Predictive adaptive response

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A predictive adaptive response (PAR) is a developmental trajectory taken by an organism during a period of developmental plasticity in response to perceived environment al cues. [1] This PAR does not confer an immediate advantage to the developing organism; however, if the PAR correctly anticipates the postnatal environment it will be advantageous in later life, if the environment the organism is born into differs from that anticipated by the PAR it will result in a mismatch. [2] PAR mechanisms were first recognized in research done on human fetuses that investigated whether poor nutrition results in the inevitable diagnosis of Type 2 diabetes in later life. [3] PARs are thought to occur through epigenetic mechanisms that alter gene expression, such as DNA methylation and histone modification, and do not involve changes to the DNA sequence of the developing organism. [4] Examples of PARs include greater helmet development in Daphnia cucullata in response to maternal exposure to predator pheromones, [5] rats exposed to glucocorticoid during late gestation led to an intolerance to glucose as adults, [6] and coat thickness determination in vole pups by the photoperiod length experienced by the mother. [7] Two hypotheses to explain PAR are the "thrifty phenotype" hypothesis and the developmental plasticity hypothesis.

Contents


The thrifty phenotype hypothesis

The thrifty phenotype hypothesis is the idea that if an organism suffers from inadequate nutrition in fetal development it will subsequently be predisposed to certain genetic outcomes as an adult. A study done examining glucose tolerance of individuals born during a famine in the Netherlands in 1944-1945 favors the “thrifty phenotype” hypothesis. [8] The results of the experiment showed that exposure to famine, particularly in late gestation, led to a decrease in the glucose tolerance of the adults. [8] Other studies on humans have shown cardiovascular and diabetes mortality has been shown to correspond to the nutrition uptake of the parents and grandparents of an offspring during their years before puberty, [9] hypertension in both sexes is the highest in individuals that had been small babies with large placentas, [10] and larger female babies have decreased ovarian suppression compared to smaller babies after intermediate levels of activity in adulthood. [11] All these studies support the thrifty phenotype hypothesis because the prenatal environment determined the phenotype that would be expressed later in life.

The developmental plasticity hypothesis

Another proposed hypothesis for the presence of PARs is the developmental plasticity hypothesis. A longitudinal study performed in Helsinki, Finland investigated whether catch-up growth of smaller children increased the risk of coronary heart disease later in life. [12] The results of this study coincide with the developmental plasticity hypothesis because as the nutrition of the small participants improved after birth, these undernourished small individuals grew at a quicker rate and had an increased chance of coronary heart disease. [12]   Another study further confirms the longitudinal study performed in Finland by showing that low weight children develop visceral fat during the catch-up growth period which can potentially result in diabetes later in life. [13] Infants that have a low birth weight have been shown to have a reduction in functioning cells, which would instantly have a negative effect on their adult life. [14] Additionally, a study testing drastic changes in childhood body-mass index showed that after two years of age, thin infants who have a comparatively large body-mass index from their birth weight are associated with disorders such as diabetes. [15] The developmental plasticity hypothesis is apparent in each of these findings because the post birth development determines the health of the individual during adulthood.

Potential future impacts

Continued research into predictive adaptive responses has the potential to gain crucial insight into the reasons diseases such as diabetes are so widespread. [16]

Related Research Articles

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In biology, epigenetics is the study of heritable phenotype changes that do not involve alterations in the DNA sequence. The Greek prefix epi- in epigenetics implies features that are "on top of" or "in addition to" the traditional genetic basis for inheritance. Epigenetics most often involves changes that affect gene activity and expression, but the term can also be used to describe any heritable phenotypic change. Such effects on cellular and physiological phenotypic traits may result from external or environmental factors, or be part of normal development.

Insulin resistance (IR) is a pathological condition in which cells fail to respond normally to the hormone insulin.

A maternal effect is a situation where the phenotype of an organism is determined not only by the environment it experiences and its genotype, but also by the environment and genotype of its mother. In genetics, maternal effects occur when an organism shows the phenotype expected from the genotype of the mother, irrespective of its own genotype, often due to the mother supplying messenger RNA or proteins to the egg. Maternal effects can also be caused by the maternal environment independent of genotype, sometimes controlling the size, sex, or behaviour of the offspring. These adaptive maternal effects lead to phenotypes of offspring that increase their fitness. Further, it introduces the concept of phenotypic plasticity, an important evolutionary concept. It has been proposed that maternal effects are important for the evolution of adaptive responses to environmental heterogeneity.

The thrifty phenotype hypothesis says that reduced fetal growth is strongly associated with a number of chronic conditions later in life, including coronary heart disease, stroke, diabetes, and hypertension. This increased susceptibility is said to result from adaptations made by the fetus in an environment limited in its supply of nutrients. The thrifty phenotype is a component of the fetal origins hypothesis.

Phenotypic plasticity Trait change of an organism in response to environmental variation

Phenotypic plasticity refers to some of the changes in an organism's behavior, morphology and physiology in response to a unique environment. Fundamental to the way in which organisms cope with environmental variation, phenotypic plasticity encompasses all types of environmentally induced changes that may or may not be permanent throughout an individual's lifespan. The term was originally used to describe developmental effects on morphological characters, but is now more broadly used to describe all phenotypic responses to environmental change, such as acclimation (acclimatization), as well as learning. The special case when differences in environment induce discrete phenotypes is termed polyphenism.

