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Scholarly Works (12 results)

  • Thesis
  • Peer Reviewed
UCLA Electronic Theses and Dissertations (2018)

The number of persons aged 65 years and older is expected to double to 92 million in the US by 2060, representing a potentially large social and financial burden of age-related neurodegenerative diseases such as Alzheimer’s disease (AD) and dementias and Parkinson’s disease (PD).Thus effective preventative public health strategies are essential. Regular physical activity (PA) and an active lifestyle have many health benefits, and evidence has accumulated that PA preserves brain structures and functions via multiple physiologic mechanisms, including mediation of inflammation and a general reduction of cardiovascular risk factors.

In the Parkinson’s Environment and Gene (PEG) case-control population-based study, we enrolled 357 incident PD cases and 341 controls in central California and assessed PA levels via self-report of (1) overall PA over 4 age periods; (2) competitive sports; and (3) occupational histories. Our findings suggest that higher lifetime moderate to vigorous activity, especially consistently high level of such activities throughout adulthood and sports activities in youth were negatively associated with PD risk, but we found no beneficial role for occupational physical activity.

We further examine how PA at the late-life influence the risk of dementia/cognitive impairment without dementia (CIND) using a prospective cohort, Sacramento Area Latino Study on Aging (SALSA) study, in which 1789 older Mexican Americans were enrolled at baseline and a majority actively followed between 1998 and 2008. We used Cox proportional hazards regression models to estimate the individual and joint effects of PA, apolipoprotein E (APOE) ε4 and diabetes status on risk of dementia/CIND and observed a nearly 10-fold increased risk among those with all three risk factors. Results from mediation analyses indicate that some of the PA effects on mortality and dementia/CIND but not depression might be mediated through well-known inflammatory pathways represented by biomarkers, specifically interleukins 6 (IL-6) and/or tumor necrosis factor - alpha (TNF-α). However, a large proportion of the PA effects on mortality, cognition, and mood seems to operate independently of the inflammatory pathways or the biomarkers we had available and thus remain unexplained.

Taken together, our results provide support for the hypothesis that PA protects against the onset of neurodegenerative diseases and all-cause mortality, and they suggest that anti-inflammatory action may partly explain the protective effects of PA on dementia/CIND and mortality.

    Cover page: Influences of Physical Activity on Risk of Parkinson’s Disease and Cognitive Decline in Elderly Hispanics
    • Article
    • Peer Reviewed
    UCLA Previously Published Works (2016)

    Introduction

    While regular exercise has been shown to alleviate the motor symptoms of Parkinson's disease (PD), it remains unclear whether a physically active lifestyle may prevent PD.

    Methods

    To examine physical activities across the lifespan and risk of PD, we relied on data from a population-based case-control study that enrolled 357 incident PD cases and 341 controls. We assessed physical activity levels via self-report of (1) overall physical activity (PA) over 4 age periods; (2) competitive sports; and (3) occupational histories.

    Results

    PD risks were lower comparing the overall PA highest quartile (moderate to vigorous activities ≥180 metabolic equivalent task-hours/week (MET-h/wk)) with the lowest quartile (<47.8 MET-h/wk) in age-period 18-24 years (adjusted odds ratio (OR) 0.64, 95% confidence interval (CI) 0.40-1.02), and 45-64 years (OR 0.50, 95%CI 0.31-0.83) but not in age-period 25-44. Individuals who consistently engaged in overall PA at high levels (before age 65 years) had a 51% lower PD risk than those with low levels. Also, having participated in competitive sports prior to age 25 was inversely associated with PD (OR 0.53, 95% CI 0.31-0.91 for high level versus never). There was no association for measures of occupational physical activity though.

