Purpose

The number of American Indian and Alaska Native (AI/AN) people living with dementia is expected to increase 5-fold by 2060. Social determinants of health may explain disparities in the incidence of Alzheimer disease (AD) but remain largely overlooked.

Methods

We examined the time trend of AD mortality rates and associations of the percentage of AI/ANs, density of primary care physicians and neurologists, area deprivation index, rurality, and Indian Health Service region with AD mortality in 646 purchased/referred care delivery area counties.

Results

AD mortality rates significantly increased over time. Counties with higher concentrations of AI/AN people had lower AD mortality. More deprived counties had 34% higher AD mortality compared with less deprived counties. AD mortality was 20% lower in nonmetro counties than in metro counties.

Conclusions

Findings have implications for prioritizing areas where more resources for AD care, education, or outreach are needed.

Objective

Posttraumatic stress disorder (PTSD) is highly comorbid with chronic pain conditions that often co-occur such as migraine headaches, temporomandibular disorder, irritable bowel syndrome, fibromyalgia, chronic fatigue syndrome, chronic prostatitis/chronic pelvic pain syndrome, and tension headaches. Using a genetically informative sample, the current study evaluated the genetic and environmental factors contributing to the co-occurrence of PTSD and chronic pain conditions.

Methods

Data from 4680 male twins in the Vietnam Era Twin Registry were examined. Biometric modeling was used to estimate genetic and environmental variance components and genetic and environmental correlations between PTSD and multiple chronic pain conditions.

Results

Heritabilities were estimated at 43% (95% confidence interval [CI] = 15%-63%) for PTSD and 34% (95% CI = 27%-41%) for the combined history of any one or more pain condition. Specific pain condition heritabilities ranged from 15% (95% CI = 0%-48%) for tension headaches to 41% (95% CI = 27%-54%) for migraine headaches. Environmental influences accounted for the remaining variance in pain conditions. The genetic correlation between PTSD and combined history of any one or more pain condition was rg= 0.61 (95% CI = 0.46-0.89) and ranged for individual pain conditions from rg= 0.44 (95% CI = 0.24-0.77) for migraine headache to rg= 0.75 (95% CI = 0.52-1.00) for tension headaches.

Conclusions

PTSD and chronic pain conditions are highly comorbid, and this relationship can be explained by both genetic and environmental overlap. The precise mechanisms underlying these relationships are likely diverse and multifactorial.

Objective

To evaluate the genetic and environmental relationship among prostatitis and other urological conditions, including benign prostatic hyperplasia (BPH) and prostate cancer (CaP), a classical twin design and biometric modeling was used. While prostatitis-characterized by pain and voiding symptoms, no clear etiology, and functional and quality of life impairments-co-occurs with other urinary conditions, the degree of shared overlapping etiologic processes among them remains unclear. We examined the contribution of genetic and environmental factors to these conditions and the etiology of their associations at the level of genetic and environmental influences.

Methods

4380 monozygotic and dizygotic male twin pairs from the Vietnam Era Twin Registry reported lifetime physician-diagnosed prostatitis (combined acute and chronic), bladder problems, enlarged prostate/BPH, and CaP. Multivariate biometrical modeling estimated the magnitude of genetic and environmental influences for each condition, as well as their genetic and environmental covariance. The common pathway model tested the assumption that covariation among these urinary conditions is determined by a single latent factor.

Results

Overall prevalence of prostatitis was 2.7%. Heritability estimates ranged from 19% for bladder problems to 42% for CaP. Significant shared environmental influences were present for CaP (12%), enlarged prostate/BPH (10%) but were smaller than genetic influences. A reduced one factor common pathway model provided the best fit, suggesting that covariation among the conditions is determined by a shared latent factor.

Conclusion

We identified a common, genetically-influenced factor that accounts for much of the comorbidity among these 4 disease conditions. Nonshared environmental factors also make a significant contribution.

Objectives

Chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) is characterized by pain and voiding symptoms in the absence of an obvious infection or other cause. CP/CPPS frequently occurs with non-urological chronic overlapping pain conditions (COPCs) of unknown etiology. We conducted a co-twin control study in men discordant for chronic prostatitis (CP), an overarching diagnosis of which approximately 90% is CP/CPPS. The primary aim was to investigate the contribution of familial factors, including shared genetic and common environmental factors, to the comorbidity of CP and COPCs.

