Cheitlin MD, Hutter, AM, Faxon DP, et al. Use of sildenafil (Viagra) in patients with cardiovascular disease. J Am Coll Cardiol 1999;33:273–82.[ISI][Medline]
  53. Mittleman MA, Maclure M, Sherwood JB, et al. Triggering acute myocardial infarction onset by episodes of anger. Determinants of Myocardial Infarction Onset Study Investigators. Circulation 1995;92:1720–5.[Abstract/Free Full Text]
  54. Mussleman DL, Evans DL, Nemeroff CB. The relationship of depression to cardiovascular disease. Arch Gen Psychiatry 1998;55:580–92.[Abstract/Free Full Text]
Received for publication May 19, 1999. Accepted for publication December 9, 1999.