Prime mover or fellow traveller: 25-hydroxy vitamin D’s seasonal variation, cardiovascular disease and death in the Scottish Heart Health Extended Cohort (SHHEC)

Hugh Tunstall-Pedoe (Lead / Corresponding author), Mark Woodward, Maria Hughes, Annie Anderson, Gwen Kennedy, Jill Belch, Kari Kuulasmaa, MORGAM Investigators

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Abstract

BACKGROUND: Theoretical links between seasonal lack of sunlight, hypovitaminosis D and excess cardiovascular disease and death prompted our adding novel to conventional cohort analyses. 

METHODS: We tested three postulates on 13 224 Scottish Heart Health Extended Cohort participants, assayed for 25-hydroxyvitamin D (25OHD) and followed for 22 years. (i) Endpoints enumerated by month of occurrence mirror annual seasonal oscillation in 25OHD. (ii) Endpoint seasonality is increased in people with below median 25OHD. (iii) Low 25OHD predicts endpoints independently of major risk factors. 

RESULTS: Baseline median 25OHD level was 36.4 (other quartiles 26.7, 51.7) nmol/l. The March trough was half the August peak, both well after seasonal solstices. (i) There was no demonstrable monthly variation in First Cardiovascular Event (n = 3307). Peaks and troughs for All Death and Cardiovascular Death (n = 2987, 1350) were near the solstices, earlier than extremes of 25OHD. (ii) Endpoint variability showed no difference between those above and below median 25OHD. (iii) Cox model hazard ratios (HR), by decreasing 25OHD, increased modestly and nonspecifically for all endpoints examined, with no threshold, the gradients diminishing by  ∼ : 60% following multiple adjustment. For Cardiovascular Disease, HR, by 20 (∼SD) nmol/l decrease, = 1.224 (1.175, 1.275) adjusted for age and sex; additionally adjusted for family history, deprivation index, smoking, systolic blood pressure, total and HDL cholesterol, = 1.093 (1.048, 1.139); All Deaths = 1.238 (1.048, 1.139) and 1.098 (1.050, 1.149). 25OHD made no independent contribution to cardiovascular discrimination and reclassification. CONCLUSIONS: Our analyses challenge vitamin D's alleged role as major prime mover in cardiovascular disease and mortality.

Original languageEnglish
Pages (from-to)1602-1612
Number of pages11
JournalInternational Journal of Epidemiology
Volume44
Issue number5
Early online date21 Jun 2015
DOIs
Publication statusPublished - 21 Jun 2015

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Vitamins
Cardiovascular Diseases
Health
Blood Pressure
Social Adjustment
Sunlight
Proportional Hazards Models
HDL Cholesterol
Cohort Studies
Smoking
Mortality

Keywords

  • Vitamin D
  • causality
  • seasonality
  • cardiovascular disease
  • mortality
  • cohort study

Cite this

@article{4402ca638b2d412bae3a11b21abc688f,
title = "Prime mover or fellow traveller: 25-hydroxy vitamin D’s seasonal variation, cardiovascular disease and death in the Scottish Heart Health Extended Cohort (SHHEC)",
abstract = "BACKGROUND: Theoretical links between seasonal lack of sunlight, hypovitaminosis D and excess cardiovascular disease and death prompted our adding novel to conventional cohort analyses. METHODS: We tested three postulates on 13 224 Scottish Heart Health Extended Cohort participants, assayed for 25-hydroxyvitamin D (25OHD) and followed for 22 years. (i) Endpoints enumerated by month of occurrence mirror annual seasonal oscillation in 25OHD. (ii) Endpoint seasonality is increased in people with below median 25OHD. (iii) Low 25OHD predicts endpoints independently of major risk factors. RESULTS: Baseline median 25OHD level was 36.4 (other quartiles 26.7, 51.7) nmol/l. The March trough was half the August peak, both well after seasonal solstices. (i) There was no demonstrable monthly variation in First Cardiovascular Event (n = 3307). Peaks and troughs for All Death and Cardiovascular Death (n = 2987, 1350) were near the solstices, earlier than extremes of 25OHD. (ii) Endpoint variability showed no difference between those above and below median 25OHD. (iii) Cox model hazard ratios (HR), by decreasing 25OHD, increased modestly and nonspecifically for all endpoints examined, with no threshold, the gradients diminishing by  ∼ : 60{\%} following multiple adjustment. For Cardiovascular Disease, HR, by 20 (∼SD) nmol/l decrease, = 1.224 (1.175, 1.275) adjusted for age and sex; additionally adjusted for family history, deprivation index, smoking, systolic blood pressure, total and HDL cholesterol, = 1.093 (1.048, 1.139); All Deaths = 1.238 (1.048, 1.139) and 1.098 (1.050, 1.149). 25OHD made no independent contribution to cardiovascular discrimination and reclassification. CONCLUSIONS: Our analyses challenge vitamin D's alleged role as major prime mover in cardiovascular disease and mortality.",
keywords = "Vitamin D, causality, seasonality, cardiovascular disease, mortality, cohort study",
author = "Hugh Tunstall-Pedoe and Mark Woodward and Maria Hughes and Annie Anderson and Gwen Kennedy and Jill Belch and Kari Kuulasmaa and {MORGAM Investigators}",
note = "{\circledC} The Author 2015; all rights reserved. Published by Oxford University Press on behalf of the International Epidemiological Association.",
year = "2015",
month = "6",
day = "21",
doi = "10.1093/ije/dyv092",
language = "English",
volume = "44",
pages = "1602--1612",
journal = "International Journal of Epidemiology",
issn = "0300-5771",
publisher = "Oxford University Press",
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}

