Preventing Chronic Disease David Barker Professor of Clinical - - PowerPoint PPT Presentation

preventing chronic disease
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Preventing Chronic Disease David Barker Professor of Clinical - - PowerPoint PPT Presentation

Preventing Chronic Disease David Barker Professor of Clinical Epidemiology, University of Southampton Professor of Cardiovascular Medicine, Oregon Health and Science University The fetal origins of chronic disease Coronary heart disease,


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Preventing Chronic Disease

David Barker Professor of Clinical Epidemiology, University

  • f Southampton

Professor of Cardiovascular Medicine, Oregon

Health and Science University

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The fetal origins of chronic disease

  • Coronary heart disease, Type 2 diabetes,

hypertension, osteoporosis and asthma originate in developmental plasticity, in response to malnutrition during fetal life and infancy

  • Certain cancers also originate in this way
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≤ 5.5

  • 6.5
  • 7.5
  • 8.5
  • 9.5

>9.5

Birthweight (pounds)

20 40 60 80 100 120

Standardised Mortality Ratio Men

≤ 5.5

  • 6.5
  • 7.5
  • 8.5
  • 9.5

>9.5

Birthweight (pounds)

20 40 60 80 100 120

Women

Mortality from coronary heart disease in 15726 men and women in Hertfordshire

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Hazard ratios for coronary heart disease in men

16 17 18 19 20 21 22 23 24 25 26 27 >27

Weight at one year (pounds)

0.5 1 1.5 2 2.5 3

Hazard ratio

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Programming

Malnutrition and other adverse environmental exposures during development alter gene expression and programme the body’s structures and functions for life. Adverse exposures also result in slow growth and small body size.

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  • Much of human development is completed

during the first 1000 days after conception.

  • Each system and organ has a critical, often

brief, period during which it has to develop.

  • Most critical periods occur in utero

Critical periods

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During normal human growth the development of low priority organs, such as the lungs and kidneys, is traded-off to protect high priority organs, importantly the brain.

Trade offs

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Small body size at birth

People who were small at birth are biologically different:

  • Reduced functional capacity e.g. fewer nephrons, less muscle
  • Altered metabolic settings e.g. insulin resistance
  • Altered hormonal production e.g. stress responses, sex hormones
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Associations between early growth and later disease extend across the range of fetal and infant growth. This implies that what are regarded as normal variations in the supply

  • f nutrients to the baby have important

long–term effects.

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Fetal nutrition

Size at birth is the product of the fetus’s trajectory of growth, which is set soon after conception, and the materno-placental capacity to supply sufficient nutrients to maintain this trajectory.

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Fetal Nutrition

The fetus is nourished by

  • the mother’s diet
  • the nutrients stored in her body
  • her metabolism
  • the placenta’s ability to transport nutrients from mother to baby
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Pelvic diameters

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Hazard ratios for ovarian cancer according to mothers’ interspinous diameter and age at menarche

2 4 6 8 10 25 25.1-26.0 26.1-27.0 >27.0 Menarche at age 14 years or less p for trend 0.002 Menarche at age 15 years or more p for trend 0.63

Interspinous diameter (cm) H a z a r d r a t i

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Lung cancer according to head circumference at birth

0.5 1 1.5

  • 33
  • 34
  • 35
  • 36

>36 Head circumference (cm) Hazard ratio

p for trend=0.001

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Lung cancer according to placental area

0.5 1 1.5 2 2.5 3 3.5

  • 200
  • 240
  • 280
  • 320

>320

East

Placental area (cm2) Hazard ratio

p for trend=0.004

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The causes of chronic disease are linked to variations in the normal processes of development that programme a few key systems - the immune system, anti-oxidant defences, inflammatory responses and the number and quality of stem cells.

Chronic disease