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Published in final edited form as: Prostate. 2024 Jan 9;84(5):417–425. doi: 10.1002/pros.24656

Link between Circadian Rhythm and Benign Prostatic Hyperplasia (BPH)/Lower Urinary Tract Symptoms (LUTS)

Dana Cavanaugh 1,2, Alfonso Urbanucci 3,4, Nihal E Mohamed 1,2, Ashutosh K Tewari 1,2, Mariana Figueiro 2,5,*, Natasha Kyprianou 1,2,6,*
PMCID: PMC10922447  NIHMSID: NIHMS1951521  PMID: 38193363

Abstract

Background:

Benign prostatic hyperplasia (BPH) is the most common urologic disease in aging males, affecting 50% of men over 50 and up to 80% of men over 80 years old. Its negative impact on health-related quality of life (HRQoL) implores further investigation into its risk factors and strategies for effective management. Although the exact molecular mechanisms underlying pathophysiological onset of BPH are poorly defined, the current hypothesized contributors to BPH and lower urinary tract symptoms (LUTS) include aging, inflammation, metabolic syndrome, and hormonal changes. These processes are indirectly influenced by circadian rhythm disruption. In this article, we review the recent evidence on the potential association of light changes/circadian rhythm disruption and the onset of BPH and impact on treatment.

Methods:

A narrative literature review was conducted using PubMed and Google Scholar to identify supporting evidence. The articles referenced ranged from 1975 to 2023.

Results:

A clear relationship between BPH/LUTS and circadian rhythm disruption is yet to be established. However, common mediators influence both diseases, including pro-inflammatory states, metabolic syndrome, and hormonal regulation that can be asserted to circadian disruption. Some studies have identified a possible relationship between general LUTS and sleep disturbance, but little research has been done on the medical management of these diseases and how circadian rhythm disruption further affects treatment outcomes.

Conclusions:

There is evidence to implicate a relationship between BPH/LUTS and circadian rhythm disruptions. However, there is scarce literature on potential specific link in medical management of the disease and treatment outcomes with circadian rhythm disruption. Further study is warranted to provide BPH patients with insights into circadian rhythm directed appropriate interventions.

Keywords: Circadian rhythm disruption, light, benign prostate growth, benign prostatic hyperplasia, lower urinary tract symptoms, risk factors, therapeutic management, racial disparities

1. Introduction

Background

Benign prostatic hyperplasia (BPH) is a condition that affects the aging male population, with onset of symptoms occurring around age 50. This urologic disease affects over 200 million men worldwide, and in the United States (US), accounts for about 23 million clinic visits and 1.2 million Emergency Department (ED) visits1. By the age 80, over 80% of men are diagnosed with BPH2, deeming it the most common urologic disease in men3. BPH is characterized as an enlargement of the prostate gland due to the proliferation of prostatic stromal and epithelial cells in the transitional zone4. The enlargement of the gland restricts urine flow through the prostatic urethra, causing lower urinary track symptoms (LUTS)4. These symptoms include frequent urination, incomplete bladder emptying, increased urgency, difficulty starting a stream, and nocturia. Of those individuals reporting symptoms of LUTS, 30–48% experience moderate-to-severe symptoms5. Although not life-threatening, these symptoms can significantly impair individuals’ health-related quality of life (HRQoL) and may lead to complications such as urinary tract infections, urinary retention and bladder stones6.

The current treatment options for BPH range from pharmacological intervention to surgery, depending on the size of the prostate, patient’s age and overall health, and severity of symptoms. Patients are commonly prescribed α−1 adrenoceptor antagonists (including tamsulosin, alfuzosin, doxazosin, terazosin), that function to relax the smooth muscle of the bladder neck and prostate4. Smooth muscle relaxation reduces prostatic tone, thereby decreasing urinary obstruction and allowing for urine flow7. Within 1 to 2 weeks of starting treatment with α−1 adrenergic antagonists, obstructive and irritative LUTS from BPH have been demonstrated to improve7. α−1 adrenergic antagonists not only work on the prostatic and bladder smooth muscle, but also cause vasodilation of the systemic vasculature, resulting in a lowering of blood pressure8. Because of this vasodilation, α−1 antagonists can have adverse effects of syncope, dizziness, and headache. To avoid complications from these adverse effects, such as falls, it is recommended that patients should take α−1 antagonists at night to prevent orthostatic hypotension8,9. BPH is also medically managed using 5-α reductase inhibitors, such as finasteride. Normal and abnormal prostate growth is stimulated by dihydrotestosterone (DHT), a potent androgen formed from testosterone by the enzyme 5-α reductase10,11 consequential to binding/activating the androgen receptor (AR) signaling. 5-α reductase inhibitors target the conversation of testosterone to DHT, significantly lowering both circulating and intraprostatic levels of the active androgen, thus reducing the size of the prostate gland12.

