scholarly journals Higher blood high density lipoprotein and apolipoprotein A1 levels are associated with reduced risk of developing amyotrophic lateral sclerosis

2021 ◽  
pp. jnnp-2021-327133
Author(s):  
Alexander G Thompson ◽  
Kevin Talbot ◽  
Martin R Turner

BackgroundPremorbid body mass index, physical activity, diabetes and cardiovascular disease have been associated with an altered risk of developing amyotrophic lateral sclerosis (ALS). There is evidence of shared genetic risk between ALS and lipid metabolism. A very large prospective longitudinal population cohort permits the study of a range of metabolic parameters and the risk of subsequent diagnosis of ALS.MethodsThe risk of subsequent ALS diagnosis in those enrolled prospectively to the UK Biobank (n=502 409) was examined in relation to baseline levels of blood high and low density lipoprotein (HDL, LDL), total cholesterol, total cholesterol:HDL ratio, apolipoproteins A1 and B (apoA1, apoB), triglycerides, glycated haemoglobin A1c (HbA1c) and creatinine, plus self-reported exercise and body mass index.ResultsControlling for age and sex, higher HDL (HR 0.84, 95% CI 0.73 to 0.96, p=0.010) and apoA1 (HR 0.83, 95% CI 0.72 to 0.94, p=0.005) were associated with a reduced risk of ALS. Higher total cholesterol:HDL was associated with an increased risk of ALS (HR 1.17, 95% CI 1.05 to 1.31, p=0.006). In models incorporating multiple metabolic markers, higher LDL or apoB was associated with an increased risk of ALS, in addition to a lower risk with higher HDL or apoA. Coronary artery disease, cerebrovascular disease and increasing age were also associated with an increased risk of ALS.ConclusionsThe association of HDL, apoA1 and LDL levels with risk of ALS contributes to an increasing body of evidence that the premorbid metabolic landscape may play a role in pathogenesis. Understanding the molecular basis for these changes will inform presymptomatic biomarker development and therapeutic targeting.

Author(s):  
I. Cotter ◽  
C. Healy ◽  
R. King ◽  
DR. Cotter ◽  
M. Cannon

Abstract Background. Abnormal body mass index (BMI) has been associated with development of psychopathology. This association in children is well documented, for both overweight and underweight children. However, the association between change in BMI and the development of psychopathology has been less investigated. Aim. To investigate the association between change in BMI between childhood and adolescence and psychopathology in adolescence. Methods. Data from the Growing Up in Ireland cohort were used. We investigated the ’98 cohort (also known as the child cohort) at age 9/13. BMI, defined using internationally recognised definitions as underweight, healthy or overweight, was used as the exposure, and abnormal Strength and Difficulties Questionnaire scores were used as the outcome. Logistic regression was undertaken for the analysis. All analyses were adjusted for confounders. Results. A change to overweight from healthy BMI was significantly associated with increased risk of psychopathology (adjusted OR 1.66; 95% CI 1.19–2.32). Both change from underweight to healthy (adjusted OR 0.12; 95% CI 0.03–0.43) or from overweight to healthy (adjusted OR 0.47; 95% CI 0.79–0.8) was associated with a significantly reduced risk of developing psychopathology. Discussion. As a child’s BMI returns to within the healthy range, their risk of adolescent psychopathology is reduced. Interventions to restore healthy BMI, in both underweight and overweight, children may reduce their risk of adolescent psychopathology.


2017 ◽  
Vol 88 (12) ◽  
pp. 1033-1041 ◽  
Author(s):  
Martin Gorges ◽  
Pauline Vercruysse ◽  
Hans-Peter Müller ◽  
Hans-Jürgen Huppertz ◽  
Angela Rosenbohm ◽  
...  

2017 ◽  
Vol 30 (2) ◽  
pp. 67-76 ◽  
Author(s):  
Jorge Mario Rodríguez-Fernández ◽  
Emily Danies ◽  
José Martínez-Ortega ◽  
William C. Chen

Objective: The aim of this study was to explore the association of body mass index (BMI), waist circumference (WC), and BMI and WC changes over time with cognitive decline in a nationally representative sample. Methods: A total of 5239 participants (≥65 years) were followed for 3 years as part of the National Health and Aging Trends Study. Cox proportional hazard regression was applied to model the risk of cognitive decline. Results: BMI, after adjusting for WC and main confounders, was associated with reduced risk of cognitive decline (hazard ratio [HR] 0.97 for each unit BMI increase, 0.95-0.99). After stratifying by gender and age, this effect remained significant among females and young elders ≤80 years. A BMI decrease and WC increase >10% over the study period were associated with increased risk of cognitive decline (HR 1.98, 1.16-3.38; HR 1.30, 1.04-1.62, respectively). Conclusion: In the elderly individuals, lean mass, as measured by BMI adjusted for WC, was associated with reduced risk of cognitive decline. Loss of lean mass and gain of fat mass, as measured by WC adjusted for BMI, were associated with elevated risk of cognitive decline.