Methods

Data from 6824 male twins in the Vietnam Era Twin Registry were examined to evaluate the association between self-reported lifetime physician diagnosis of CP with COPCs including fibromyalgia, chronic fatigue syndrome, irritable bowel syndrome, temporomandibular disorder, tension headaches, and migraine headaches. Random effects logistic regression models were used and within-pair analyses evaluated confounding effects of familial factors on the associations.

Results

There were significant associations between CP and all 6 examined COPCs. After adjusting for shared familial influences in within twin pair analyses, the associations for all COPCs diminished but remained significant. Familial confounding was strongest for the association of CP with fibromyalgia and temporomandibular disorder and smallest for irritable bowel syndrome.

Conclusions

CP and COPCs are highly comorbid. These associations can be partially explained by familial factors. The mechanisms underlying these relationships are likely diverse and multifactorial. Future longitudinal research can help to further elucidate specific genetic and environmental mechanisms and determine potentially causal relationships between CP and its comorbidities.

Purpose

Symptoms of urinary irritation, urgency, frequency and obstruction, known as lower urinary tract symptoms, are common in urological practice. However, little is known about the etiology or pathogenesis of lower urinary tract symptoms, especially the relative contributions of genetic and environmental factors to the development of these symptoms. We used a classic twin study design to examine the relative contributions of genetic and environmental factors to the occurrence of lower urinary tract symptoms in middle-aged men.

Materials and methods

Twins were members of the Vietnam Era Twin Registry. We used a mail survey to collect data on lower urinary tract symptoms using the I-PSS (International Prostate Symptom Score) instrument. Twin correlations and biometric modeling were used to determine the relative genetic and environmental contributions to variance in I-PSS total score and individual items.

Results

Participants were 1,002 monozygotic and 580 dizygotic middle-aged male twin pairs (mean age 50.2 years, SD 3.0). Nearly 25% of the sample had an I-PSS greater than 8, indicating at least moderate lower urinary tract symptoms. The heritability of the total I-PSS was 37% (95% CI 32-42). Heritability estimates ranged from 21% for nocturia to 40% for straining, with moderate heritability (34% to 36%) for urinary frequency and urgency.

Conclusions

Genetic factors provide a moderate contribution (20% to 40%) to lower urinary tract symptoms in middle-aged men, suggesting that environmental factors may also contribute substantially to lower urinary tract symptoms. Future research is needed to define specific genetic and environmental mechanisms that underlie the development of these symptoms and conditions associated with lower urinary tract symptoms.

Posttraumatic stress disorder (PTSD) and eating disorders (ED) frequently co-occur, but the mechanisms underlying this association remain unclear. EDs are characterized by features of maladaptive eating behaviors including disinhibited eating and cognitive dietary restraint. Identifying the genetic overlap between PTSD symptoms and maladaptive eating behaviors may elucidate biological mechanisms and potential treatment targets. A community sample of 400 same-sex twins (102 monozygotic and 98 dizygotic pairs) completed the PTSD Checklist-Civilian (PCL-C) for PTSD symptoms and the Three-Factor Eating Questionnaire-Reduced (TFEQ-R18) for eating behaviors (uncontrolled eating, emotional eating, and cognitive dietary restraint). We used biometric modeling to examine the genetic and environmental relationships between PCL-C and TFEQ-R18 total and subscales scores. Heritability was estimated at 48% for PTSD symptoms and 45% for eating behavior overall. Bivariate models revealed a significant genetic correlation between PTSD symptoms and eating behavior overall (rg =.34; CI:.07,.58) and Uncontrolled Eating (rg =.53; CI:.24,.84), and a significant environmental correlation between PTSD symptoms and Emotional Eating (re =.30; CI:.12,.45). These findings suggest the influence of common etiology. Future research and clinical efforts should focus on developing integrated treatments.

Objectives

Hypothalamic-pituitary-adrenal (HPA) axis dysregulation is associated with chronic pain. Studying pain sensitivity and the HPA axis could elucidate the role of stress in chronic pain development, which might be influenced by familial factors, including genes.

