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Article ; Online: POHaD: why we should study future fathers.

Soubry, Adelheid

2018 Volume 4, Issue 2, Page(s) dvy007

Abstract: The growing field of 'Developmental Origin of Health and Disease' (DOHaD) generally reflects environmental influences from mother to child. The importance of maternal lifestyle, diet and other environmental exposures before and during gestation period is ...

Abstract	The growing field of 'Developmental Origin of Health and Disease' (DOHaD) generally reflects environmental influences from mother to child. The importance of maternal lifestyle, diet and other environmental exposures before and during gestation period is well recognized. However, few epidemiological designs explore potential influences from the paternal environment on offspring health. This is surprising given that numerous animal models have provided evidence that the paternal environment plays a role in a non-genetic inheritance of pre-conceptional exposures through the male germ line. Recent findings in humans suggest that the epigenome of sperm cells can indeed be affected by paternal exposures. Defects in epigenetic sperm mechanisms may result in persistent modifications, affecting male fertility or offspring health status. We addressed this issue at the LATSIS Symposium 'Transgenerational Epigenetic Inheritance: Impact for Biology and Society', in Zürich, 28-30 August 2017, and here provide important arguments why environmental and lifestyle-related exposures in young men should be studied. The
Language	English
Publishing date	2018-04-26
Publishing country	England
Document type	Journal Article
ZDB-ID	2831217-X
ISSN	2058-5888 ; 2058-5888
ISSN (online)	2058-5888
ISSN	2058-5888
DOI	10.1093/eep/dvy007
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Article ; Online: Epigenetics as a Driver of Developmental Origins of Health and Disease: Did We Forget the Fathers?

Soubry, Adelheid

BioEssays : news and reviews in molecular, cellular and developmental biology

2017 Volume 40, Issue 1

Abstract: What are the effects of our environment on human development and the next generation? Numerous studies have provided ample evidence that a healthy environment and lifestyle of the mother is important for her offspring. Biological mechanisms underlying ... ...

Abstract	What are the effects of our environment on human development and the next generation? Numerous studies have provided ample evidence that a healthy environment and lifestyle of the mother is important for her offspring. Biological mechanisms underlying these environmental influences have been proposed to involve alterations in the epigenome. Is there enough evidence to suggest a similar contribution from the part of the father? Animal models provide proof of a transgenerational epigenetic effect through the paternal germ line, but can this be translated to humans? To date, literature on fathers is scarce. Human studies do not always incorporate appropriate tools to evaluate paternal influences or epigenetic effects. In reviewing the literature, I stress the need to explore and recognize paternal contributions to offspring's health within the Developmental Origins of Health and Disease hypothesis, and coin this new concept the Paternal Origins of Health and Disease paradigm (POHaD). A better understanding of preconceptional origins of disease through the totality of paternal exposures, or the paternal exposome, will provide evidence-based public health recommendations for future fathers.
MeSH term(s)	Animals ; Diet ; Disease Models, Animal ; Epigenesis, Genetic ; Epigenomics ; Fathers ; Gene-Environment Interaction ; Germ Cells ; Humans ; Infertility, Male/genetics ; Life Style ; Male ; Obesity/genetics ; Paternal Exposure ; Stress, Physiological/genetics
Language	English
Publishing date	2017-11-23
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	50140-2
ISSN	1521-1878 ; 0265-9247
ISSN (online)	1521-1878
ISSN	0265-9247
DOI	10.1002/bies.201700113
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Article ; Online: Epigenetic inheritance and evolution: A paternal perspective on dietary influences.

Soubry, Adelheid

Progress in biophysics and molecular biology

2015 Volume 118, Issue 1-2, Page(s) 79–85

Abstract: The earliest indications for paternally induced transgenerational effects from the environment to future generations were based on a small number of long-term epidemiological studies and some empirical observations. Only recently have experimental animal ...