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Canalisation (genetics)

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Transgenerational epigenetic inheritance

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Extended evolutionary synthesis

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References

  1. ↑ Low, F.M., Gluckman, P.D., Hanson, M.A.: Developmental Plasticity, Epigenetics and Human Health. Evol. Biol. 39, 650-665 (2012)
  2. ↑ Godfrey, K.M., Lillycrop, K.A., Burdge, G.C., Gluckman, P.D., Hanson, M.A.: Epigenetic mechanisms and the mismatch concept of the developmental origins of health and disease. Pediatr. Res. 61, 5R-10R (2007)
  3. ↑ Hales, C.N.; Barker, D.J. (1992). "Type 2 (non-insulin-dependent) diabetes mellitus: The thrifty phenotype hypothesis". Diabetologia. 35 (7): 595–601. doi: 10.1007/BF00400248 . PMID   1644236.
  4. ↑ Tammen, S.A.; Friso, S.; Choi, S.W. (2013). "Epigenetics: The link between nature and nurture". Mol. Aspects Med. 34 (4): 753–764. doi:10.1016/j.mam.2012.07.018. PMC   3515707 . PMID   22906839.
  5. ↑ Agrawal, A.A.; Laforsch, C.; Tollrian, R. (1999). "Transgenerational induction of defences in animals and plants". Nature. 401 (6748): 60–63. Bibcode:1999Natur.401...60A. doi:10.1038/43425. S2CID   4326322.
  6. ↑ Nyirenda, M.J.; Lindsay, R.S.; Kenyon, C.J.; Burchell, A.; Seckl, J.R. (1998). "Glucocorticoid exposure in late gestation permanently programs rat hepatic phosphoenolpyruvate carboxykinase and glucocorticoid receptor expression and causes glucose intolerance in adult offspring". Journal of Clinical Investigation. 101 (10): 2174–2181. doi:10.1172/JCI1567. PMC   508805 . PMID   9593773.
  7. ↑ Lee, T.M.; Zucker, I. (1988). "Vole infant development is influenced perinatally by maternal photoperiodic history". Am. J. Physiol. 255 (5): R831–R838. doi:10.1152/ajpregu.1988.255.5.r831. PMID   3056043.
  8. 1 2 Ravelli, A.; Meulen, J.V.; Michels, R.; Osmond, C.; Barker, D.; Hales, C.; Bleker, O. (1998). "Glucose tolerance in adults after prenatal exposure to famine". The Lancet. 351 (9097): 173–177. doi:10.1016/S0140-6736(97)07244-9. PMID   9449872. S2CID   39879127.
  9. ↑ Kaati, G.; Bygren, L.; Edvinsson, S. (2002). "Cardiovascular and diabetes mortality determined by nutrition during parents' and grandparents' slow growth period". European Journal of Human Genetics. 10 (11): 682–688. doi: 10.1038/sj.ejhg.5200859 . PMID   12404098.
  10. ↑ Barker, D.J.; Bull, A.R.; Osmond, C.; Simmonds, S.J. (1990). "Fetal and placental size and risk of hypertension in adult life". BMJ. 301 (6746): 259–262. doi:10.1136/bmj.301.6746.259. PMC   1663477 . PMID   2390618.
  11. ↑ Jasienska, Grazyna; Thune, Inger; Ellison, P.T. (August 22, 2006). "Fatness at birth predicts adult susceptibility to ovarian suppression: An empirical test of the Predictive Adaptive Response hypothesis". PNAS. 103 (34): 12759–12762. doi: 10.1073/pnas.0605488103 . PMC   1568921 . PMID   16908839.
  12. 1 2 Eriksson, J.G.; Forsen, T.; Tuomilehto, J.; Winter, P.D.; Osmond, C.; Barker, D.J. (1999). "Catch-up growth in childhood and death from coronary heart disease: Longitudinal study". BMJ. 318 (7181): 427–431. doi:10.1136/bmj.318.7181.427. PMC   27731 . PMID   9974455.
  13. ↑ Ibanez, L; Suarez, L.; Lopez-Bermejo, A.; Diaz, M.; Valls, C.; Zegher, F.D. (2008). "Early Development of Visceral Fat Excess after Spontaneous Catch-Up Growth in Children with Low Birth Weight". The Journal of Clinical Endocrinology & Metabolism. 93 (3): 925–928. doi: 10.1210/jc.2007-1618 . PMID   18089700.
  14. ↑ Widdowson, E.M.; Crabb, D.E.; Milner, R.D. (1972). "Cellular Development of Some Human Organs Before Birth". Archives of Disease in Childhood. 47 (254): 652–655. doi:10.1136/adc.47.254.652. PMC   1648291 . PMID   5046781.
  15. ↑ Bhargava, S.K.; Sachdev, H.S.; Fall, C.H.; Osmond, C.; Lakshmy, R.; Barker, D.J.; Sushant K. Dey, Biswas; Ramji, Siddarth; Reddy, K.S. (2004). "Relation of Serial Changes in Childhood Body-Mass Index to Impaired Glucose Tolerance in Young Adulthood". New England Journal of Medicine. 350 (9): 865–875. doi:10.1056/NEJMoa035698. PMC   3408694 . PMID   14985484.
  16. ↑ Bateson, P.; Barker, D.; Clutton-Brock, T.; Deb, D.; Dudine, B.; Foley, R.A.; Gluckman, P.; Godfrey, K.; Sultan, S.E. (2004). "Developmental plasticity and human health". Nature. 430 (6998): 419–421. Bibcode:2004Natur.430..419B. doi:10.1038/nature02725. PMID   15269759. S2CID   4374045.
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