Methods

Associations between pain sensitivity and salivary cortisol and familial confounding in these associations were examined in 88 female, community-based twin pairs (75% monozygotic, mean age 29 y). Cortisol was assessed after 0.25 mg dexamethasone (DEX), recovery from 0.25 mg DEX, and after 0.5 mg DEX. Cold pressor task (CPT) pain ratings were obtained at threshold and at tolerance. Conditioned pain modulation (CPM) was examined using thermal heat as the testing stimulus and hot water as the conditioning stimulus. Generalized estimating equation models were used and adjusted for baseline pain rating, age, and other relevant covariates.

Results

After controlling for baseline cortisol, greater cortisol suppression following DEX administration and lower recovery cortisol levels were associated with higher pain ratings at tolerance during the CPT (Bs=-2.42 to -17.82; Ps=0.031 to<0.001) as well as with reduced CPM (Bs=-0.92 to -1.68; Ps=0.003 to 0.046). Interestingly, familial confounding was evident in the CPT and CPM during recovery from DEX administration, but not immediately following DEX administration.

Discussion

These findings contribute to understanding possible mechanisms underlying chronic pain by demonstrating that HPA axis response to negative feedback is related to pain sensitivity.

Background

Given high rates of cancer mortality in Native communities, we examined how urban American Indian and Alaska Native elders talk about colorectal cancer (CRC) and CRC screening.

Methods

We conducted seven focus groups with a total of 46 participants in two urban clinics in the Pacific Northwest to assess participant awareness, perceptions, and concerns about CRC and CRC screening. Using speech codes theory, we identified norms that govern when and how to talk about CRC in this population.

Results

Our analyses revealed that male participants often avoided screening because they perceived it as emasculating, whereas women often avoided screening because of embarrassment and past trauma resulting from sexual abuse. Both men and women used humor to mitigate the threatening nature of discussions about CRC and CRC screening.

Conclusions

We offer our analytic results to assist others in developing culturally appropriate interventions to promote CRC screening among American Indians and Alaska Natives.

OBJECTIVES:Limited research suggests commonalities between urologic chronic pelvic pain syndromes (UCPPS) and other non-urologic chronic overlapping pain conditions (COPCs) including fibromyalgia, chronic fatigue syndrome, and irritable bowel syndrome. The goal of this case-control study was to examine similarities and differences between UCPPS and these other COPCs. METHODS:As part of the Multidisciplinary Approach to the Study of Chronic Pelvic Pain Research Network, we examined 1,039 individuals with UCPPS (n=424), non-urologic COPCs (n=200), and healthy controls (n=415). Validated standardized measures were used to assess urological symptoms, non-urological pain symptoms, and psychosocial symptoms and traits. RESULTS:Participants with UCPPS had more urologic symptoms than non-urologic COPCs or healthy controls (P<0.001); non-urological COPC group also had significantly worse urological symptoms than healthy controls (P<0.001). Participants with non-urological COPCs reported more widespread pain than those with UCPPS (P<0.001), yet both groups had similarly increased symptoms of anxiety, depression, negative affect, perceived stress, neuroticism, and lower levels of extraversion than healthy controls (P<0.001). Participants with UCPPS with and without COPCs reported more catastrophizing than those with non-urological COPCs (P<0.001). DISCUSSION:Findings are consistent with the hypothesis of common underlying biopsychosocial mechanisms and can guide the comprehensive assessment and treatment of these conditions regardless of the primary site of pain or diagnosis. Heightened catastrophizing in UCPPS should be examined to inform psychosocial interventions and improve patient care.

Background

There is a dearth of knowledge about the link between cortisol and pain sensitivity.

Purpose

We examined the association of salivary cortisol with indices of cold pain sensitivity in 198 female twins and explored the role of familial confounding.

Methods

Three-day saliva samples were collected for cortisol levels and a cold pressor test was used to collect pain ratings and time to threshold and tolerance. Linear regression modeling with generalized estimating equations examined the overall and within-pair associations.

Results

Lower diurnal variation of cortisol was associated with higher pain ratings at threshold (p = 0.02) and tolerance (p < 0.01). The relationship of diurnal variation with pain ratings at threshold and tolerance was minimally influenced by familial factors (i.e., genetics and common environment).

Conclusions

Understanding the genetic and non-genetic mechanisms underlying the link between HPA axis dysregulation and pain sensitivity may help to prevent chronic pain development and maintenance.