The pathogenesis of BPH is driven by deregulation of tissue homeostasis mediated by chronic inflammation, aging, hormonal changes, and metabolic syndrome, defined as a group of risk factors specific for cardiovascular disease13–16. There is growing evidence that expansion of inflammatory states, regulation of hormones, such as antidiuretic hormone and testosterone, and disease progression can be regulated by the circadian clock17,18.

Circadian rhythms are oscillations of biological processes that repeat themselves at about every 24-hours19. These rhythms are regulated by an internal “biological clock” that is located in the suprachiasmatic nuclei (SCN) of the anterior hypothalamus20. The master biological clock generates and regulates biological and behavioral processes such as sleep/wake cycle, core body temperature, metabolism, and hormonal regulation21. Peripheral systems, organs, and cells also exhibit circadian rhythms driven by peripheral oscillators, which are controlled by the master biological clock22. The circadian cellular protein machinery is under the control of an intense chain of transcriptional and translational feedback loops which rely on divergent interactions of key transcription factors during the “day phase” versus, others in the “night phase”23. This circadian clock transcriptional-translational feedback loop dictates the 24-hour cycle. During the day phase, transcription factors CLOCK and BMAL1 heterodimerize to induce the transcription of target genes Period and Cryptochrome, which are translated into proteins PER and CRY. PER and CRY form complexes that accumulate in the nucleus into the late evening. During the night phase, PER and CRY proteins dimerize and act as negative regulators by repressing CLOCK/BMAL1 transcription of Period and Cryptochrome, creating a negative feedback loop. Once the PER:CRY complexes’ are degraded due to relatively short half-lives, the CLOCK:BMAL1 complex is no longer inhibited, marking the start of the next cycle the following morning24. The master clock in the SCN therefore works in concert to synchronize these peripheral oscillators on a cellular level22. Such internal synchronization is critically important in regulating cell cycle, DNA repair, apoptosis, and immune modulation at the cellular level25. The master biological clock is influenced by environmental factors, most notably the exposure to light-dark patterns reaching the back of the eye26. There is a direct neural track from the retina to the SCN that transmits environmental light signals to the master biological clock27. Entrainment is the term used to describe when environmental cues and human physiological processes are in sync. Individuals experiencing chronic fluctuations in their light-dark exposures, such as shift workers, those experiencing chronic jet lag, and those with noise/light pollution, can be at risk for desynchronization of oscillations and cellular processes28. Evidence demonstrates that circadian rhythm disruption can cause a vast range of complications, such as metabolic disorders, cancer, and cardiovascular disease29–31.

Rationale and Knowledge Gap:

The literature is scarce when it comes to reporting the relationship between circadian rhythm disruption and the pathogenesis of BPH/LUTS. Given that some primary treatments of BPH, such as α−1 antagonists, have a time component to their administration, it is important to assess how circadian disruption affects the management of these diseases.

Objective:

In this review, we focus on the relationship between circadian rhythm disruption and the progression and management of BPH/LUTS. We present this article in accordance with the narrative review reporting checklist.

2. Methods

The literature was reviewed using PubMed and Google Scholar. Articles were identified from 1975–2023. Key phrases searched were descriptive of BPH mediators, circadian rhythm mediators, BPH/LUTS and circadian rhythm relationship/association, BPH management, and effects of circadian rhythm disruption on medical management. Journal articles as well as web-based guidelines were included.

3. Discussion

3.1. Circadian Rhythm Disruption in Human Disease: Epidemiological Insights

BPH and circadian rhythm disruption are independently prevalent conditions that have significant healthcare burdens and impairments to HRQoL. HRQoL is a multidimensional construct that describes individuals perceived physical, mental, and social health. A causative relationship between BPH and circadian rhythm disruption has not yet formatively been explored. Doing so can provide insight into how to provide high quality care for these patients and best practices for medical management.