    Conclusion

    The long prodromal stage of PD makes it difficult to conclude whether insidious disease leads to a reduction of physical activity years before motor symptom onset and PD diagnosis. However, sports activities and high levels of overall PA in youth appear protective unless they are markers for biologic or genetic factors that lower PD risk.
      Cover page: Lifetime occupational and leisure time physical activity and risk of Parkinson's disease.
      • Article
      • Peer Reviewed
      UC San Francisco Previously Published Works (2019)
      A higher level of physical activity (PA) is associated with decreased risk of mortality, dementia, and depression, yet the mechanisms involved are not well understood, and little evidence exists for Mexican Americans. With data from the Sacramento Area Latino Study on Aging (1998-2007), we used Cox proportional hazards regression to separately evaluate associations of baseline PA level with mortality, dementia/cognitive impairment without dementia (CIND), and depressive symptoms, and we estimated the mediating effects of inflammatory markers in additive hazard models. A low level of PA (<35 metabolic equivalent of task-hours/week) was associated with increased mortality (hazard ratio (HR) = 1.50, 95% confidence interval (CI): 1.20, 1.88), dementia/CIND (HR = 1.37, 95% CI: 0.96, 1.96), and depressive symptoms (HR = 1.23, 95% CI: 1.00, 1.52). A low PA level added 512 (95% CI: -34, 1,058) cases of dementia/CIND per 100,000 person-years at risk (direct effect), while, through a mediating path, interleukin 6 (IL-6) added another 49 (95% CI: 5, 94) cases, or 9% of the total effect. For mortality, 8%-10% of the PA total effect was mediated through IL-6, tumor necrosis factor α (TNF-α), or TNF-α receptors. None of the inflammatory markers mediated the association between PA and depressive symptoms. Our results suggest that antiinflammation (especially as assessed by IL-6 and TNF-α levels) may partly explain how PA protects against dementia/CIND and mortality.
        Cover page: The Roles of Physical Activity and Inflammation in Mortality, Cognition, and Depressive Symptoms Among Older Mexican Americans
        • Article
        • Peer Reviewed
        UCLA Previously Published Works (2018)

        Introduction

        The etiologies of dementia are complex and influenced by genetic and environmental factors including medical conditions.

        Methods

        We used Cox regression model to estimate the individual and joint effects of physical activity (PA), apolipoprotein E (APOE) ε4, and diabetes status on risk of dementia and cognitive impairment without dementia (CIND) among 1438 cognitively intact Mexican American elderly who were followed up to 10 years.

        Results

        The risk of developing dementia/CIND was increased more than threefold in APOE ε4 carriers or diabetics with low levels of PA compared with ε4 noncarriers or nondiabetics who engaged in high PA (ε4: hazard ratio [HR] = 3.44, 95% confidence interval [CI] = 1.85-6.39; diabetes: HR = 3.11, 95% CI = 1.87-5.18); the presence of all three risk factors increased risk by nearly 10-fold (HR = 9.49, 95% CI = 3.57-25.3).

        Discussion

        PA in elderly Hispanics protects strongly against the onset of dementia/CIND, especially in APOE ε4 carriers and those who have diabetes.
          Cover page: Physical activity modifies the influence of apolipoprotein E ε4 allele and type 2 diabetes on dementia and cognitive impairment among older Mexican Americans
          • Article
          • Peer Reviewed
          UCLA Previously Published Works (2024)
          INTRODUCTION: Post-operative prescription opioid use is a known risk factor for persistent opioid use. Despite the increased utilization of robotic-assisted surgery (RAS) for inguinal hernia repair (IHR), little is known whether this minimally invasive approach results in less opioid consumption. In this study, we compare long-term opioid use between RAS versus laparoscopic (Lap) versus open surgery for IHR. METHODS: A retrospective cohort study of opioid-naïve patients who underwent outpatient primary IHR was conducted using the Merative™ MarketScan® (Previously IBM MarketScan®) Databases between 2016 and 2020. Patients not continuously enrolled 180 days before/after surgery, who had malignancy, pre-existing chronic pain, opioid dependency, or invalid prescription fill information were excluded. Among patients exposed to opioids peri-operatively, we assessed long-term opioid use as any opioid prescription fill within 90 to 180 days post-surgery. Secondary outcomes were controlled substance schedule II/III opioid fill, and high-dose opioid fill defined as > 50 morphine milligram equivalent per day. An Inverse-probability of treatment weighted logistic regression was used to compare outcomes between groups with p-value of < 0.05 considered statistically significant. RESULTS: A total of 41,271 patients were identified (2070 (5.0%) RAS, 16,704 (40.5%) Lap, and 22,497 (54.5%) open surgery). RAS was associated with less likelihood of prescription fills for any opioid (OR 0.78, 95% CI 0.60 to 0.98 versus Lap; OR 0.67, 95% CI 0.52 to 0.85 versus open), and schedule II/III opioid (OR 0.74, 95% CI 0.56 to 0.96 versus Lap; OR 0.68, 95% CI 0.51 to 0.88 versus open), but comparable high-dose opioid fill (OR 0.95, 95% CI 0.54 to 1.55 versus Lap; OR 0.96, 95% CI 0.56 to 1.52 versus open). Lap and open surgery had no significant difference. CONCLUSION: In this cohort of patients derived from a national commercial claims dataset, patients undergoing RAS had a decreased risk of long-term opioid use compared to laparoscopic and open surgery patients undergoing IHR.
            Cover page: New persistent opioid use following robotic-assisted, laparoscopic and open surgery inguinal hernia repair.
            • Article
            • Peer Reviewed
            UCLA Previously Published Works (2020)
            Low physical activity (PA) among older adults increases the risk of cardiovascular disease (CVD) and mortality through metabolic disorders such as type 2 diabetes. We aimed to elucidate the extent to which diabetes mediates the effect of nonoccupational PA levels on CVD and mortality among older Mexican Americans. This study included 1,676 adults from the Sacramento Area Latino Study on Aging (1998-2007). We employed Cox proportional hazards regression models to investigate associations of PA level with all-cause mortality, fatal CVD, and nonfatal CVD events. Utilizing causal mediation analysis within a counterfactual framework, we decomposed the total effect of PA into natural indirect and direct effects. Over a median of 8 years of follow-up, low PA (<25th percentile) was associated with increased risks of all-cause mortality (hazard ratio (HR) = 1.36, 95% confidence interval (CI): 1.06, 1.75), fatal CVD (HR = 2.05, 95% CI: 1.42, 2.97), and nonfatal CVD events (HR = 1.67, 95% CI: 1.18, 2.37) in comparison with high PA (>75th percentile). Diabetes mediated 11.0%, 7.4%, and 5.2% of the total effect of PA on all-cause mortality, fatal CVD, and nonfatal CVD events, respectively. Our findings indicate that public health interventions targeting diabetes prevention and management would be a worthwhile strategy for preventing CVD and mortality among older Mexican Americans with insufficient PA levels.
              Cover page: Mediation of the Associations of Physical Activity With Cardiovascular Events and Mortality by Diabetes in Older Mexican Americans
              • Article
              • Peer Reviewed
              UCLA Previously Published Works (2019)

