The evolutionary biology of child health

被引:26
作者
Crespi, Bernard [1 ]
机构
[1] Simon Fraser Univ, Dept Biol Sci, Burnaby, BC V5A 1S6, Canada
基金
加拿大自然科学与工程研究理事会;
关键词
evolutionary medicine; child health; cancer; growth; HUMAN LIFE-HISTORY; PARENT-OFFSPRING CONFLICT; FOR-GESTATIONAL-AGE; BECKWITH-WIEDEMANN-SYNDROME; SILVER-RUSSELL-SYNDROME; IMPRINTED GENE NETWORK; PRADER-WILLI-SYNDROME; WEIGHT-GAIN; BIRTH-WEIGHT; PUBERTAL DEVELOPMENT;
D O I
10.1098/rspb.2010.2627
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
I apply evolutionary perspectives and conceptual tools to analyse central issues underlying child health, with emphases on the roles of human-specific adaptations and genomic conflicts in physical growth and development. Evidence from comparative primatology, anthropology, physiology and human disorders indicates that child health risks have evolved in the context of evolutionary changes, along the human lineage, affecting the timing, growth-differentiation phenotypes and adaptive significance of prenatal stages, infancy, childhood, juvenility and adolescence. The most striking evolutionary changes in humans are earlier weaning and prolonged subsequent pre-adult stages, which have structured and potentiated maladaptations related to growth and development. Data from human genetic and epigenetic studies, and mouse models, indicate that growth, development and behaviour during pre-adult stages are mediated to a notable degree by effects from genomic conflicts and imprinted genes. The incidence of cancer, the primary cause of non-infectious childhood mortality, mirrors child growth rates from birth to adolescence, with paediatric cancer development impacted by imprinted genes that control aspects of growth. Understanding the adaptive significance of child growth and development phenotypes, in the context of human-evolutionary changes and genomic conflicts, provides novel insights into the causes of disease in childhood.
引用
收藏
页码:1441 / 1449
页数:9
相关论文
共 104 条
[1]   Association between small for gestational age and paternally inherited 5′ insulin haplotypes [J].
Adkins, R. M. ;
Krushkal, J. ;
Klauser, C. K. ;
Magann, E. F. ;
Morrison, J. C. ;
Somes, G. .
INTERNATIONAL JOURNAL OF OBESITY, 2008, 32 (02) :372-380
[2]  
Alexander R.D., 1974, Annual Rev Ecol Syst, V5, P325, DOI 10.1146/annurev.es.05.110174.001545
[3]  
[Anonymous], 2010, EVOLUTIONARY BIOL HU
[4]  
[Anonymous], 1999, ANIM BEHAV, DOI DOI 10.1006/ANBE.1999.1378
[5]  
[Anonymous], 1999, CANC INCIDENCE SURVI
[6]   ZAC, LIT1 (KCNQ1OT1) and p57KIP2 (CDKN1C) are in an imprinted gene network that may play a role in Beckwith-Wiedemann syndrome [J].
Arima, T ;
Kamikihara, T ;
Hayashida, T ;
Kato, K ;
Inoue, T ;
Shirayoshi, Y ;
Oshimura, M ;
Soejima, H ;
Mukai, T ;
Wake, N .
NUCLEIC ACIDS RESEARCH, 2005, 33 (08) :2650-2660
[7]   The malnourished baby and infant [J].
Barker, DJP .
BRITISH MEDICAL BULLETIN, 2001, 60 :69-88
[8]   Reproductive conflicts in social animals: who has power? [J].
Beekman, M ;
Komdeur, J ;
Ratnieks, FLW .
TRENDS IN ECOLOGY & EVOLUTION, 2003, 18 (06) :277-282
[9]  
Bogin B, 1997, YEARB PHYS ANTHROPOL, V40, P63
[10]   Evolutionary perspective on human growth [J].
Bogin, B .
ANNUAL REVIEW OF ANTHROPOLOGY, 1999, 28 :109-153