Various factors can disrupt circadian rhythms, including shift work, chronic jet lag, exposure to electric light at night, and environmental noise pollution32–35. It is estimated that about 25% of the US populations are rotating shift workers, which amounts to between 26 and 38 million US adults36. A 2021 meta-analysis of the prevalence of shift work disorder (SWD) conducted by Pallesen et al. found that among shift workers, 26.5% suffered from SWD37. SWD is defined by the American Sleep Disorders Association as insomnia/excessive sleepiness resulting in reduction in sleep time caused by the misalignment between the timing of the master biological clock and sleep time, with symptoms lasting for at least three months38. Sleep disturbances from SWD are associated with significant clinical distress and impairment of social, occupational, and overall level of functioning39. There is a significant body of evidence in the literature detailing the consequences of shift work on physiological and psychological disease. Shift work is associated with increased incidence of myocardial infarction and ischemic stroke40, metabolic syndrome41, cancer42, gastrointestinal disorders43, and reproductive complications, including reduced conception rates and increased miscarriage rates44. Additionally, shift workers are at an increased risk of mental health disorders, including depression, anxiety, suicidal ideation, and impaired cognitive function, as a result of poor sleep quality and duration45,46.

Studies have found that jet lag caused from international flights crossing multiple time zones, and chronic jet lag, such as those of flight crews, often manifest symptoms of disturbed sleep, dysmorphic mood, and gastrointestinal disorders47. Circadian rhythm disruption is also seen in those experiencing environment noise pollution and night-time light pollution. Nocturnal noise pollution, such as from transportation, can disrupt sleep quality and sleep architecture, causing a greater risk of cardiovascular and metabolic pathologies perhaps due to the release of stress hormones, particularly cortisol48. Noise pollution is associated with the dysregulation of the master biological clock, affecting peripheral clock mechanisms49. Nocturnal light may also impact sleep and lead to circadian rhythm disruption; significantly it was reported that over 80% of humans and 99% of those living in the US and Europe are exposed to some kind of light at night50. Light at night can come from TVs, computer screens, smartphones, and e-readers, as well as environmental factors like living in an urban setting47. Exposure to light at night, depending on the amount of light and duration of exposure, can lead to circadian and sleep disruption47.

3.2. Impact of Circadian Rhythm Disruption on the Prostate Health

The association between circadian rhythm disruption and prostatic health has been best explored in prostate cancer. There is a wealth of evidence to suggest that circadian rhythm disruption can influence tumorigenesis51 through the downregulation of tumor suppressive genes52, disruption of the immune system53, and decreased release of melatonin which has anti-tumor properties54. Certain circadian machinery has been demonstrated to be associated with prostate cancer treatment resistance. Prostate cancer cells treated with long-term exposure to enzalutamide, an androgen receptor (AR)-targeting monotherapy, revealed massive epigenomic reprogramming in response to treatment toward elements that induce pro-survival signaling. These elements were notably found to be enriched for the circadian clock core regulator ARNTL. Post-treatment ARNTL levels were associated with patients’ clinical outcomes, and ARNTL knockout strongly decreased prostate cancer cell growth. Thus, at the molecular level, an intense reprogramming of the chromatin structure and activation of the central circadian clock regulator ARNTL transcription factor can mechanistically drive tumor plasticity in advanced therapeutically resistant prostate cancer55. This study also suggests that androgen receptor signaling and its therapeutic targeting can, per se, modulate the circadian rhythm of not only prostate cells, but, potentially influence all tissues under endocrine control that express the androgen receptor (AR) and maintain an intact androgen signaling dynamic. Regarding other prostatic diseases, there has been limited work so far to evaluate circadian rhythm disruption on BPH development and therapeutic response to medications (5-α reductase inhibitors and/or α−1 adrenergic antagonists).