Abstract	The earliest indications for paternally induced transgenerational effects from the environment to future generations were based on a small number of long-term epidemiological studies and some empirical observations. Only recently have experimental animal models and a few analyses on human data explored the transgenerational nature of phenotypic changes observed in offspring. Changes include multiple metabolic disorders, cancer and other chronic diseases. These phenotypes cannot always be explained by Mendelian inheritance, DNA mutations or genetic damage. Hence, a new compelling theory on epigenetic inheritance is gaining interest, providing new concepts that extend Darwin's evolutionary theory. Epigenetic alterations or "epimutations" are being considered to explain transgenerational inheritance of parentally acquired traits. The responsible mechanisms for these epimutations include DNA methylation, histone modification, and RNA-mediated effects. This review explores the literature on a number of time-dependent environmentally induced epigenetic alterations, specifically those from dietary exposures. We suggest a role for the male germ line as one of nature's tools to capture messages from our continuously changing environment and to transfer this information to subsequent generations. Further, we open the discussion that the paternally inherited epigenetic information may contribute to evolutionary adaptation.
MeSH term(s)	Animals ; Diet ; Environmental Exposure ; Epigenesis, Genetic ; Evolution, Molecular ; Fathers ; Humans ; Inheritance Patterns/genetics
Language	English
Publishing date	2015-07
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	209302-9
ISSN	1873-1732 ; 0079-6107
ISSN (online)	1873-1732
ISSN	0079-6107
DOI	10.1016/j.pbiomolbio.2015.02.008
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Article ; Online: A multifactorial model for the etiology of neuropsychiatric disorders: the role of advanced paternal age.

Vervoort, Ine / Delger, Chantal / Soubry, Adelheid

Pediatric research

2021 Volume 91, Issue 4, Page(s) 757–770

Abstract: Mental or neuropsychiatric disorders are widespread within our societies affecting one in every four people in the world. Very often the onset of a mental disorder (MD) occurs in early childhood and substantially reduces the quality of later life. ... ...

Abstract	Mental or neuropsychiatric disorders are widespread within our societies affecting one in every four people in the world. Very often the onset of a mental disorder (MD) occurs in early childhood and substantially reduces the quality of later life. Although the global burden of MDs is rising, mental health care is still suboptimal, partly due to insufficient understanding of the processes of disease development. New insights are needed to respond to this worldwide health problem. Next to the growing burden of MDs, there is a tendency to postpone pregnancy for various economic and practical reasons. In this review, we describe the current knowledge on the potential effect from advanced paternal age (APA) on development of autism spectrum disorder, schizophrenia, attention-deficit/hyperactivity disorder, bipolar disorder, obsessive-compulsive disorder, and Tourette syndrome. Although literature did not clearly define an age cut-off for APA, we here present a comprehensive multifactorial model for the development of MDs, including the role of aging, de novo mutations, epigenetic mechanisms, psychosocial environment, and selection into late fatherhood. Our model is part of the Paternal Origins of Health and Disease paradigm and may serve as a foundation for future epidemiological research designs. This blueprint will increase the understanding of the etiology of MDs and can be used as a practical guide for clinicians favoring early detection and developing a tailored treatment plan. Ultimately, this will help health policy practitioners to prevent the development of MDs and to inform health-care workers and the community about disease determinants. Better knowledge of the proportion of all risk factors, their interactions, and their role in the development of MDs will lead to an optimization of mental health care and management. IMPACT: We design a model of causation for MDs, integrating male aging, (epi)genetics, and environmental influences. It adds new insights into the current knowledge about associations between APA and MDs. In clinical practice, this comprehensive model may be helpful in early diagnosis and in treatment adopting a personal approach. It may help in identifying the proximate cause on an individual level or in a specific subpopulation. Besides the opportunity to measure the attributed proportions of risk factors, this model may be used as a blueprint to design prevention strategies for public health purposes.
MeSH term(s)	Attention Deficit Disorder with Hyperactivity/psychology ; Autism Spectrum Disorder ; Child, Preschool ; Female ; Humans ; Male ; Paternal Age ; Pregnancy ; Risk Factors ; Schizophrenia/etiology ; Schizophrenia/genetics
Language	English
Publishing date	2021-03-05
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	4411-8
ISSN	1530-0447 ; 0031-3998
ISSN (online)	1530-0447
ISSN	0031-3998
DOI	10.1038/s41390-021-01435-4
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Article: Correction to: Male Obesity: Epigenetic Origin and Effects in Sperm and Offspring.

Houfflyn, Sam / Matthys, Christophe / Soubry, Adelheid

Current molecular biology reports

2018 Volume 4, Issue 1, Page(s) 24

Abstract: This corrects the article DOI: 10.1007/s40610-017-0083-5.]. ...

