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A paradigm is a framework or theory which guides or establishes a set of practices or ways of working in a particular subject area. Epidemiology describes patterns of disease in a defined population providing understanding of the causes and so controls of disease in that population. Epidemiological paradigms are therefore frameworks or theories that explain and guide the ways we address patterns of disease and ill health in particular populations.
There are generally considered to be three main epidemiological paradigms:
1.1 Addressing ill health
Conditions during pregnancy have long term effects on adult life. Addressing adult chronic disease requires reducing adverse conditions or exposures in pregnant women and their developing foetuses.
1.2 Overview of theory
The foetal origins hypothesis 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.
For example, a foetus that is undernourished makes changes to its structures and organ functions to adapt to the lack of nourishment. The baby may or may not be born at a low birth weight as an immediately apparent indication of its lack of nourishment but will be less able to ‘cope’ with a normal level of nutrition due to the previous adaptation to under nutrition. The growing child and later adult are therefore at a greater risk of developing obesity and subsequent chronic disease. Conversely a child or adult who continues to experience under nutrition after birth is more able to ‘deal’ with it than a normally nourished foetus exposed to under nutrition as a child or adult.
The theory is built on the concept of foetal plasticity or the ability of the foetus to adapt to its surrounding environment and possible adverse conditions by making changes to its structures or cells. Once these changes have been made they cannot be undone which then impacts on later health and disease.
1.3 Supporting evidence
1.3.1. The Dutch Famine
During World War II a 3 month blockade of 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:
a) The first trimester: likely to be born at a normal birth weight having ‘caught up’ with typical development, but who were
at a higher risk of developing high blood pressure, diabetes and obesity in later life.
b) The third trimester: likely to be born small and stay small throughout their lives but who were not at a greater risk of
developing obesity of chronic disease.
Effects (coronary heart disease, obesity, renal disease and non-insulin dependent diabetes) were continued to be seen in the offspring of individuals who were foetuses at the time of the famine (Langley-Evans 2006, Rosebloom et al 2001).
1.3.2. 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:
a) Those born before the siege and exposed to starvation as growing children
b) Those born during the siege
c) Those born at the same time but outside of the siege area
No evidence was found of a relationship between maternal malnutrition during pregnancy and glucose intolerance, dyslipidaemia, hypertension or cardiovascular disease in adulthood. Authors suggested this may be due to the continued starvation following birth, concluding that intrauterine malnutrition has a greater impact when postnatal nutrition is sufficient, i.e. at a normal level.
1.4. Limitations of evidence
Main criticisms of the foetal origins hypothesis are targeted at the limitations in the methodology of the research carried out. 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 carried out by Huxley et al, showing that effect size for associations between birth weight and risk of vascular disease decrease as cohort size increases, suggest that any evidence seen is a result of publication bias and measurement error (in Langley Evans).
2. Life course
2.1 Addressing ill health
The risk of chronic disease development is dependent on the 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.
The life course approach combines elements of both the foetal origins hypothesis and the adult lifestyle theory and has evolved in response to some of the limitations identified in both of these frameworks.
It develops the premise that different biological and social factors throughout life independently, cumulatively and interactively influence health and disease in later life. 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. Cumulative effects during an individual’s lifetime may also occur 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. In addition, there is evidence that during childhood and adolescence social and cognitive skills, coping strategies, attitudes and values are more easily acquired than at a later age; skills which have strong implication for future health and wellbeing.
There are four conceptual models of the life course approach:
a) The critical period model: when an ‘insult’ during a particular period of development has a lasting or lifelong effect.
(See foetal origins hypothesis).
b) The critical period model with later effect modifiers: when later life risk factors modify changes made during the
critical period. For example, the impact of normal nutrition on a baby who has experienced intrauterine under
nutrition (see foetal origins hypothesis).
c) Accumulation of risk with independent and uncorrelated insults: the gradual accumulation of different risk factors
and their impact on long term health and wellbeing. An accumulation of risk is likely to have greater impact than
a single risk or exposure.
d) Accumulation of risks with correlated insults: Chains or clusters of risk where one adverse or protective experience
leads to another in a cumulative way. This may be biological or social. For example, repeated respiratory disease
in childhood may result in increased absence from school, lower education attainment, increased risk of smoking
and reduced likelihood of successful quitting.
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.
3. Adult lifestyle/risk factors
3.1 Addressing ill health
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.
The adult lifestyle approach focuses on how adult behaviours such as smoking, diet or exercise impact on the development of chronic disease and ill health. 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).
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. Contextual issues such as poor housing are often at a national policy level whereas a lifestyle approach is at an individual level and carries an inherent risk of ‘blaming the victim’ for their ill health.
- Barker DJP. In utero programming of chronic disease. Clinical Science. 1998. 95:115-128
- Doll R, Peto R (1981) The causes of cancer: quantitative estimates of avoidable risks of cancer in the United States today. J Natl Cancer Inst 66: 1191–1308
- Hu FB, Manson JE, Meir J. Diet, lifestyle and the risk of type 2 diabetes mellitus in women. N Engl J Med. 2001; 345:790-797
- Kuh D, Ben-Shlomo Y, Lynch J et al. Life course epidemiology. J Epidemiol Community Health. 2003; 57:778-783
- Langley-Evans. Developmental programming of health and disease. Proc Nutr Soc. 2006: 65(1):97-105
- Roseboom TJ, van der Meulen JH, Rayelli AC et al. Effects of prenatal exposure to the Dutch famine on adult disease in later life: an overview. Twin Res. 2001: 4(5):293-8
- Stanner SA & Yudkin JS. Fetal programming and the Leningrad siege study. Twin Res. 4(5): 287-92
- World Health Organisation. A life course approach to health. WHO (200): Geneva
© Hannah Pheasant 2008, Mary Hall 2017