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The Complex Interplay of Modifiable Risk Factors Affecting Prostate Cancer Disparities in African American Men - Beyond the Abstract

There is a preponderance of scientific evidence that men of African ancestry in the U.S. have a disproportionate burden of prostate cancer, with mortality rates approximately 2.1 times higher than men of European ancestry, particularly between ages 40-60.1 Despite significant advancements in screening, diagnosis, and treatment modalities, these benefits remain inequitably distributed across population groups.2 This persistent gap reveals a complex, multifactorial etiology that transcends genetics alone, demanding a more comprehensive understanding of the forces at play.

This manuscript calls for a broader examination of these underlying factors. We illuminate how a complex network of factors—from dietary patterns and environmental exposures to healthcare access and research representation gaps—converge to shape outcomes for prostate cancer in men of African ancestry in the U.S.3 This commentary integrates challenging perspectives to illuminate the intricate interplay between biology and social context, what we conceptualize as the "socioeconomic web" of prostate cancer outcomes.

Through systematic examination of diet, social determinants of health, screening practices, vitamin D status, and clinical research inclusion, researchers seek to shift the analytical lens from individual-level behaviors (or biology) toward structural and systemic contributors. Addressing these multifaceted elements that impact prostate cancer outcomes demands more than scientific insight-it requires intentional, balanced resources across research, clinical practice, and policy domains.

Diet-Related Risk and Protective Factors

Although dietary patterns have been shown to influence prostate cancer risk and progression, studies agree that no specific diet can prevent or eliminate the disease. Nonetheless, studies are ongoing to elucidate the potential for dietary components to enhance current prostate cancer treatments and interventions, thus offering another innovative approach to mitigating prostate cancer outcomes. For example, recent studies emphasize the protective benefits of plant-based diets in prostate cancer management. In a large multiethnic cohort of prostate cancer survivors, men in the highest quintile of a healthful plant-based diet index demonstrated a 25% lower all-cause mortality risk compared to those in the lowest quintile.4 Similarly, cruciferous vegetable consumption appeared protective. A 2023 meta-analysis revealed that men with the highest intake experienced approximately 13% lower prostate cancer risk than those with minimal consumption.5 Soy products were also reported to significantly reduce prostate cancer risk among men of African ancestry in the U.S. and Hispanic men with regular soy consumption, whereas no comparable benefit was observed in Caucasian or Japanese men;6 thus, suggesting that increasing soy and plant protein consumption may represent a modifiable protective factor specifically for high-risk populations.

The emerging evidence consistently indicates that diets rich in fruits, vegetables, legumes, and whole grains—particularly cruciferous varieties—correlate with reduced cancer risk and improved outcomes. Conversely, the Western dietary pattern, characterized by high saturated fat, processed meat, and refined sugar intake, has consistently correlated with elevated prostate cancer risk, especially for high-risk populations. For example, red meat consumption and how that red meat is prepared may expose individuals to carcinogenic compounds, such as PhIP, which form DNA adducts in prostate tissue and elevate cancer risk.7 Research demonstrates that these dietary exposures contribute not only to incidence but also to aggressiveness and recurrence rates. Interestingly, a large prospective NIH-AARP (National Institute of Health - American Association of Retired Persons) Diet and Health Study showed red meats cooked at high temperatures were associated with an increased risk of prostate cancer (HR=1.18, 95%CI=1.00–1.38 and HR=1.22, 95%CI=1.03–1.44, for the upper two intake tertiles),7 thus suggesting, red meats cooked at high temperatures were positively associated with prostate cancer risk among African-American men. This was later supported by a comparative analysis of nutrient intake in the Prostate, Lung, Colorectal, and Ovarian (PLCO) cohort that found men of African ancestry in the U.S. in the U.S. consumed more organ meats, more processed meat, and fewer protective nutrients such as fiber and antioxidants than their European counterparts.8 Although these dietary patterns are often perceived as minor contributory factors underlying prostate cancer outcomes observed,9 these findings are not to be interpreted in a vacuum. These dietary patterns must be taken into consideration with well-established data that show that dietary patterns are significantly associated with the socioeconomic and neighborhood deprivation status that high-risk populations (i.e., men of African ancestry in the U.S.) are often impacted by. Research consistently demonstrates that people living in "food deserts"—areas with limited access to nutritious food options—tend to develop poor dietary habits. These same communities experience higher rates of diet-related health problems commonly associated with the Western diet, such as obesity, diabetes, and cardiovascular disease.10 Taken together, dietary intervention holds significant promise, particularly when designed with cultural and socioeconomic realities in mind. Tailored nutritional education, subsidies for fresh produce in underserved neighborhoods, and culturally appropriate food marketing may increase both uptake and sustainability. Addressing diet represents not merely health promotion but a pathway toward balanced health resource distribution.