Abstract	[This corrects the article DOI: 10.1007/s40610-017-0083-5.].
Language	English
Publishing date	2018-01-15
Publishing country	Switzerland
Document type	Published Erratum
ISSN	2198-6428
ISSN	2198-6428
DOI	10.1007/s40610-017-0084-4
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Article ; Online: Transgenerational epigenetic effects from male exposure to endocrine-disrupting compounds: a systematic review on research in mammals.

Van Cauwenbergh, Olivia / Di Serafino, Alessandra / Tytgat, Jan / Soubry, Adelheid

Clinical epigenetics

2020 Volume 12, Issue 1, Page(s) 65

Abstract: Assessing long-term health effects from a potentially harmful environment is challenging. Endocrine-disrupting compounds (EDCs) have become omnipresent in our environment. Individuals may or may not experience clinical health issues from being exposed to ...

Abstract	Assessing long-term health effects from a potentially harmful environment is challenging. Endocrine-disrupting compounds (EDCs) have become omnipresent in our environment. Individuals may or may not experience clinical health issues from being exposed to the increasing environmental pollution in daily life, but an issue of high concern is that also the non-exposed progeny may encounter consequences of these ancestral exposures. Progress in understanding epigenetic mechanisms opens new perspectives to estimate the risk of man-made EDCs. However, the field of epigenetic toxicology is new and its application in public health or in the understanding of disease etiology is almost non-existent, especially if it concerns future generations. In this review, we investigate the literature on transgenerational inheritance of diseases, published in the past 10 years. We question whether persistent epigenetic changes occur in the male germ line after exposure to synthesized EDCs. Our systematic search led to an inclusion of 43 articles, exploring the effects of commonly used synthetic EDCs, such as plasticizers (phthalates and bisphenol A), pesticides (dichlorodiphenyltrichloroethane, atrazine, vinclozin, methoxychlor), dioxins, and polycyclic aromatic hydrocarbons (PAHs, such as benzo(a)pyrene). Most studies found transgenerational epigenetic effects, often linked to puberty- or adult-onset diseases, such as testicular or prostate abnormalities, metabolic disorders, behavioral anomalies, and tumor development. The affected epigenetic mechanisms included changes in DNA methylation patterns, transcriptome, and expression of DNA methyltransferases. Studies involved experiments in animal models and none were based on human data. In the future, human studies are needed to confirm animal findings. If not transgenerational, at least intergenerational human studies and studies on EDC-induced epigenetic effects on germ cells could help to understand early processes of inheritance. Next, toxicity tests of new chemicals need a more comprehensive approach before they are introduced on the market. We further point to the relevance of epigenetic toxicity tests in regard to public health of the current population but also of future generations. Finally, this review sheds a light on how the interplay of genetics and epigenetics may explain the current knowledge gap on transgenerational inheritance.
MeSH term(s)	Animals ; Atrazine/toxicity ; Benzhydryl Compounds/toxicity ; Benzo(a)pyrene/toxicity ; DDT/toxicity ; Dioxins/toxicity ; Endocrine Disruptors/toxicity ; Epigenesis, Genetic/drug effects ; Male ; Mammals ; Mice ; Paternal Inheritance ; Phenols/toxicity ; Phthalic Acids/toxicity
Chemical Substances	Benzhydryl Compounds ; Dioxins ; Endocrine Disruptors ; Phenols ; Phthalic Acids ; Benzo(a)pyrene (3417WMA06D) ; DDT (CIW5S16655) ; bisphenol A (MLT3645I99) ; Atrazine (QJA9M5H4IM)
Language	English
Publishing date	2020-05-12
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Systematic Review
ZDB-ID	2553921-8
ISSN	1868-7083 ; 1868-7075
ISSN (online)	1868-7083
ISSN	1868-7075
DOI	10.1186/s13148-020-00845-1
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Article ; Online: Male age interferes with embryo growth in IVF treatment.

Van Opstal, Jolien / Fieuws, Steffen / Spiessens, Carl / Soubry, Adelheid

Human reproduction (Oxford, England)

2020 Volume 36, Issue 1, Page(s) 107–115

Abstract: Study question: Does male age affect embryo growth or quality in couples undergoing IVF treatment?: Summary answer: Advanced paternal age (APA) is negatively associated with the chance of an optimal eight-cell embryo on the third day of development.!# ...

