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Biography
Richard Lea is Professor of Reproductive Biology in the School of Veterinary Medicine at the University of Nottingham (UK). For more than 25 years, his research has focussed on the effects of environmental contaminants on human and animal reproductive health, and he is internationally recognised for his work on animal models and sentinels that address environmental concerns. Professor Lea served as Chair of the Society for Reproduction and Fertility (2021-24), previously SRF Programme Chair (2018-21) and Treasurer (2010-15). He was awarded the SRF Anne McLaren Distinguished Scientist award at the Fertility 2026 International Conference, and the Society for Reproductive Biology (SRB: Australia, New Zealand) Founders' Medal and Oration at the SRB 2024 International conference in Adelaide. He is chair of an International initiative to establish an International Federation of Reproductive Science (IFRS), currently across 7 countries with a steering committee comprised of the SRF, SRB and the Society for the Study of Reproduction (SSR: USA, Canada). He is Chair of the UK Association of Veterinary Ethics Committees (AVEC) as well as Nottingham Vet School Committee for Animal Research and Ethics. He is a sought-after speaker and regularly features on TV programmes, documentaries, radio interviews and podcasts aimed at raising awareness of fertility and reproductive health.
Expertise Summary
Professor Lea is internationally renowned for his expertise on environmental impacts on fertility and reproductive health. His knowledge and experience includes both human and animal reproduction and he teaches veterinary reproduction in the School of Veterinary Medicine and Science.
Professor Lea is also a recognised expert in research ethics and to this end has Chaired the Vet School Committee for Animal Research and Ethics (CARE) for more than 10 years and he also chairs the Association of Veterinary Ethics Committees (AVEC) comprised of representatives from all accredited Vet School ethics Committees across the UK and 4 large private veterinary practices. The overarching aim of AVEC is to harmonise standards of ethical review by veterinary ethics committees.
Research Summary
Exposure to environmental chemicals during fetal and pre-pubertal development has been associated with perturbed reproductive development in humans and animals. In the male, effects include… read more
Recent Publications
LEA, RICHARD G., AMEZAGA, MARIA R., LOUP, BENOIT, MANDON-PEPIN, BEATRICE, STEFANSDOTTIR, AGNES, FILIS, PANAGIOTIS, KYLE, CAROL, ZHANG, ZULIN, ALLEN, CERI, PURDIE, LAURA, JOUNEAU, LUC, COTINOT, CORINNE, RHIND, STEWART M., SINCLAIR, KEVIN D. and FOWLER, PAUL A., 2016. The fetal ovary exhibits temporal sensitivity to a 'real-life' mixture of environmental chemicals SCIENTIFIC REPORTS. 6, LEA RICHARD G, BYERS ANDREW S, SUMNER REBECCA N, RHIND STEWART M, ZHANG ZULIN, FREEMAN SARAH L, MOXON RACHEL, RICHARDSON HOLLY M, GREEN MARTIN, CRAIGON JIM and ENGLAND GARY CW, 2016. Environmental chemicals impact dog semen quality in vitro and may be associated with a temporal decline in sperm motility and increased cryptorchidism Scientific Reports. 6, srep31281 REMNANT, J. G., LEA, R. G., ALLEN, C. E., HUXLEY, J. N., ROBINSON, R. S. and BROWER, A. I., 2014. Novel gonadal characteristics in an aged bovine freemartin ANIMAL REPRODUCTION SCIENCE. 146(1-2), 1-4 CARVALHO, A. VITORINO, REINAUD, P., FORDE, N., HEALEY, G. D., EOZENOU, C., GIRAUD-DELVILLE, C., MANSOURI-ATTIA, N., GALL, L., RICHARD, C., LONERGAN, P., SHELDON, I. M., LEA, R. G. and SANDRA, O., 2014. SOCS genes expression during physiological and perturbed implantation in bovine endometrium REPRODUCTION. 148(6), 545-557
Current Research
Exposure to environmental chemicals during fetal and pre-pubertal development has been associated with perturbed reproductive development in humans and animals. In the male, effects include sub-fertility, malformations at birth (cryptorchidism, hypospadias) and testicular cancer and in the female, exposure has been associated with precocious puberty, premature menopause and polycystic ovarian disease. Although the developing fetus in utero is reported to be particularly sensitive to exposure via the mother, the pre-pubertal infant and adult are also sensitive to exposure. professor Lea's research program has focused on the effects of environmental chemicals, at environmentally relevant concentrations, on reproductive and metabolic function in the sheep, dog and rodent.