The pathogenesis of BPH is characterized by a multilayered complexity, with diverse cellular processes (apoptosis, epithelial-to-mesenchymal transition, inflammation) contributing to its development and severity of symptoms. It has been suggested that chronic prostatic inflammation causes increased severity of BPH/LUTS2. Being in a pro-inflammatory state may cause chronic tissue damage of the prostate, and with repeated subsequent wound healing, the prostate tissue proliferates and becomes enlarged. Disruption to circadian rhythms has been found to elevate inflammatory response to lipopolysaccharides (LPS), increasing the pathogenicity of inflammatory markers56 and thus upregulating immune response. Inflammatory cells and immune response in the gut microbiome also exhibit circadian rhythms. Circadian disturbances in rats are associated with an increased upregulation of pro-inflammatory cytokines IL-1A, IL-17RA, and Stat3 expression in the colon mucosa, leading to both acute and delayed colitis-associated inflammation57,58. Clinical studies have shown that night-shift workers with circadian rhythm disorders have significantly elevated inflammatory markers59, implicating an effect of circadian rhythm disorders on BPH/LUTS through pro-inflammatory states (Fig. 1).

Figure 1:

Figure 1:

Open in a new tab

Schema summarizing the relationships between circadian rhythm/sleep disruption and prostatic diseases through shared mediators. There is an established correlation between cellular circadian rhythm disruption and prostate cancer, represented by the solid arrow.

Relationships with between circadian rhythm disruption and prostatic disorders through shared mediators is represented by faded arrows. Circadian rhythm disruption leads to pro-inflammatory states, potentially influencing BPH. Circadian rhythm disruption is also indirectly associated (via metabolic syndrome) with BPH. Sleep disruption leads to decreased testosterone secretion, that ultimately impact LUTS. The relationship between circadian rhythm disruption and BPH treatment management strategies, including medication administration, have not yet been determined, and is represented by the dashed arrow.

A potential association between development and progression of BPH/LUTS with metabolic syndrome60 has also been postulated. Metabolic syndrome is characterized as a risk cluster including central obesity, hypertension, hyperglycemia, and hyperlipemia61 . The evidence suggests that metabolic syndrome increases the risk of more severe LUTS symptoms, such as nocturia, in men with BPH62. Circadian rhythm disruption can also impact metabolic syndrome clinical outcomes. Adipose tissue, similar to prostate tissue, has peripheral clock genes that regulate adipokines involved in glucose and lipid metabolism63. Studies show that simulation of jet lag increases body weight and glucose intolerance in comparison to the normal 12 hours of light and dark63,64. One may also consider that since circadian rhythm disruption is associated with the metabolic syndrome, and metabolic syndrome is a risk factor of BPH progression, circadian rhythm disruption may be indirectly associated with the BPH symptom severity. A recent study by Xiong et al.65, evaluated the “Circadian Syndrome” (CircS), proposed by Zimmet et al. in 2019 as a re-clustering of metabolic syndrome to underline the vital impact circadian rhythm disruption has on the components of metabolic syndrome66. This investigative team proposed that since circadian rhythms play such a defining role in metabolic processes, metabolic syndrome should be expanded and reclassified as Circadian Syndrome with the addition of sleep disturbances, depression, steatohepatitis, and cognitive dysfunction66. By redefining the cluster as Circadian Syndrome, Zimmet et al. suggest that CircS is a more comprehensive research criterion. Over four years, Xiong et al. compared the incidence of BPH in those experiencing CircS to metabolic syndrome. Participants were classified as having CircS if they had ≥4 components (depression, reduced sleep duration, abdominal obesity, hypertension, hyperglycemia, high triglycerides, and low HDL cholesterol), whereas they were classified as having MetS if they had ≥3 components. It was found that individuals with CircS have a 3.62% higher risk of BPH/LUTS than those with MetS. The addition of reduced sleep duration and depression to the MetS risk cluster, which underlines circadian rhythm disruption, had a higher predictive power than MetS alone. This points to CircS, with the additional inclusion of sleep disturbances and depression, as a better predictor of BPH incidence and prevalence than MetS.

