scholarly journals Sauna bathing is inversely associated with dementia and Alzheimer's disease in middle-aged Finnish men

2016 ◽  
Vol 46 (2) ◽  
pp. 245-249 ◽  
Author(s):  
Tanjaniina Laukkanen ◽  
Setor Kunutsor ◽  
Jussi Kauhanen ◽  
Jari Antero Laukkanen

Abstract Background there are no previous studies linking repeated heat exposure of sauna and the risk of memory diseases. We aimed to investigate whether frequency of sauna bathing is associated with risk of dementia and Alzheimer's disease. Setting prospective population-based study. Methods the frequency of sauna bathing was assessed at baseline in the Kuopio Ischaemic Heart Disease population-based prospective cohort study of 2,315 apparently healthy men aged 42–60 years at baseline, with baseline examinations conducted between 1984 and 1989. Hazard ratios (HRs) with 95% confidence intervals (CIs) for dementia and Alzheimer's disease were ascertained using Cox-regression modelling with adjustment for potential confounders. Results during a median follow-up of 20.7 (interquartile range 18.1–22.6) years, a total of 204 and 123 diagnosed cases of dementia and Alzheimer's disease were respectively recorded. In analysis adjusted for age, alcohol consumption, body mass index, systolic blood pressure, smoking status, Type 2 diabetes, previous myocardial infarction, resting heart rate and serum low-density lipoprotein cholesterol, compared with men with only 1 sauna bathing session per week, the HR for dementia was 0.78 (95% CI: 0.57–1.06) for 2–3 sauna bathing sessions per week and 0.34 (95% CI: 0.16–0.71) for 4–7 sauna bathing sessions per week. The corresponding HRs for Alzheimer's disease were 0.80 (95% CI: 0.53–1.20) and 0.35 (95% CI: 0.14–0.90). Conclusion in this male population, moderate to high frequency of sauna bathing was associated with lowered risks of dementia and Alzheimer's disease. Further studies are warranted to establish the potential mechanisms linking sauna bathing and memory diseases.

2018 ◽  
Vol 27 (6) ◽  
pp. 562-569 ◽  
Author(s):  
Tanjaniina Laukkanen ◽  
Jari A. Laukkanen ◽  
Setor K. Kunutsor

Objective: Sauna bathing has been suggested to promote mental well-being and relaxation, but the evidence is uncertain with respect to mental disorders. We aimed to assess the association of frequency of sauna bathing with risk of psychosis in the Kuopio Ischemic Heart Disease prospective population-based study. Subjects and Methods: Baseline sauna bathing habits were assessed in 2,138 men aged 42–61 years who had no history of psychotic disorders. Participants were classified into three groups based on the frequency of sauna bathing (once, 2–3, and 4–7 times per week). Results: During a median follow-up of 24.9 years, 203 psychotic disorders were recorded. A total of 537, 1,417, and 184 participants reported having a sauna bath once a week, 2–3 times, and 4–7 times per week, respectively. In Cox regression analysis adjusted for age, compared to men who had 1 sauna session per week, the hazard ratio (95% confidence intervals) of psychosis for 4–7 sauna sessions per week was 0.23 (0.09–0.58). In a multivariable model adjusted for several risk factors and other potential confounders, the corresponding hazard ratio was 0.21 (0.08–0.52). The association was similar after further adjustment for total energy intake, socioeconomic status, physical activity, and C-reactive protein (0.22 [0.09–0.54]) and was unchanged on additional adjustment for duration of a sauna session and temperature of the sauna bath (0.23 [0.09–0.57]). Conclusion: Our study suggests a strong inverse and independent association between frequent sauna bathing and the future risk of psychotic disorders in a general male population.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
G Pesau ◽  
C Hoebaus ◽  
B Zierfuss ◽  
R Koppensteiner ◽  
G H Schernthaner

Abstract Background and introduction Endothelial dysfunction and associated cells are an important cornerstone in the development and progression of peripheral artery disease (PAD). Endothelial progenitor cells (EPC) are released from the bone marrow and have exhibited the potential for cardiovascular repair. Higher EPC levels have been linked to longer event-free survival in coronary artery disease. Similar evaluation of EPC on mortality in PAD is lacking. Purpose The current study aimed to evaluate the possible association between EPC levels and mortality in PAD patients. Methods EPC were measured in 367 PAD patients (age 69.22±10.3, 66.5% male, Fontaine stage I-II) by flow cytometry using the cell surface marker CD34+ and CD309+. Patients were followed for seven years to assess all cause and cardiovascular mortality. Patients were categorized into quartiles according to EPC levels for further analyses. Statistics included Kaplan-Meier and Cox regression. Results 89 patients died over the observation period. ICD-codes indicated a cardiovascular cause in 58 patients. The group with the highest count of EPC showed a trend towards higher all-cause mortality (p=0.070) and a significant association with cardiovascular mortality (p=0.002). Multivariable adjustment for age, c-reactive protein, systolic blood pressure, renal function (creatinine and urinary albumin), low density lipoprotein cholesterol, HbA1c, and smoking status revealed the EPC quartile to be an independent risk factor for cardiovascular mortality (p=0.016). Conclusion Increased levels of CD34+CD309+ cells are independently associated with long-term cardiovascular mortality in PAD patients.


2005 ◽  
Vol 26 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Rangaraj K. Gopalraj ◽  
Haiyan Zhu ◽  
Jeremiah F. Kelly ◽  
Marta Mendiondo ◽  
Joseph F. Pulliam ◽  
...  