Social Determinants of Health and Neighborhood Effects

Social determinants of health (SDOH), non-medical factors that affect health outcomes, encompass health care and quality, neighborhood and built environment, social and community context, education access and quality, and economic stability. Downstream impacts of SDOH include limited high-quality care access, neighborhood deprivation, residential segregation, poverty, and chronic discrimination exposure. Numerous studies confirm that even after adjusting for insurance status and income, variations in PCa treatment and outcomes persist. Access to health care and quality of health care are often compromised due to implicit bias and challenges that continue to influence whether patients receive early screening, appropriate treatment, and access to cutting-edge therapies. Lillard et al. note that institutional factors driving PCa outcome variations include widespread medical system mistrust, suboptimal patient-physician communication, and insufficient tailored information among men of African ancestry in the U.S.11 Economic barriers—including screening and treatment costs and employment disruption—further delay care-seeking behaviors.11 While it is often cautioned against attributing PCa outcome variations to biology alone, we contend, as do Johnson et al.,3 that the biological consequences of social exposures must not be ignored but rather prioritized.

Consistent with these factors, epidemiological data demonstrate that certain population groups have a higher risk and tend to present with PCa at younger ages and with more advanced disease. One analysis reported men of African ancestry in the U.S. were diagnosed approximately two years earlier than their white counterparts and experienced shorter post-diagnosis survival even after stage adjustment.12 These outcome variations reflect both heightened baseline risk and reduced access to preventive services and timely intervention. In summary, poverty and healthcare service gaps compound biological risk; addressing these social determinants is as crucial as targeting genetic factors.

Medical system mistrust, rooted in historical exploitation and ongoing service gaps, presents an additional challenge. From the Tuskegee Syphilis Study to contemporary reports of undertreatment and dismissal in clinical settings, men of certain ancestral origins have rational grounds for healthcare institution skepticism.13 This mistrust contributes to care-seeking delays, screening recommendation skepticism, and low clinical trial participation. Overcoming this challenge requires not merely patient education but institutional accountability, community partnership with racially diverse healthcare providers, and structural reform.

Furthermore, implicit healthcare system bias often results in differential treatment recommendations for men of select ancestral origins compared to their counterparts, even with similar clinical presentations.14 Studies demonstrate that some population groups are less likely to receive aggressive treatment options like radical prostatectomy or radiation therapy and more likely to be directed toward watchful waiting or less intensive management approaches.14 Research also suggests that healthcare providers hold biased beliefs regarding the pain tolerance of some population groups.15 These outcome variations reflect the need to improve health outcomes across all communities.

Neighborhood deprivation, a community-level assessment of social factors such as poverty, employment, and housing, has increasingly been incorporated in the design of multi-level studies elucidating variations in health outcomes across population groups. In a recent review article by Fuemmeler et al., the authors highlighted how neighborhood conditions can impact cancer biology, specifically stage, tumor progression, and survival.16 The findings suggest the need for further examination of potential mediators of neighborhood conditions and prostate cancer outcomes, such as chronic stress, exposure to environmental toxins, and inadequate nutrition, and how they might exert psychophysiological effects, including altered hormone levels, inflammation, and epigenetic changes that influence cancer biology, such as tumorigenesis. In a case-control study, Pichardo et al. found neighborhood conditions moderated the relationship between West African genetic ancestry and prostate cancer risk. Those with increased West African genetic ancestry who resided in neighborhoods with limited access to resources had an increased odds of prostate cancer than those living in more affluent neighborhoods.17 The NIH's framework for health outcome gaps strongly supports this expanded research design, advocating for multi-level models that incorporate SDOH into mechanistic and translational research design.

Regions with documented healthcare access limitations remain one of the most enduring structural mechanisms shaping cancer outcome variations. These regions are disproportionately concentrated in neighborhoods with limited access to health-promoting resources such as quality grocery stores, recreational spaces, and specialty healthcare providers.18 These "health deserts" not only constrain prevention and early detection opportunities but also reinforce intergenerational disadvantage patterns. Living in high-poverty, high-crime areas correlates with elevated allostatic load—the cumulative physiological burden of chronic stress—which increases cancer susceptibility and accelerates progression.18 Thus, residential zip code may be as determinative as genetic code in shaping prostate cancer outcomes. Ultimately, neglecting social context in PCa care reinforces the misleading dichotomy between biology and environment, rather than recognizing their profound interconnection. These domains are not mutually exclusive but synergistic—the social becomes biological over time, inscribed into cellular pathways and disease trajectories. Thus, care models and research paradigms that omit or deprioritize SDOH remain fundamentally incomplete. Achieving healthcare access across all communities requires a paradigm shift, recognizing social determinants not as peripheral considerations but as core variables that should shape research design, clinical guidelines, and public health strategies.

