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The thrifty phenotype hypothesis.

C N Hales1, D J Barker

  • 1Department of Clinical Biochemistry, University of Cambridge, Addenbrooke's Hospital, Cambridge, UK.

British Medical Bulletin
|January 26, 2002
PubMed
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Poor early-life nutrition may permanently alter glucose-insulin metabolism, increasing type 2 diabetes risk. This thrifty phenotype hypothesis links fetal growth to insulin resistance and secretion capacity.

Area of Science:

  • Endocrinology
  • Metabolic Syndrome
  • Developmental Biology

Background:

  • The thrifty phenotype hypothesis links early-life nutrition to chronic disease risk.
  • Poor fetal and infant growth are associated with type 2 diabetes and metabolic syndrome.
  • Permanent changes in glucose-insulin metabolism are proposed mechanisms.

Purpose of the Study:

  • To review evidence supporting the thrifty phenotype hypothesis.
  • To examine the relationship between early nutrition, insulin secretion, and insulin resistance.
  • To discuss the roles of genetics and environment.

Main Methods:

  • Review of epidemiological studies worldwide.
  • Analysis of data on glucose-insulin metabolism across different age groups.

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  • Discussion of contributing factors like obesity, aging, and physical inactivity.

    • Main Results:

    • Epidemiological evidence largely supports the hypothesis.
    • A clear relationship exists between early nutrition and insulin resistance.
    • The link with insulin secretion capacity is less consistent.
    • The relative contributions of genes and environment are debated.

    Conclusions:

    • Early-life nutrition significantly impacts long-term metabolic health.
    • Insulin resistance is a key outcome, while insulin secretion effects require further study.
    • Maternal hyperglycemia and postnatal growth trajectories warrant further investigation.