Abstract	Study question: Does male age affect embryo growth or quality in couples undergoing IVF treatment? Summary answer: Advanced paternal age (APA) is negatively associated with the chance of an optimal eight-cell embryo on the third day of development. What is known already: Literature shows that APA is associated with decreased sperm quality and fecundity. However, the effect of male age on embryo growth in an IVF setting remains inconclusive. Literature concerning male influences on IVF success is scarce and approaches used to analyse embryo outcomes differ by study. Study design, size, duration: This study was part of the longitudinal Epigenetic Legacy of Paternal Obesity (ELPO) study for which fathers and mothers were followed from pre-pregnancy until the birth of their child. Couples were recruited from April 2015 to September 2017. A total of 1057 embryos from 87 couples were studied. Participants/materials, setting, methods: Dutch-speaking couples planning to undergo an IVF treatment were recruited at the Leuven University Fertility Center in Flanders, Belgium. Anthropometrics were documented and compared to the general Flemish population. Semen characteristics, pregnancy rates and the following embryo characteristics were recorded: number of blastomeres, symmetry and percentage fragmentation. Statistical modelling was applied taking into account correlation of within-cycle outcomes and use of multiple cycles per couple. Main results and the role of chance: We observed a significant inverse association between APA and a key determinant for scoring of embryo quality: older men were less likely to produce an embryo of eight blastomeres at Day 3, compared to younger fathers; odds ratio for the effect of 1 year equals 0.960 (95% CI: 0.930-0.991; P = 0.011). Our finding remained significant after adjusting for female age and male and female BMI. Degree of fragmentation and symmetry were not significantly related to male age. Limitations, reasons for caution: Because of the study's small sample size and its monocentric nature, a larger study is warranted to confirm our results. In addition, distribution of BMI and level of education were not representative of the general Flemish population. Although we corrected for BMI status, we do not exclude that obesity may be one of the determinants of infertility in our study population. Furthermore, it is known from other European countries that a higher education eases access to fertility treatment. Hence, caution should be taken when interpreting our findings from a fertility setting to the general population. Wider implications of the findings: We suggest a heightened need for future research into male age and its potential effects on embryo growth, embryo quality and ART outcomes. Clinical decision-making and preventative public health programmes would benefit from a better understanding of the role of men, carried forward by the Paternal Origins of Health and Disease (POHaD) paradigm. We hope the current finding will encourage others to examine the role of the sperm epigenome in embryo development according to paternal age. Study funding/competing interest(s): This work was supported by a research grant from KU Leuven University (OT/14/109). The authors declare no competing financial, professional or personal interests. Trial registration number: KU Leuven S57378 (ML11309), B322201523225.
MeSH term(s)	Aged ; Belgium ; Child ; Europe ; Female ; Fertilization in Vitro ; Humans ; Infertility ; Male ; Pregnancy ; Pregnancy Rate
Language	English
Publishing date	2020-11-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	632776-x
ISSN	1460-2350 ; 0268-1161 ; 1477-741X
ISSN (online)	1460-2350
ISSN	0268-1161 ; 1477-741X
DOI	10.1093/humrep/deaa256
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Article: Opposing Epigenetic Signatures in Human Sperm by Intake of Fast Food Versus Healthy Food.

Soubry, Adelheid / Murphy, Susan K / Vansant, Greet / He, Yang / Price, Thomas M / Hoyo, Cathrine

Frontiers in endocrinology

2021 Volume 12, Page(s) 625204

Abstract: Animal experiments have demonstrated that diets high in fats create a harmful environment for developing sperm cells, contributing to impaired reproductive health and induced risk for chronic diseases in the next generation. Changes at the level of the ... ...