Prostate Cancer Screening: Policy Changes and Persistent Barriers

Screening policy changes over the past decade have had profound and uneven impacts across populations. Following the USPSTF's (U.S. Preventative Services Task Force) 2012 recommendation against routine PSA screening, metastatic prostate cancer incidence rose among U.S. men aged 50-74.19 Recognizing the limitations of this one-size-fits-all approach, the USPSTF revised its position in 2018, recommending that men aged 55-69 engage in individualized, informed screening decisions.20 Professional organizations have increasingly emphasized risk stratification in their guidelines, with the American Cancer Society now advising that high-risk individuals, including all population groups, begin screening discussions at age 45.21,22

Despite these policy adjustments, screening uptake remains limited in practice. Survey data indicate that PSA testing rates remain suboptimal in many communities. Notably, modeling analyses suggest that more intensive screening among all population groups could yield greater mortality reductions than in the general population, reflecting their higher baseline incidence rates.23 Unfortunately, challenges including limited care access, medical mistrust, and inadequate awareness continue to suppress screening participation.

Lillard et al. emphasize that prostate cancer outcomes in select population groups are more severe partly because they are "less likely to be screened or to receive treatment."11 Community-based surveys have identified practical obstacles—competing priorities, transportation challenges, and confusion about screening locations—as significant deterrents. To reduce these limitations, experts recommend culturally tailored education initiatives, improved healthcare access, and inclusion of all population groups on guideline development panels to ensure high-risk populations receive appropriate early screening recommendations.

Environmental Factors and Hormonal Pathways in Prostate Cancer Outcomes

Vitamin D synthesis depends heavily on ultraviolet B radiation from sunlight, but environmental factors create differential exposure patterns. For example, certain population groups tend to be more innately deficient in vitamin D due to higher melanin levels that provide natural sun protection while simultaneously reducing vitamin D production from the same environmental UV exposure.24 This biological adaptation to ancestral environments creates significantly lower average serum 25-hydroxyvitamin D concentrations in modern settings.

The resulting vitamin D deficiency has profound implications for prostate cancer outcomes. Duraki et al. describe robust evidence linking vitamin D deficiency with lethal prostate cancer.24 Observational data demonstrate that lower vitamin D levels at diagnosis correlate with higher Gleason grade, advanced stage, and greater metastatic burden, particularly among men of African ancestry in the U.S.25 Mechanistic investigations support this relationship through genomic analyses showing that vitamin D receptor signaling differs in tumors from various ancestral origins, potentially influencing tumor progression patterns.26

However, supplementation strategies remain unclear. The Vitamin D and Omega-3 trial (VITAL) found no overall cancer prevention benefit after 5 years, yet prostate cancer incidence among certain population groups was reduced by 23% (P < 0.07)27, suggesting that targeted supplementation may address environmentally-induced gaps more effectively in this population.

Another potential contributing factor involves glucocorticoid receptor signaling in prostate cancer progression. Glucocorticoid receptor signaling in prostate cancer progression has been shown to be problematic for men of African ancestry in the U.S., due to enhanced physiological responses to glucocorticoids, which may accelerate tumor development and create more aggressive disease patterns.28 Environmental stressors, including systemic racism and socioeconomic challenges, create chronic psychosocial stress that dysregulates cortisol production. These population groups exhibit enhanced physiological responses to glucocorticoids, partly attributed to cumulative environmental stress exposure resulting in chronically elevated cortisol levels and sustained glucocorticoid receptor signaling 28

Environmentally-driven hormonal dysregulation creates a cascade of molecular changes that promote aggressive prostate cancer. For example, chronically elevated cortisol levels, increased glucocorticoid receptor expression, and sustained glucocorticoid receptor signaling in men of African descent have been partially attributed to cumulative psychosocial stress. 28 Specifically, hyperactive glucocorticoid receptor signaling induces local lasting changes in DNA methylation, which shape subsequent responses to glucocorticoid exposure and accelerate epigenetic ageing associated with cancer.29,30 Additionally, glucocorticoid receptor overexpression in hormone-resistant prostate cancer enables bypass of androgen receptor pathways while directly activating oncogenic target genes.28,29,31

These environmentally-mediated hormonal pathways present significant clinical challenges. The enhanced glucocorticoid receptor signaling observed in some population subgroups complicates treatment since glucocorticoids are integral components of standard prostate cancer regimens. Future therapeutic strategies must account for how environmental factors influence both vitamin D deficiency and cortisol dysregulation to develop more effective, personalized approaches for reducing prostate cancer mortality for all men.