Additional studies have evaluated the association between circadian rhythm disruption and specific LUTS, such as nocturia and nocturnal polyuria (NP) mediated through circadian-driven hormonal processes. Water homeostasis and micturition follow a circadian pattern. The kidney and bladder are two genitourinary organs whose function is dictated by their own peripheral circadian clocks which can be affected by master circadian clock disruption67,68. Significantly, fluid intake, urine production, urine storage, and diuresis follow distinct circadian rhythms, with urination occurring less frequently at night69. This process follows a diurnal pattern controlled by the master circadian clock in the SCN. Based on this knowledge, it has been hypothesized that the release of antidiuretic hormone (ADH), which controls diuresis, follows a circadian pattern. ADH is normally released at night to decrease diuresis70, a process that can be impaired by circadian disruption, contributing to nocturia71,72. One must also consider however that LUTS, such as nocturia and NP, may occur independently of a BPH diagnosis. Circadian rhythm disruption may affect nocturia and NP without mechanisms specific to BPH.

Additional evidence suggests an relationship between LUTS/BPH and sleep disturbance, without directly implicating circadian rhythm disruption73–75. However, frequent night urination is significantly associated with reduced time and quality of sleep, thus, leading to chronic day-time tiredness and circadian rhythm disruption76. Reduced sleep quality and time can also cause hormonal abnormalities, including low testosterone, increased stress hormone levels such as cortisol, and lower thyroid levels which in turn could be associated with increased circadian rhythm disruption77,78. Furthermore, Arauju et al. found that poor sleep quality increased the risk of obstructive and irritative LUTS, and sleep restriction increased the risk of irritative LUTS by two-fold. This study however did not evaluate specifically a diagnosis of BPH, but rather only general LUTS73. Another study tracked shift workers and found a correlation between impaired sleep quality and more significant LUTS74. These disruptions in sleep and increased incidence of LUTS could be related to androgen secretion75. Testosterone secretion is associated with sleep/wake cycles in a diurnal rhythm, in which serum concentration increases during sleep and decreases during wakefulness79 (Fig. 1). The regulation of testosterone therefore is critically influenced by sleep disruption: serum testosterone levels inappropriately fall during nighttime awakening80. It should be noted that this study found that the amount of sleep was more significant to testosterone regulation than the timing (night vs. day) of sleep, suggesting that sleep restriction decreases serum testosterone concentration80. Significantly enough, BPH has been shown to be modulated by decreased testosterone levels81,82. This indicates a potential relationship between BPH/LUTS progression and sleep disturbance mediated through decreased testosterone levels from reduced sleep.

3.3. Racial Disparities and Circadian Rhythm Association in BPH/LUTS

In the US, the Prostate Cancer Prevention Trial reported a 41% increased incidence risk of Black and Hispanic men having BPH/LUTS compared to that of White men1,83. Furthermore, the risk of progressing from mild to moderate/severe BPH were 68% higher than White men83. In the Flint Men’s Health Study of African American men, although 37% had moderate-to-severe LUTS impairment, only 8.2% were diagnosed with BPH before the study and 3% reported being medically treated for BPH84. The significant difference in the proportion of Black men who had LUTS and who were diagnosed and treated with BPH suggests that many Black men are being underdiagnosed and untreated. Among White men, the decision to receive medical care for LUTS is in function of symptom severity, but this relationship in Black men has not been determined85. Racial disparities in BPH evaluation and management may arise from a myriad of socioeconomic determinants of health (SDOH) related factors, including socioeconomic status, access to healthcare, and bias and discrimination in healthcare settings. Barriers to quality healthcare, as a result of economic burden and difficulty paying healthcare costs, were associated with worsening LUTS86. In a retrospective study on men presenting to the Emergency Department (ED) with acute urinary retention, Black and Hispanic men were more likely to present at ED than any other group, implicating that these patients may be untreated/undertreated for BPH in the outpatient setting87 and rather reach healthcare for acute episodes. In fact, when controlling for economic factors, Black men were less likely to report a previous BPH diagnosis88. The California Medicaid program indicated that Black men with BPH, who were receiving the same insurance benefits, were 15.4% less likely to be medically treated during their first year of diagnosis than White patients89. This highlights additional underpinnings beyond socioeconomic status in racial disparity in BPH diagnosis and management. Furthermore, cultural differences in BPH/LUTS symptom reporting and symptom attribution may lead to under-reporting of symptoms experienced, less help-seeking behaviors, and delayed clinical care thus contributing to existing racial disparities in BPH90–92.