2019 ◽  
Author(s):  
Ping Zeng ◽  
Xinghao Yu ◽  
Haibo Xu

Background: Inverse association between premorbid body mass index (BMI) and amyotrophic lateral sclerosis (ALS) has been discovered in observational studies; however, whether this association is causal remains largely unknown. Methods: We employed a two-sample Mendelian randomization approach to evaluate the causal relationship of genetically increased BMI with the risk of ALS. The analyses were implemented using summary statistics obtained for the independent instruments identified from large-scale genome-wide association studies of BMI (up to ~770,000 individuals) and ALS (up to ~81,000 individuals). The causal relationship between BMI and ALS was estimated using inverse-variance weighted methods and was further validated through extensive complementary and sensitivity analyses. Findings: Using 1,031 instruments strongly related to BMI, the causal effect of per one standard deviation increase of BMI was estimated to be 1.04 (95% CI 0.97~1.11, p=0.275) in the European population. The null association between BMI and ALS discovered in the European population also held in the East Asian population and was robust against various modeling assumptions and outlier biases. Additionally, the Egger-regression and MR-PRESSO ruled out the possibility of horizontal pleiotropic effects of instruments. Interpretation: Our results do not support the causal role of genetically increased or decreased BMI on the risk of ALS.


2017 ◽  
Vol 185 (5) ◽  
pp. 362-371 ◽  
Author(s):  
Daniela Mariosa ◽  
John D. Beard ◽  
David M. Umbach ◽  
Rino Bellocco ◽  
Jean Keller ◽  
...  

2019 ◽  
Vol 8 (10) ◽  
pp. 1725 ◽  
Author(s):  
Yinkun Yan ◽  
Lydia A. Bazzano ◽  
Markus Juonala ◽  
Olli T. Raitakari ◽  
Jorma S. A. Viikari ◽  
...  

Background: Data are limited regarding the association of cumulative burden and trajectory of body mass index (BMI) from early life with adult lipid disorders. Methods: The study cohort consisted of 5195 adults who had BMI repeatedly measured 4 to 21 times from childhood and had blood lipid measurements of low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides (TG) and information on lipid-lowering medications in the last adult survey. The area under the curve (AUC) was calculated as a measure of long-term burden (total AUC) and trends (incremental AUC) of BMI. Results: Participants with dyslipidemia, high LDL-C, low HDL-C and high TG had consistently and significantly higher BMI levels from childhood to adulthood compared to those with normal lipid levels. After adjusting for age, race, sex, and cohort, increased risk of adult dyslipidemia was significantly associated with higher values of childhood BMI, adulthood BMI, total AUC and incremental AUC, with odds ratio (95% confidence interval) = 1.22 (1.15–1.29), 1.85 (1.74–1.97), 1.61 (1.52–1.71), and 1.59 (1.50–1.69), respectively, and p < 0.001 for all. The association patterns were similar in most race–sex subgroups. Conclusions: Adults with dyslipidemia versus normal lipid levels have consistently higher levels and distinct life-course trajectories of BMI, suggesting that the impact of excessive body weight on dyslipidemia originates in early life.


Author(s):  
Éilis J. O'Reilly ◽  
Hao Wang ◽  
Marc G. Weisskopf ◽  
Kathryn C. Fitzgerald ◽  
Guido Falcone ◽  
...  

2013 ◽  
Vol 3 (4) ◽  
pp. 80 ◽  
Author(s):  
Maximilien C. Goris Gbenou

Recent studies have demonstrated an association between higher body mass index and increased aggressiveness in prostate cancer. The present narrative review, based on a search of Medline® and Embase® databases from October 1982 to October 2012, explores the relationship between higher body mass index and localized prostate cancer. In particular, the current epidemiological and mechanistic evidence for interactions between obesity and prostate cancer are discussed. Obesity is associated with alterations in androgen levels, decreased sex hormone binding globulin and increased estrogen levels, insulin resistance, hyperglycemia, alterations in plasma lipoprotein levels particularly raised triglycerides and reduced high density lipoprotein, decreased levels of adiponectin, and increased levels of circulating insulin-growth factor- 1, leptin and dietary saturated fats. Obese men have more aggressive prostate cancer with a greater percentage prostate involvement, increased tumor volume and higher-grade disease, enlarged prostates, high prostate-specific antigen levels, increased risk of having positive margins and recurrence. Moreover, there is strong evidence of the beneficial effects of functional foods for the treatment of obesity. Additionally, an increasing number of studies support that obesity-induced inflammation plays an important role in the development of obesity-related pathologies. Despite, the beneficial role of nutriment in prostate cancer control, the use of functional foods in prostate cancer is not recommended for lack of large epidemiological studies. This data supports the hypothesis that obese men have more aggressive prostate cancers and that the obesity is a modifiable risk factor of prostate cancer. Key Words: prostate cancer, metabolic syndrome, obesity, high BMI, risk factor, diet, functional foods.


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