TY - JOUR

T1 - Prime mover or fellow traveller

T2 - 25-hydroxy vitamin D’s seasonal variation, cardiovascular disease and death in the Scottish Heart Health Extended Cohort (SHHEC)

AU - Tunstall-Pedoe, Hugh

AU - Woodward, Mark

AU - Hughes, Maria

AU - Anderson, Annie

AU - Kennedy, Gwen

AU - Belch, Jill

AU - Kuulasmaa, Kari

AU - MORGAM Investigators

N1 - © The Author 2015; all rights reserved. Published by Oxford University Press on behalf of the International Epidemiological Association.

PY - 2015/6/21

Y1 - 2015/6/21

N2 - BACKGROUND: Theoretical links between seasonal lack of sunlight, hypovitaminosis D and excess cardiovascular disease and death prompted our adding novel to conventional cohort analyses. METHODS: We tested three postulates on 13 224 Scottish Heart Health Extended Cohort participants, assayed for 25-hydroxyvitamin D (25OHD) and followed for 22 years. (i) Endpoints enumerated by month of occurrence mirror annual seasonal oscillation in 25OHD. (ii) Endpoint seasonality is increased in people with below median 25OHD. (iii) Low 25OHD predicts endpoints independently of major risk factors. RESULTS: Baseline median 25OHD level was 36.4 (other quartiles 26.7, 51.7) nmol/l. The March trough was half the August peak, both well after seasonal solstices. (i) There was no demonstrable monthly variation in First Cardiovascular Event (n = 3307). Peaks and troughs for All Death and Cardiovascular Death (n = 2987, 1350) were near the solstices, earlier than extremes of 25OHD. (ii) Endpoint variability showed no difference between those above and below median 25OHD. (iii) Cox model hazard ratios (HR), by decreasing 25OHD, increased modestly and nonspecifically for all endpoints examined, with no threshold, the gradients diminishing by  ∼ : 60% following multiple adjustment. For Cardiovascular Disease, HR, by 20 (∼SD) nmol/l decrease, = 1.224 (1.175, 1.275) adjusted for age and sex; additionally adjusted for family history, deprivation index, smoking, systolic blood pressure, total and HDL cholesterol, = 1.093 (1.048, 1.139); All Deaths = 1.238 (1.048, 1.139) and 1.098 (1.050, 1.149). 25OHD made no independent contribution to cardiovascular discrimination and reclassification. CONCLUSIONS: Our analyses challenge vitamin D's alleged role as major prime mover in cardiovascular disease and mortality.

AB - BACKGROUND: Theoretical links between seasonal lack of sunlight, hypovitaminosis D and excess cardiovascular disease and death prompted our adding novel to conventional cohort analyses. METHODS: We tested three postulates on 13 224 Scottish Heart Health Extended Cohort participants, assayed for 25-hydroxyvitamin D (25OHD) and followed for 22 years. (i) Endpoints enumerated by month of occurrence mirror annual seasonal oscillation in 25OHD. (ii) Endpoint seasonality is increased in people with below median 25OHD. (iii) Low 25OHD predicts endpoints independently of major risk factors. RESULTS: Baseline median 25OHD level was 36.4 (other quartiles 26.7, 51.7) nmol/l. The March trough was half the August peak, both well after seasonal solstices. (i) There was no demonstrable monthly variation in First Cardiovascular Event (n = 3307). Peaks and troughs for All Death and Cardiovascular Death (n = 2987, 1350) were near the solstices, earlier than extremes of 25OHD. (ii) Endpoint variability showed no difference between those above and below median 25OHD. (iii) Cox model hazard ratios (HR), by decreasing 25OHD, increased modestly and nonspecifically for all endpoints examined, with no threshold, the gradients diminishing by  ∼ : 60% following multiple adjustment. For Cardiovascular Disease, HR, by 20 (∼SD) nmol/l decrease, = 1.224 (1.175, 1.275) adjusted for age and sex; additionally adjusted for family history, deprivation index, smoking, systolic blood pressure, total and HDL cholesterol, = 1.093 (1.048, 1.139); All Deaths = 1.238 (1.048, 1.139) and 1.098 (1.050, 1.149). 25OHD made no independent contribution to cardiovascular discrimination and reclassification. CONCLUSIONS: Our analyses challenge vitamin D's alleged role as major prime mover in cardiovascular disease and mortality.

KW - Vitamin D

KW - causality

KW - seasonality

KW - cardiovascular disease

KW - mortality

KW - cohort study

U2 - 10.1093/ije/dyv092

DO - 10.1093/ije/dyv092

M3 - Article

C2 - 26095374

VL - 44

SP - 1602

EP - 1612

JO - International Journal of Epidemiology

JF - International Journal of Epidemiology

SN - 0300-5771

IS - 5

ER -