              Background

              Lifestyle factors may contribute to the development of Parkinson's disease, but little is known about factors that influence progression. The objective of the current study was to examine whether caffeine or alcohol consumption, physical activity, or cigarette smoking is associated with progression and survival among PD patients.

              Methods

              We assessed lifelong coffee, tea, and alcohol consumption, smoking, and physical activity in a prospective community-based cohort (n = 360). All patients were passively followed for mortality (2001-2016); 244 were actively followed on average ± SD 5.3 ± 2.1 years (2007-2014). Movement disorder specialists repeatedly assessed motor function (Hoehn & Yahr) and cognition (Mini-Mental State Exam). We used Cox proportional hazards models and inverse probability weights to account for censoring.

              Results

              Coffee, caffeinated tea, moderate alcohol consumption, and physical activity were protective against at least 1 outcome. Smoking and heavy alcohol consumption were associated with increased risks. Coffee was protective against time to Hoehn & Yahr stage 3 (hazard ratio, 0.52; 95% confidence interval, 0.28-1.01), cognitive decline (hazard ratio, 0.23; 95% confidence interval, 0.11, 0.48), and mortality (hazard ratio, 0.47; 95% confidence interval, 0.32-0.69). Relative to moderate drinkers, those who never drank liquor and those who drank more heavily were at an increased risk of Hoehn & Yahr 3 (hazard ratio, 3.48; 95% confidence interval, 1.90-6.38; and hazard ratio, 2.16; 95% confidence interval, 1.03, 4.54, respectively). A history of competitive sports was protective against cognitive decline (hazard ratio, 0.46; 95% confidence interval, 0.22-0.96) and Hoehn & Yahr 3 (hazard ratio, 0.42; 95% confidence interval, 0.23-0.79), as was physical activity measured by metabolic-equivalent hours. Current cigarette smoking was associated with faster cognitive decline (hazard ratio, 3.20; 95% confidence interval, 1.02-10.01).

              Conclusions

              This population-based study suggests that lifestyle factors influence PD progression and mortality. © 2019 International Parkinson and Movement Disorder Society.
                Cover page: The association between lifestyle factors and Parkinson's disease progression and mortality
                • Article
                • Peer Reviewed
                UCLA Previously Published Works (2023)

                Background

                Both air pollution and noise exposures have separately been shown to affect cognitive impairment. Here, we examine how air pollution and noise exposures interact to influence the development of incident dementia or cognitive impairment without dementia (CIND).

                Methods

                We used 1,612 Mexican American participants from the Sacramento Area Latino Study on Aging conducted from 1998 to 2007. Air pollution (nitrogen dioxides, particulate matter, ozone) and noise exposure levels were modeled with a land-use regression and via the SoundPLAN software package implemented with the Traffic Noise Model applied to the greater Sacramento area, respectively. Using Cox proportional hazard models, we estimated the hazard of incident dementia or CIND from air pollution exposure at the residence up to 5-years prior to diagnosis for the members of each risk set at event time. Further, we investigated whether noise exposure modified the association between air pollution exposure and dementia or CIND.

