2a Epidemiological Paradigms Flashcards

1
Q

What is an epidemiologcial paradigm?

A

Epidemiological paradigms are frameworks or theories that explain and guide the ways we address patterns of disease and ill health in particular populations. Effectivly theories about how disease occurs.

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2
Q

What are the three main epidemiological paradigms?

A

1) Programming also called Foetal origins hypothesis also The Barker Hypothesis also The Thrifty phenotype hypothesis

2) Life course

3) Adult lifestyle/risk factors

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3
Q

What is the epidemiologcial paradigm of “Programming” (also called “Foetal origins hypothesis” also called “The Barker Hypothesis” also called “The Thrifty phenotype hypothesis”

A

Traces causes of disease back to critical periods in the life of the developing foetus in the uterus. It suggests that adverse environmental exposures during critical periods of foetal growth and development impact upon or change the ‘programming’ of the structure or functions of organs, tissues or cells in the developing foetus. Changes made are permanent, although not always immediately apparent, even if the adverse conditions are later removed. Changes made as a foetus impacts on the growing child and adult by affecting how the body responds to normal or adverse conditions.

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4
Q

What is the evidence for the epidemiologcial paradigm of “Programming” (also called “Foetal origins hypothesis” also called “The Barker Hypothesis” also called “The Thrifty phenotype hypothesis”.

A

1) The Dutch Famine
During a period in World War II, the Western Netherlands reduced daily caloric intake to around 30% of daily need. Subsequent analysis of health records reviewed the effects of foetal starvation during. Poor long term health outcomes (such as strokes, heart disease etc) continued to be seen in the offspring of individuals who were foetuses at the time of the famine.

The Leningrad Siege Study

Long term outcomes in three groups of subjects exposed to intrauterine starvation during the 3-year siege of Leningrad in World War II were analysed. No evidence was found of a relationship between maternal malnutrition during pregnancy and fetal disease in adulthood. This may show that intrauterine malnutrition has a greater impact when postnatal nutrition is sufficient, i.e. at a normal level. I.e. The malnourished children learnt to adapt to changing environments.

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5
Q

What are the main criticisms for the epidemiologcial paradigm of “Programming” (also called “Foetal origins hypothesis” also called “The Barker Hypothesis” also called “The Thrifty phenotype hypothesis”.

A

There are many limitations in the methodology of the research used to evidence it. This includes the reliability of obtaining historical data about adult subjects, the quality of cohort selection, the difficulty in adjusting for confounders such as maternal stress during famine, and the poor proxy that birth weight is for maternal nutrition.

Meta analyses show that effect size for associations between birth weight and risk of vascular disease decrease as cohort size increases, suggesting that any evidence seen is a result of publication bias and measurement error.

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6
Q

What is the life course epidemiologcial paradigm?

A

That the risk of chronic disease development is independently, cumulatively and interactively influenced by biological, behavioural and psychosocial processes that operate throughout the life of an individual or population. Addressing chronic disease therefore requires a recognition and understanding of these critical factors.

These start even before conception, accumulate throughout pregnancy, childhood and early adulthood and impact either negatively or positively on future health, wellbeing, social development and behaviour. These may also act across generations.

The framework further recognises that there are particular critical periods of development such as in utero, early infancy and during childhood and adolescence, when exposures have more influence on future health and health risk than at other times.

There are 4 models of the life course approach:
* The critical period model: when an ‘insult’ during a particular period of development has a lasting or lifelong effect.
* The critical period model with later effect modifiers: when later life risk factors modify changes made during the critical period.
* Accumulation of risk with independent and uncorrelated insults: An accumulation of risk is likely to have greater impact than a single risk or exposure.
* Accumulation of risks with correlated insults: Chains or clusters of risk where one adverse or protective experience leads to another in a cumulative way.

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7
Q

What are the main criticisms for the life course epidemiologcial paradigm

A

Main limitations of this theory centre on limitations in research methodology particularly around the difficulty in carrying out and following up subjects in long term cohort studies or across generations.

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8
Q

What is the adult lifestyle/risk factors epidemiolgical paradigm?

A

The main causes of morbidity and mortality are as a result of poor lifestyle behaviour choices. Providing information and education will therefore help people to change their behaviour to improve their health.

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9
Q

What is the evidence for the adult lifestlye/risk factors epidemiological paradigm?

A

It is based on evidence from cohort studies such as that of Doll & Peto (1981) establishing a causal association between lung cancer and smoking, or diet and type II diabetes (Hu et al 2001).

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10
Q

What are the limitations of the adult lifestyle/risk factors epidemiolgical paradigm?

A

The framework does not take into account why people make choices in the first place, failing to recognise the factors that influence behaviours such as socio-economic status and/or environmental factors.

It therefore limits any approach of addressing potential risk to simply addressing individual behaviours and ignores the context in which those behaviours may occur.

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