Preconception origins of asthma, allergies and lung function: The influence of previous generations on the respiratory health of our children

被引:15
作者
Svanes, Cecilie [1 ,2 ]
Holloway, John W. W. [3 ]
Krauss-Etschmann, Susanne [4 ,5 ]
机构
[1] Univ Bergen, Ctr Int Hlth, Dept Global Publ Hlth & Primary Care, Bergen, Norway
[2] Haukeland Hosp, Dept Occupat Med, Bergen, Norway
[3] Univ Southampton, Fac Med, Human Dev & Hlth, Southampton, England
[4] German Ctr Lung Res DZL, Res Ctr Borstel, Airway Res Ctr North ARCN, Div Early Life Origins Chron Lung Dis, Borstel, Germany
[5] Christian Albrechts Univ Kiel, Inst Expt Med, Kiel, Germany
关键词
asthma; epigenetics; lung function; non-genetic heredity; overweight; HIGH-FAT DIET; TRANSGENERATIONAL INHERITANCE; EPIGENETIC INHERITANCE; DEVELOPMENTAL ORIGINS; CIGARETTE-SMOKING; PRENATAL EXPOSURE; HUMAN SPERMATOZOA; PARENTAL SMOKING; CHILDHOOD ASTHMA; SMALL RNAS;
D O I
10.1111/joim.13611
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Emerging research suggests that exposures occurring years before conception are important determinants of the health of future offspring and subsequent generations. Environmental exposures of both the father and mother, or exposure to disease processes such as obesity or infections, may influence germline cells and thereby cause a cascade of health outcomes in multiple subsequent generations. There is now increasing evidence that respiratory health is influenced by parental exposures that occur long before conception. The strongest evidence relates adolescent tobacco smoking and overweight in future fathers to increased asthma and lower lung function in their offspring, supported by evidence on parental preconception occupational exposures and air pollution. Although this literature is still sparse, the epidemiological analyses reveal strong effects that are consistent across studies with different designs and methodologies. The results are strengthened by mechanistic research from animal models and (scarce) human studies that have identified molecular mechanisms that can explain the epidemiological findings, suggesting transfer of epigenetic signals through germline cells, with susceptibility windows in utero (both male and female line) and prepuberty (male line).The concept that our lifestyles and behaviours may influence the health of our future children represents a new paradigm. This raises concerns for future health in decades to come with respect to harmful exposures but may also open for radical rethinking of preventive strategies that may improve health in multiple generations, reverse the imprint of our parents and forefathers, and underpin strategies that can break the vicious circle of propagation of health inequalities across generations.
引用
收藏
页码:531 / 549
页数:19
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