                Results

                In total, 104 incident dementia and 159 incident dementia/CIND cases were identified during the 10 years of follow-up. For each ∼2 µg/m3 increase in time-varying 1- and 5-year average PM2.5 exposure, the hazard of dementia increased 33% (HR = 1.33, 95%CI: 1.00, 1.76). The hazard ratios for NO2-related dementia/CIND and PM2.5-related dementia were stronger in high-noise (≥65 dB) exposed than low-noise (<65 dB) exposed participants.

                Conclusion

                Our study indicates that PM2.5 and NO2 air pollution adversely affect cognition in elderly Mexican Americans. Our findings also suggest that air pollutants may interact with traffic-related noise exposure to affect cognitive function in vulnerable populations.
                  Cover page: Air pollution and traffic noise interact to affect cognitive health in older Mexican Americans
                  • Article
                  • Peer Reviewed
                  UC San Francisco Previously Published Works (2020)

                  Background

                  Recently, it has been suggested that environmental exposures from traffic sources including noise may play a role in cognitive impairment in the elderly. The objective of the study was to investigate the association between local traffic-related noise pollution and incident dementia or cognitive impairment without dementia (CIND) during a 10-year follow-up period.

                  Methods

                  1612 Mexican-American participants from the Sacramento Area Latino Study on Aging (SALSA) were followed every 12-15 months via home visits from 1998 to 2007. We used the SoundPLAN software package to estimate noise originating from local traffic with the input of Annual Average Daily Traffic (AADT) data from Metropolitan Planning Organizations (MPO) based on geocoded residential addresses at baseline (1998-1999). We estimated the risks of incident dementia or CIND from 24-hour and nighttime noise exposure using Cox proportional hazard models.

                  Results

                  During the follow-up, we identified 159 incident dementia or CIND cases in total. Per 11.6 dB (interquartile range width) increase in 24-hour noise, the hazard of developing dementia or CIND increased (hazard ratio = 1.3 [1.0, 1.6]) during follow-up; estimates were slightly lower (hazard ratio = 1.2 [0.97, 1.6]) when adjusting for modeled local air pollution exposure from traffic sources. Overall, the risk of dementia/CIND was elevated when 24-hour and nighttime noise were higher than 75 and 65 dB respectively. See video Abstract: http://links.lww.com/EDE/B728.

                  Conclusions

                  In our study, traffic-related noise exposure was associated with increased risk of dementia or CIND in elderly Mexican-Americans. Future studies taking into account other noise sources and occupational noise exposure before retirement are needed.
                    Cover page: Traffic-related Noise Exposure and Late-life Dementia and Cognitive Impairment in Mexican-Americans.
                    • Article
                    • Peer Reviewed
                    UC San Francisco Previously Published Works (2020)
                    Cognitive impairment has been linked to traffic-related air pollution and noise exposure as well as to metabolic syndrome or some of its individual components. Here, we investigate whether the presence of metabolic dysfunction modifies associations between air pollution or noise exposures and incident dementia or cognitive impairment without dementia (CIND).

                    Methods

                    For 1,612 elderly Mexican-American participants of the Sacramento Area Latino Study on Aging (SALSA) followed for up to 10 years, we estimated residential-based local traffic-related exposures relying on the California Line Source Dispersion Model version 4 (CALINE4) for nitrogen oxides (NOx) and the SoundPLAN software package (Version 8.0; NAVCON, Fullerton, CA) that implements the Federal Highway Administration Traffic Noise Model (TNM) for noise, respectively. We used Cox proportional hazard models to estimate the joint effects of NOx or noise exposures and obesity, hyperglycemia, or low high-density lipoprotein (HDL) cholesterol.

                    Results

                    The risk of developing dementia/CIND among participants with hyperglycemia who also were exposed to high levels of NOx (≥3.44 parts per billion [ppb] [75th percentile]) or noise (≥65 dB) was 2.4 (1.4, 4.0) and 2.2 (1.7, 3.9), respectively. For participants with low HDL-cholesterol, the estimated hazard ratios for dementia/CIND were 2.5 (1.4, 4.3) and 1.8 (1.0, 3.0) for those also exposed to high levels of NOx (≥3.44 ppb) or noise (≥65 dB), respectively, compared with those without metabolic dysfunction exposed to low traffic-related air pollution or noise levels.

                    Conclusions

                    Exposure to traffic-related air pollution or noise most strongly increases the risk of dementia/CIND among older Mexican-Americans living in California who also exhibit hyperglycemia or low HDL-cholesterol.
                      Cover page: Metabolic dysfunction modifies the influence of traffic-related air pollution and noise exposure on late-life dementia and cognitive impairment
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