2019 ◽  
Vol 2 (1) ◽  
Author(s):  
Donald R Royall ◽  
Raymond F Palmer ◽  

Abstract Dementia severity can be quantitatively described by the latent dementia phenotype ‘δ’ and its various composite ‘homologues’. We have explored δ’s blood-based protein biomarkers in the Texas Alzheimer’s Research and Care Consortium. However, it would be convenient to replicate them in the Alzheimer’s Disease Neuroimaging Initiative. To that end, we have engineered a δ homologue from the observed cognitive performance measures common to both projects [i.e. ‘d:Texas Alzheimer’s Research and Care Consortium to Alzheimer’s Disease Neuroimaging Initiative’ (dT2A)]. In this analysis, we confirm 13/22 serum proteins as partial mediators of age’s effect on dementia severity as measured by dT2A in the Texas Alzheimer’s Research and Care Consortium and then replicate 4/13 in the Alzheimer’s Disease Neuroimaging Initiative’s plasma data. The replicated mediators of age-specific effects on dementia severity are adiponectin, follicle-stimulating hormone, pancreatic polypeptide and resistin. In their aggregate, the 13 confirmed age-specific mediators suggest that ‘cognitive frailty’ pays a role in dementia severity as measured by δ. We provide both discriminant and concordant support for that hypothesis. Weight, calculated low-density lipoprotein and body mass index are partial mediators of age’s effect in the Texas Alzheimer’s Research and Care Consortium. Biomarkers related to other disease processes (e.g. cerebrospinal fluid Alzheimer’s disease-specific biomarkers in the Alzheimer’s Disease Neuroimaging Initiative) are not. It now appears that dementia severity is the sum of multiple independent processes impacting δ. Each may have a unique set of mediating biomarkers. Age’s unique effect appears to be at least partially mediated through proteins related to frailty. Age-specific mediation effects can be replicated across cohorts and biofluids. These proteins may offer targets for the remediation of age-specific cognitive decline (aka ‘senility’), help distinguish it from other determinants of dementia severity and/or provide clues to the biology of Aging Proper.


2011 ◽  
Vol 19 (3) ◽  
pp. 523-533 ◽  
Author(s):  
Amal Khanolkar ◽  
Denny Vågerö ◽  
Ilona Koupil

Background: Social status is associated with cardiovascular disease (CVD) prevalence and incidence. Aims: to investigate relationships between socioeconomic position (SEP) and common CVD biomarkers including adiponectin not previously investigated in a Swedish-population sample, and to assess if these associations changed with age. Design: Population-based longitudinal cohort study of men born 1920–24 with clinical measurements, blood samples, questionnaire data, and register-based information on SEP and cause of death. Methods: A total of 2322 men attended an investigation at age 50 of which 1221 attended a reinvestigation at age 70. Association between SEP and CVD biomarkers [cholesterol, low-density lipoprotein/high-density lipoprotein (LDL/HDL), apolipoprotein (Apo) ApoB/ApoA1, and adiponectin] were analysed by linear regression (adjusted for age, body mass index, and physical activity). SEP was measured as occupational class and educational level. CVD mortality over 36 years of follow-up was analysed by Cox regression. Results: At age 50, we found a significant inverse association of education with cholesterol level, LDL/HDL ratio and ApoB/ApoA1 ratio. Cholesterol was also associated with occupational class, statistically significant after adjustment for all covariates. At age 70, no significant associations were found between either measurement of SEP and any of the biomarkers studied. Highest educated men had decreased risk for CVD mortality during follow-up. Conclusions: Associations of SEP with cholesterol levels and LDL/HDL ratio that exist at age 50 are no longer apparent in the same group of men at age 70. We found no significant association between SEP and adiponectin levels at age 70.


2016 ◽  
Vol 64 (2) ◽  
pp. 392-399 ◽  
Author(s):  
Altan Onat ◽  
Günay Can ◽  
Neslihan Çoban ◽  
İbrahim Dönmez ◽  
Hakan Çakır ◽  
...  

Owing to the scarcity of available information, we aimed to assess the association of migration inhibitory factor (MIF)-173 G/C genotypes and serum lipoprotein(Lp)(a) with incident metabolic syndrome (MetS) and all-cause mortality, respectively. In population based, middle-aged adults (n=1297), stratified by gender and presence of MetS, we used Lp(a) quintiles to identify non-linear associations with outcomes using Cox regression models, adjusted for MIF genotype, age, smoking status, high density lipoprotein cholesterol, and systolic blood pressure. After 5.2 years of follow-up, 151 cases of incident MetS and 123 deaths were recorded. For incident MetS, adjusted HRs increased in each gender across four declining quintiles, starting from the highest quintile in men and from quintile 4 in women. The MIF CC-GC genotype appeared to contribute to the risk estimates in men. Similarly adjusted models in the whole sample disclosed that all-cause mortality tended to be inversely associated with Lp(a) quintiles and yielded an HR (2.42 (95% CI 1.03 to 5.81)) in men in quintile 2, whereas the MIF genotype additively predicted mortality (HR 1.79 (95% CI 1.01 to 3.18)) only in men. Excess risk of death was additively conferred on Turkish men by the MIF CC-GC genotype and by apparently reduced circulating Lp(a) assays, supporting the notion that ‘low’ serum Lp(a), mediating autoimmune activation, is a major determinant of metabolic disease risk and death. Damaged MIF protein and more complex autoimmune activation in women may be responsible from lack of relationship to MetS/mortality.


Sign in / Sign up

Export Citation Format

Share Document