Clinical Trial Participation: The Representation Crisis

Unfortunately, some population groups have limited representation in prostate cancer clinical research studies, limiting our comprehensive understanding of observed outcome variations.32 A recent systematic analysis of 51 prostate cancer treatment trials found that only 6.7% of enrolled participants were men of African ancestry in the U.S. Similarly, negligible representation of various ethnic groups has been reported for characterized screening and prevention trials.33 This limited participation reflects systemic challenges: medical research mistrust, socioeconomic obstacles, and insufficient targeted recruitment strategies.

The argument that randomized clinical trials control for confounding factors becomes insufficient when some population groups are systematically excluded or underrepresented in those very trials. The practical consequence is that most pivotal studies do not include uniform numbers of all population groups. Paradoxically, when adequately powered analyses are possible, certain population groups often demonstrate equivalent or superior therapeutic responses compared to other counterparts.

For example, pooled analyses from Sipuleucel-T trials revealed that men of African ancestry in the U.S. experienced significantly longer overall survival than other participants.34 Similarly, a 2024 meta-analysis examining FDA-approved metastatic castration-resistant prostate cancer systemic therapies found that men of African ancestry in the U.S. consistently demonstrated survival advantages compared to other ethnic groups, regardless of treatment class.35

These findings suggest underlying biological or tumor-immune differences and underscore that select population groups derive substantial benefit from existing therapeutic approaches. They also highlight the imperative to increase uniform enrollment in clinical trials to enable reliable ancestral-stratified analyses. Recent recommendations emphasize community engagement strategies, patient navigation services, and diverse trial leadership—approaches demonstrated to improve uniform recruitment and retention.

Inclusive research participation represents an ethical imperative. Broader demographic participation ensures statistical power adequacy for detecting effects in historically neglected subpopulations. As regulatory bodies, including the FDA and NIH, establish comprehensive excellence requirements for funded trials, research priorities should focus on designing studies that are simultaneously scientifically rigorous and socially responsive.

Future Directions: From Insight to Action

Moving forward, our primary objective must be translating these insights into concrete action. Lifestyle interventions encompassing dietary modification, physical activity, and nutritional supplementation should be specifically tailored to men of African ancestry in the U.S. communities, incorporating culturally appropriate guidance on healthful eating practices. Concurrently, health policy must address screening equity through expanded access and trust-building initiatives to ensure early identification of high-risk individuals.

Research initiatives must prioritize full participation. While funding agencies and investigators increasingly mandate community engagement plans, sustained effort remains essential. Ongoing investigations for prostate cancer are analyzing biomarker profiles in various populations of men, potentially uncovering biological factors that interact with social determinants. Integrative methodological approaches—combining genomic data with precise measurement of dietary patterns, environmental exposures, and healthcare access—will prove crucial for fully elucidating the "socioeconomic web" underlying prostate cancer disparities.

Conclusion

Prostate cancer outcome variations across population groups in the U.S. arise from complex interactions among factors extending far beyond biology alone. Recent evidence reinforces that dietary pattern, screening practices, vitamin D status, and research participation each significantly influence outcomes. Plant-rich diets with minimal saturated fat content may confer partial protection against cancer development, though socioeconomic barriers frequently limit access to healthful dietary choices. Evolving screening guidelines have measurably impacted stage at diagnosis, disproportionately affecting high-risk populations, while tailored screening approaches begin to address this need.

Vitamin D deficiency remains a plausible contributing factor, though supplementation benefits require further investigation. Critically, not all population groups have been included/represented in clinical research despite often demonstrating equivalent or superior treatment responses when provided appropriate access. Addressing these modifiable factors through education, policy reform, and community engagement initiatives offers a viable pathway toward narrowing the survival gap.

Written by: LaKendria K. Brown, PhD, MS,1 Brian Rivers, PhD, MPH,1 Rick Kittles, PhD,1 and Jabril Johnson, PhD2

  1. Department of Community Health and Preventive Medicine, Morehouse School of Medicine, Atlanta, GA, USA.
  2. Department of Microbiology, Biochemistry & Immunology, Morehouse School of Medicine, Atlanta, GA, USA.
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