Sheep real-life model: Pregnant ewes exposed to a cocktail of chemicals present in agricultural fertilizer (biosolids) derived from processed human sewage (common global agricultural practice) were studied as a "real-life" model of exposure. Exposure of the fetuses via the mother has been shown to adversely affect evelopment of the testes and ovaries as assessed in late gestation fetuses, pubertal and adult offspring. Furthermore, in both sexes, restricted gestational periods of exposure to fertilizer treated fields altered more gonadal genes and proteins than observed in continuously exposed animals. In addition, the mid and late gestation periods were particularly sensitive to exposure and we have identified ovarian gene pathways including enzymes involved in DNA methylation and cell signaling networks important for ovarian function such as the PTEN/PI3K pathway. Recent studies have focussed on trans-generational effects by restricting exposure to the initial F0 pregnancy. Recent findings include early puberty in F1 males, and delayed puberty in F1 females and testicular abnormalities in neonatal, pre-pubertal and adult offspring.
Dog 'canary in the coalmine' sentinel species: In a separate but complimentary project, Professor Lea has worked with a population of stud dogs used in an assistance dog breeding program. In parallel with published studies in the human, Professor Lea reported a 26-year decline in semen quality produced by the stud dogs (1988-2014) and this occurred alongside an increased incidence in cryptorchidism in the pups from the same population. A recent update study confirmed that the decline in semen quality has continued to the present day: a period of 33 years (1990-2023). Interestingly, breed differences in temporal trends are indicative of an environment by gene interaction. Additional studies illustrated that dog testes collected from the UK and Scandinavia differed in both testicular chemical profiles and pathologies, adding further weight to an environmental imfluence. Furthermore, chemicals detected in semen and testes with known endocrine disrupting activity, altered both dog and human sperm function in vitro. The convergence of dog and human data provides compelling real-world evidence that environmental chemicals represent a genuine, continuing threat to male fertility and future reproductive health.
A neonatal mouse model of ovarian follicle development has shown that that specific environmental chemicals alter early stage ovarian follicle development and this has been identified as a period of ehitened sensitivity to environmental factors.
Professor Lea has had considerable success in raising research funds from the European Union Framework 7 initiative. In 2008, the EU awarded 3 million euros to investigate the effects of environmental chemicals on female reproductive development and fertility and Professor Lea was a partner in this international initiative. Entitled "Reproductive effects of environmental chemicals in females: REEF" this program brought together 6 centres of excellence and the program officially ended in 2011. Considerable output was generated from this work including high impact factor papers and numerous presentations and representations at international and national conferences. More recently, Professor Lea was central to a 5 year successful NIH grant designed to investigate the transgenerational effects of F0 exposures vis the mother.
Past Research
Professor Lea's research career began with his PhD studies on immuno-endocrine aspects of implantation in the horse. Specifically he was interested in the formation of the endometrial cups and the maternal immunological response to these placental derived structures unique to equids. At McMaster University Professor Lea worked on the immunological basis of recurrent pregnancy failure in the human and investigated immunological and endocrine mechanisms that control this process using various strains of mice and human tissues. Professor Lea's efforts were recognised with a Prize for best clinical presentation from the Canadian Fertility and Andrology Society in 1989. This was followed by a number of papers in which he made his mark in the field of Reproductive Immunology. After 3 years in Canada, Professor Lea returned to the UK where he completed 2 fellowships in Edinburgh. For the first 3 years he worked on a rat model of diabetes associated embryopathy and demonstrated an effect of diabetes on the embryo prior to implantation. A successful MRC grant then enabled Professor Lea to move to the Centre for Reproductive Biology in Edinburgh to work on immuno-endocrine aspects of implantation and pregnancy failure
This project focussed on the role of the immune system on early pregnancy and what regulatory factors may account for recurrent pregnancy failure in the human. The altered and perturbed expression of decidua and placenta derived cytokines and developmental genes were characterised in rodent models and in a subset of women with unexplained recurrent pregnancy loss. Further studies focussed on the impact of progesterone withdrawal through in vivo treatment with mifepristone (RU486) as part of legal termination of human pregnancies. The immunological cascade of events in the decidua was characterised.
Professor Lea then moved to the Rowett Institute where he worked on the effects of nutrition on maternal immune and endocrine mechanisms important for reproductive function. This included the investigation of (1) nutrient deficiencies using rodent models, (2) mechanisms underlying the process of placental growth restriction in a sheep model of adolescent pregnancy and (3) the effects of diet, superovulation regimes and oocyte/embryo culture on DNA methylation and gene expression.
Nutrient deficiencies using rodent models
The immunomodulatory effects of pregnancy on the maternal immune system are well documented as are the effects of nutrition on immunity (e.g., trace elements, vitamins, polyunsaturated fatty acids etc). Professor Lea combined these two areas in a programme of research designed to determine how altered diet affects immune mechanisms and pathways central to reproductive success. Initially this was largely based on the normal maternal immune response to the allogeneic feto-placental unit and how this may be modified by maternal nutrition. To investigate this novel area professor Lea began by using rat models of altered maternal nutrition and demonstrated changes in immune signalling molecules (cytokines) in response to maternal dietary changes in vitamin A and iron.