Abstract	Animal experiments have demonstrated that diets high in fats create a harmful environment for developing sperm cells, contributing to impaired reproductive health and induced risk for chronic diseases in the next generation. Changes at the level of the epigenome have been suggested to underlie these observations. Human data are limited to verify this hypothesis. While we earlier demonstrated a link between male obesity and DNA methylation changes at imprinted genes in mature sperm cells and newborns, it is currently unknown if -or how- a paternal eating pattern (related to obesity) is related to indices for epigenetic inheritance. We here aim to examine a yet unexplored link between consumption of healthy (rich in vitamins and fibers) or unhealthy ("fast") foods and methylation at imprint regulatory regions in DNA of sperm. We obtained semen and data from 67 men, as part of a North Carolina-based study: The Influence of the Environment on Gametic Epigenetic Reprogramming (TIEGER) study. Dietary data included intake of fruits/nuts, vegetables/soups, whole grain bread, meat, seafood/fish, and fatty or processed food items. Multiple regression models were used to explore the association between dietary habits and clinical sperm parameters as well as DNA methylation levels, quantified using bisulfite pyrosequencing at 12 differentially methylated regions (DMRs) of the following imprinted genes:
MeSH term(s)	Adolescent ; Adult ; DNA Methylation ; Epigenesis, Genetic ; Fast Foods ; Genomic Imprinting ; Humans ; Male ; Spermatozoa/metabolism ; Young Adult
Language	English
Publishing date	2021-04-23
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2021.625204
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Article: Male Obesity: Epigenetic Origin and Effects in Sperm and Offspring.

Houfflyn, Sam / Matthys, Christophe / Soubry, Adelheid

Current molecular biology reports

2017 Volume 3, Issue 4, Page(s) 288–296

Abstract: Purpose of review: The prevalence of obesity has increased substantially in the current generations of Western countries, and the burden of obesity-related complications has been growing steadily. In men, obesity is not only a major risk factor for ... ...

Abstract	Purpose of review: The prevalence of obesity has increased substantially in the current generations of Western countries, and the burden of obesity-related complications has been growing steadily. In men, obesity is not only a major risk factor for serious chronic diseases, concern is growing that the reproductive capacity, and more particularly, their offspring's health may be affected. Obesity-related impaired spermatogenesis is associated with a decrease in microscopic and molecular sperm characteristics and pregnancy success. We hypothesize that epigenetics is an important mediator explaining interactions between an obesogenic environment and sperm/offspring outcomes. Recent findings: Recent studies have explored inter- and transgenerational epigenetic effects in sperm cells and in offspring. Father-to-child effects have been reported in relation to preconceptional nutritional and life-style related factors. Summary: Here, we summarize the current understanding about obesity and molecular or epigenetic underlying mechanisms in sperm. We identify the obesogenic environment of the father before conception as a potential origin of health or disease in the offspring and include it as part of a new concept, the
Language	English
Publishing date	2017-11-09
Publishing country	Switzerland
Document type	Journal Article ; Review
ISSN	2198-6428
ISSN	2198-6428
DOI	10.1007/s40610-017-0083-5
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Article ; Online: Extending the Developmental Origins of Health and Disease theory: does paternal diet contribute to breast cancer risk in daughters?

Romanus, Stephanie / Neven, Patrick / Soubry, Adelheid

Breast cancer research : BCR

2016 Volume 18, Issue 1, Page(s) 103

Abstract: The Developmental Origins of Health and Disease (DOHaD) theory focuses on the consequences of periconceptional and in utero exposures. A wide range of environmental conditions during early development are now being investigated as a driving force for ... ...

Abstract	The Developmental Origins of Health and Disease (DOHaD) theory focuses on the consequences of periconceptional and in utero exposures. A wide range of environmental conditions during early development are now being investigated as a driving force for epigenetic disruptions that enhance disease risk in later life, including cardiovascular, metabolic, endocrine, and mental disorders and even breast cancer. Most studies involve mother-child dyads, with less focus on environmental influences through the father. Over the last few years, however, new insights have been introduced on paternal effects and the plasticity of the epigenome of developing sperm cells have been proposed to underlie inheritable changes from ancestral exposures. The field is evolving rapidly and study results from animal models are promising. Although caution should be taken in translating animal data to humans, epidemiological findings also suggest a prominent role of the father. Therefore, we here propose an extension to the DOHaD theory to include also paternally inheritable influences.
MeSH term(s)	Breast Neoplasms/epidemiology ; Breast Neoplasms/etiology ; Disease Susceptibility ; Feeding Behavior ; Female ; Humans ; Male ; Paternal Exposure/adverse effects ; Pregnancy ; Prenatal Exposure Delayed Effects ; Risk
Language	English
Publishing date	2016-10-12
Publishing country	England
Document type	Editorial
ZDB-ID	2015059-3
ISSN	1465-542X ; 1465-5411
ISSN (online)	1465-542X
ISSN	1465-5411
DOI	10.1186/s13058-016-0760-y
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