Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Sunday, December 6, 2020

Childhood intelligence in relation to major causes of death in 68 year follow-up: prospective population study

Well I guess I'm smart enough not to die from my stroke, but obviously not smart enough to figure out how to recover.

Childhood intelligence in relation to major causes of death in 68 year follow-up: prospective population study

BMJ 2017; 357 doi: https://doi.org/10.1136/bmj.j2708 (Published 28 June 2017) Cite this as: BMJ 2017;357:j2708
  1. Catherine M Calvin, postdoctoral research assistant1 2 3,  
  2. G David Batty, reader in epidemiology2 4,  
  3. Geoff Der, senior research fellow2 5,  
  4. Caroline E Brett, lecturer in health psychology2 6,  
  5. Adele Taylor, research assistant1,  
  6. Alison Pattie, research associate1,  
  7. Iva Čukić, postdoctoral research assistant1 2,  
  8. Ian J Deary, professor of differential psychology1 2
    Author affiliations
  1. Correspondence to: I Deary I.Deary@ed.ac.uk, C Calvin catherine.calvin@psych.ox.ac.uk
  • Accepted 28 May 2017

Abstract

Objectives To examine the association between intelligence measured in childhood and leading causes of death in men and women over the life course.

Design Prospective cohort study based on a whole population of participants born in Scotland in 1936 and linked to mortality data across 68 years of follow-up.

Setting Scotland.

Participants 33 536 men and 32 229 women who were participants in the Scottish Mental Survey of 1947 (SMS1947) and who could be linked to cause of death data up to December 2015.

Main outcome measures Cause specific mortality, including from coronary heart disease, stroke, specific cancer types, respiratory disease, digestive disease, external causes, and dementia.

Results Childhood intelligence was inversely associated with all major causes of death. The age and sex adjusted hazard ratios (and 95% confidence intervals) per 1 SD (about 15 points) advantage in intelligence test score were strongest for respiratory disease (0.72, 0.70 to 0.74), coronary heart disease (0.75, 0.73 to 0.77), and stroke (0.76, 0.73 to 0.79). Other notable associations (all P<0.001) were observed for deaths from injury (0.81, 0.75 to 0.86), smoking related cancers (0.82, 0.80 to 0.84), digestive disease (0.82, 0.79 to 0.86), and dementia (0.84, 0.78 to 0.90). Weak associations were apparent for suicide (0.87, 0.74 to 1.02) and deaths from cancer not related to smoking (0.96, 0.93 to 1.00), and their confidence intervals included unity. There was a suggestion that childhood intelligence was somewhat more strongly related to coronary heart disease, smoking related cancers, respiratory disease, and dementia in women than men (P value for interactions <0.001, 0.02, <0.001, and 0.02, respectively).Childhood intelligence was related to selected cancer presentations, including lung (0.75, 0.72 to 0.77), stomach (0.77, 0.69 to 0.85), bladder (0.81, 0.71 to 0.91), oesophageal (0.85, 0.78 to 0.94), liver (0.85, 0.74 to 0.97), colorectal (0.89, 0.83 to 0.95), and haematopoietic (0.91, 0.83 to 0.98). Sensitivity analyses on a representative subsample of the cohort observed only small attenuation of the estimated effect of intelligence (by 10-26%) after adjustment for potential confounders, including three indicators of childhood socioeconomic status. In a replication sample from Scotland, in a similar birth year cohort and follow-up period, smoking and adult socioeconomic status partially attenuated (by 16-58%) the association of intelligence with outcome rates.

Conclusions In a whole national population year of birth cohort followed over the life course from age 11 to age 79, higher scores on a well validated childhood intelligence test were associated with lower risk of mortality ascribed to coronary heart disease and stroke, cancers related to smoking (particularly lung and stomach), respiratory diseases, digestive diseases, injury, and dementia.

Introduction

Findings from prospective cohort studies based on populations from Australia, Sweden, Denmark, the US, and the UK indicate that higher cognitive ability (intelligence) measured with standard tests in childhood or early adulthood is related to a lower risk of total mortality by mid to late adulthood.1 The association is evident in men and women1 2; is incremental across the full range of ability scores2 3; and does not seem to be confounded by socioeconomic status of origin or perinatal factors.1 4 5 Whereas similar gradients are also apparent for selected causes of death, such as cardiovascular disease,3 6 7 8 9 10 suicide,7 10 11 12 13 14 15 and injuries,7 16 17 the association with other leading causes remains inconclusive or little tested. Mortality surveillance for the entire population of one country born in 1936 who had an assessment of childhood intelligence provides the valuable opportunity to examine little tested associations between intelligence and mortality and consider specificity by exploring the strengths of these associations according to leading causes of death, in men and women, and over almost the entire life course.

Several hypotheses have been proposed to explain associations between intelligence and later risk of mortality.18 The suggested causal mechanisms put forward, in which cognitive ability is the exposure and disease or death the outcome, include mediation by adverse or protective health behaviours in adulthood (such as smoking, physical activity), disease management and health literacy, and adult socioeconomic status (which could, for example, indicate occupational hazards).18 Recent evidence of a genetic contribution to the association between general cognitive ability and longevity,19 however, might support a system integrity theory that posits a “latent trait of optimal bodily functioning” proximally indicated by both cognitive test performance and disease biomarkers.20 None of these possibilities are mutually exclusive. Whereas cognitive epidemiology18 makes a unique contribution to improved understanding of health inequalities in populations, by its successful application of a well validated behavioural trait that performs independently of social gradients in its association with health indices,21 22 there remains a fundamental question regarding how specific and multifaceted the link is between individual differences in intelligence and longevity. Evidence for an association with several leading causes of death has either not been replicated (dementia and respiratory disease),7 23 is conflicting (different cancer sites),5 7 8 24 25 26 27 or is hitherto untested (digestive system disease). At least six publications have compared associations between premorbid intelligence and a selection of cause specific mortalities,5 7 8 10 24 28 including some well characterised and extremely large cohorts with extensive follow-up; however, over-representation of men only samples7 10 and follow-up that was terminated in middle age5 10 has limited the generalisability of findings. Furthermore, low numbers of events for diseases common in older adult populations could have contributed to some apparently conflicting results.8 24 28

We investigated the magnitudes of the association between childhood intelligence and all major causes of death, using a whole year of birth population followed up to older age, therefore capturing sufficient numbers of cases for each outcome. Secondly, we investigated sex differences in the associations. Thirdly, we carried out sensitivity analyses to test for some possible mechanisms of association, including confounding and mediation by socioeconomic status.

 

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