Thrifty phenotype
Thrifty phenotype refers to the correlation between low birth weight of
Historical overview
The term thrifty phenotype was first coined by Charles Nicholas Hales and David Barker in a study published in 1992.[3] In their study, the authors reviewed the literature up to and addressed five central questions regarding role of different factors in type 2 diabetes on which they based their hypothesis. These questions included the following:
- The role of beta cell deficiency in type 2 diabetes.
- The extent to which beta cell deficiency contributes to insulin intolerance.
- The role of major nutritional elements in fetal growth.
- The role of abnormal amino acid supply in growth limited neonates.
- The role of malnutrition in irreversibly defective beta cell growth.
From the review of the existing literature, they posited that poor nutritional status in fetal and early neonatal stages could hamper the development and proper functioning of the pancreatic beta cells by impacting structural features of islet anatomy, which could consequently make the individual more susceptible to the development of type 2 diabetes in later life. However, they did not exclude other causal factors such as obesity, ageing and physical inactivity as determining factors of type 2 diabetes.[4]
In a later study, Barker et al.
In 1994, Phillips’ et al.
In 2001, Hales and Barker
Evolutionary rationale
Offspring
Maternal nutrition can affect the development of the unborn child in poor nutritional environments such that it will be prepared for survival within that poor environment. This results in a thrifty phenotype (Hales & Barker, 1992[8][9]). It is sometimes called Barker's hypothesis, after Professor David J. P. Barker, researching at the University of Southampton who published the theory in 1990.[10]
Metabolic
The thrifty phenotype hypothesis says that early-life
Before the term thrifty phenotype was coined, Barker had noted the phenomenon with cardiovascular disease. In his lecture paper, he discusses the role of malnutrition during fetal development in obstructed lung disease (now known as chronic obstructive pulmonary disease [COPD]), ischemic heart disease, and blood pressure. In each of these diseases, there was an association with social class and development prevalence of the disease. This was determined to be due to issues of malnutrition during key points in organ development in utero.[11]
Benefit for mother
However, environmental changes during early development may result in the selected trajectory becoming inappropriate, resulting in adverse effects on health. This paradox generates doubts about whether the thrifty phenotype is adaptive for human offspring. Thus, the thrifty phenotype should be considered as the capacity of all offspring to respond to environmental cues during early
Other consequences
Not all research into this topic has been conducted on diseases. Other research has explored the thrifty phenotype hypothesis as a causal factor for differing development into puberty and adulthood. A review on the literature, up to 2013, discussed not only the hierarchical tissue preservation within pancreatic cells, but research on limb shortening to preserve development of more vital organs and bones.[13] An example of this phenomenon is a study published in 2018 by the Royal Society, which found that hypoxic stress from differing altitudes affected offspring limb length.[14] Fetal overnutrition may also play a key role in development, increasing the likelihood of early puberty and obesity.[15]
Adverse effects
Many human diseases in adulthood are related to growth patterns during early life, determining early-life nutrition as the underlying mechanism. Individuals with a thrifty phenotype will have "a smaller body size, a lowered metabolic rate and a reduced level of behavioral activity… adaptations to an environment that is chronically short of food" (Bateson & Martin, 1999
Risk factors of thrifty phenotype include advanced maternal age and placental insufficiency.[19]
Molecular mechanisms
The ability to conserve, acquire and expend energy is believed to be an innate, ancient trait that is embedded in the genome in a way that is quite protected against mutations.[20] These changes are also believed to possibly be inherited across generations.[20] Leptin has been identified as a possible gene for the acquisition of these thrifty traits.[20]
On a larger anatomic scale, the molecular mechanisms are broadly caused by a suboptimal environment in the
See also
- Evolutionary developmental psychology
- Evolutionary physiology
- Phenotypic plasticity
- Trivers–Willard hypothesis
- Thrifty gene hypothesis
- Prenatal nutrition and birth weight
References
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