Placental growth restriction in a sheep model of adolescent pregnancy
Maternal undernutrition constitutes a major environmental influence on the developing fetus. Undernutrition before or during pregnancy, or during the postnatal period, can adversely affect the fetus and neonatal gonad development. In the sheep, maternal undernutrition is reported to reduce ovulation rates in adult female offspring suggesting that adverse effects on animal productivity may be influenced by the level of nutrition during pregnancy. Professor Lea used a sheep model of restricted food intake during early pregnancy (first 110 days of 145 day gestation) and shown each one of 3 periods of restriction during the first 1 to 2 months reduced early stage ovarian follicle numbers. This has clear implications for the longevity of adult female fertility. To provide further insight into the underlying mechanism we exposed ewes to either high or low metabolisable energy requirements from mating to slaughter at days 50, 65 or 110. Cohorts of ewes were also exposed for transitory periods prior to slaughter (0-30 days, 31 to 50 or 65 days, 66 to 110 days). Professor Lea demonstrated that the fetal ovary is sensitive to maternal undernutrition e.g. 0-30 day restriction reduced proliferation of day 65 germ cells and 0-110 day restriction altered primordial follicle bax and mcl-1 expression. In contrast, the same nutritional regime had no effect on the same markers in the developing fetal testis and concludes that the hypothalamic pituitary axis may be influenced.
In a different nutritional paradigm, overfeeding adolescent growing ewes restricts placental growth and reduces lamb birth weight. Since human adolescent pregnancy is characterised by pre-term delivery, low birth weight due to IUGR and small-for-gestational-age infants, the sheep model has been characterised as an animal model for studying the human clinical problem. Since restricted placental growth is associated with low birth weight we investigated nutrient sensitive mechanisms underlying development and function of the mid gestation placenta. Professor Lea demonstrated altered placental proliferation and apoptosis at this mid-gestation stage and concluded that this may be an early marker of reduced placenta size and hence IUGR later in gestation. In the same model, he reported that placental lactogen and progesterone levels were reduced in mid to late gestation and that this most likely reflects altered placental differentiation and/or altered maternal clearance mechanisms.
The effects of methionine deficiency on the oocyte and pre-implantation embryo in terms of DNA methylation and its developmental consequences for the foetus, neonate and adult.
In collaboration with Professors Sinclair and Young (University of, Nottingham) and Dr Rees (Rowett Research Institute, Aberdeen) Professor Lea investigated the physiological programming effects of this narrow window of altered methionine availability on pre and post-natal development using both sheep and rat models. Professor Lea's contribution to this programme was based on the possible programming effects on placental growth and function. This research was supported by the NIH with funds awarded to Sinclair, Rees, Lea and Youn
Additional past research programmes:
Causes and underlying mechanisms of pregnancy failure in domestic species.
When abortus tissue is sent to the Veterinary Laboratories Agency (VLA) for diagnosis, only 50% of investigations reveal the most likely cause. Professor Lea investigated this complex and multi factorial problem in terms of the range of pathogens investigated and other confounders. This program was supported by funds from the University of Nottingham under the Global Food Security initiative. This work was also a spin out project arising from the WildTech EU program described below.
Novel Technologies for Surveillance of Emerging and Re-emerging Infections of Wildlife
There is increasing concern over new emerging diseases threatening animal and human health, many of which have wildlife populations as a source and target. Considering the magnitude of this problem, current disease surveillance of wildlife populations across Europe is minimal. This initiative is designed to provide novel technologies which will contribute to the development of a comprehensive system of surveillance of wild animal diseases relevant to European public and animal health. Initiated by Professor Lea in the vet school, this project has allowed him to expand his portfolio and apply his technological expertise into an area of international concern both within and outside the EU. In support of this work, Professor Lea and colleagues in the vet school had considerable success in raising further funds from the EU totalling 6 million euros. The focus of the grant was to develop nucleic acid arrays for the detection of multiple pathogens in a single sample and serological arrays for investigating host response to the pathogen. A state of the art disease management system and epidemiological modelling systems were developed as part of this consortium. There were 13 partners across Europe and a network of 24 Associate Partners (wildlife specialists) involved in this program
Future Research
Professor Lea future work will focus on further developing his interests on environmental influences on fertility and reproductive health. He is currently looking to expand his work in the dog and already has access to unique data sets gathered from around the world. Professor Lea is also continuing with his work on human sperm and has very recently intiated a project to investigate environmental effects on sperm elasticiity. Professor Lea's mission is to use his data to heighten public awareness and impress upon government the urgent need for worldwide strategies to improve and protect global reproductive health.