Diverse risk factors and comorbidities contribute to the development of BPH, including metabolic syndrome and cardiovascular disease, via hormonal changes, heterogeneity of prostate cell–cell subtypes and inflammatory signaling pathways. These risk factors, potentially mediated by SDOH, disproportionately affect historically marginalized populations in the US93,94.

Black men may be at higher risk for experiencing circadian rhythm disruption due to various factors such as night shift work, environmental conditions (i.e. noise pollution, light at night exposure), socioeconomic status and chronic co-morbidities (i.e. diabetes, obesity, chronic stress, cardiovascular disease). Black and Hispanic individuals are overrepresented in night shift work: compared to White individuals, as they are twice as likely to work night shifts95,96. Racial disparities also exist in environmental conditions due to residential segregation, in which ethnic communities were only granted loans to live in less desirable and more hazardous areas97. Defined as “redlined” neighborhoods, these areas are closer to industrial plants, highways, and factories, and suffer from overcrowding98. Such conditions significantly increase noise pollution and light at night exposure99, and can contribute to circadian rhythm disruption. Furthermore, comorbidities that influence circadian rhythm disruption, such as metabolic syndrome, inflammatory states, and obesity, disproportionally affect racially diverse populations100.

In summary, disruption of circadian rhythm is a potential risk factor of BPH incidence among Black men, but further studies are needed to dissect the relationship between racial disparities in BPH evaluation and management and the factors involved in circadian rhythm disruption.

3.4. Circadian Rhythm Disruption and Medical Management of BPH

α−1 adrenoceptor antagonists are the first-life treatment prescribed to alleviate LUTS. Due to the side effect of orthostatic hypotension, it is recommended that patients take this medication at night. However, this brings into question what the proper medication management is for patients who are awake at night due to their work or lifestyle, and thus experiencing circadian rhythm disruption. Furthermore, circadian rhythms may play a role in the metabolic processing of medications and the consequential impact on the severity of side effects. This could lead to medical noncompliance, which regarding medications like 5-α reductase inhibitors, could accelerate BPH symptomatic progression. The impact of circadian rhythm disruption on effective administration of BPH medications represents a critically understudied area.

3.5. Conclusions

In the US alone, at least 800 000 and possibly as many as 3 million individuals are impacted by circadian rhythm disruption101. If shift work and jet lag are included in this definition, this statistic includes several millions of people101, affecting medical personnel, pilots, law enforcement, security, firefighters, machine operators, and those who live in noise and light polluted areas. BPH and LUTS cause significant impairment to individuals’ quality of life and increases individual and societal health burdens. Understanding the correlation between those with BPH and circadian rhythm disruption can influence management strategies, such as timing of medications and light therapy. A potential functional association between the circadian rhythm disruption with clinical progression of BPH, warrants an insightful investigation of the molecular mechanisms governing development and management of BPH in the context of circadian rhythm changes impacting the prostate and bladder microenvironment dynamics.

Moving forward, retrospective investigation of the consequences of circadian rhythm disruption on the medical management of patients with BPH can be pursued by examining clinical trials. Alternatively future designing controlled prospective trials aiming at dissecting differential timing in drug administration and management of clinical outcomes in patient cohorts with different levels of disruption of their circadian rhythms.

Acknowledgements

The authors wish to thank Dr. Steven Kaplan, Mount Sinai Urology for useful discussions.

Funding:

NCI/NIH R01 CA232574-01A1 (NK); Academy of Finland (#349314), the Norwegian Cancer Society (#198016-2018), and the Finnish Cancer Foundation and the Tampere Institute for Advanced Study (AU); The National Institute of Nursing Research 1R21 NR016518-01A1, and Pfizer Grant (#76180091) (NM); Grant #R01OH01668/NIH/NIOSH (MGF)

Abbreviations

ADH

Antidiuretic hormone

AR

Androgen receptor

BPH

Benign prostatic hyperplasia

CircS

Circadian syndrome

DHT

Dihydrotestosterone

ED

Emergency Department

HRQoL

Health-related quality of life

LPS

lipopolysaccharide

LUTS

Lower urinary track symptoms

MetS

Metabolic syndrome

SCN

Suprachiasmatic nucleus

SDOH

Social determinants of health

SWD

Shift work disorder

US

United States

Footnotes

Conflicts of Interest: There are no conflicts of interest.

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