Impact of maternal diet on the epigenome and potentially modifiable effects on offspring health
Lead Research Organisation:
MRC Unit the Gambia
Abstract
Our experiences in early life can have life-long effects on our health and wellbeing. For example, in a rural population in The Gambia in West Africa we have observed that children born in the rainy season are 6 times more likely to die between the ages of 15 and 65 than those born in the dry season. In fact there is mounting evidence that detrimental influences on lifelong health can stretch right back to the early stages of embryonic development. This underlines the importance of research into the underlying mechanisms, so that the processes linking environmental exposures to negative outcomes can be understood, and hopefully corrected.
One such possible mechanism involves a process known as methylation, which is one type of 'epigenetic' modification of the genome. Methylation requires a defined set of nutrients including folic acid and B-vitamins, both to provide the necessary chemical compounds, known as methyl groups, and to undertake the necessary metabolic conversions. Animal experiments have previously shown that supplementing the diets of female mice with these nutrients before they conceive has a profound effect on their offspring's appearance (e.g. changing their coat colour) and that these changes were associated with higher levels of methylation on their DNA. Until now it was unknown whether similar effects on offspring methylation occur in humans, but our group recently presented first-in-human evidence that they do. We have since followed up this work by looking at patterns of methylation across the genome. We found evidence of unusual or 'disrupted' methylation patterns associated with both maternal nutrient status and season of conception in certain types of genes, and notably in one gene (VTRNA2-1), where disrupted methylation has previously been linked with some forms of cancer and also with negative effects on the immune system.
With this grant we hope to extend this work in a number of ways. Firstly, we want to characterise these patterns of disruption more precisely by looking at a larger number of infants; interrogating key regions of the epigenome at high resolution using more advanced technologies; and looking for methylation effects all the year round. We hope this will provide further clues about the mechanisms underlying epigenomic disruption. Secondly, we want to investigate the effects of disrupted methylation in VTRNA2-1. Our Gambian research centre is a particularly good place to do this as we are able to link an individual's epigenetic information with medical records and other demographic data, and we can also conduct detailed laboratory investigations on blood cells in individuals known to have abberant methylation. These functional studies are an important part of the chain linking epigenetic effects to real, adverse health outcomes in people. Finally, with the help of advanced computer modelling, we will identify the specific combination of MD-related nutrients that may be causing the observed patterns of disrupted methylation. We will then develop a nutritional supplement to correct the observed suboptimal nutrient profile, and we will test its effectiveness in a randomised controlled trial. If effective, in future work we would seek to assess the effect on offspring methylation of giving this supplement to mothers-to-be. The hope is that the patterns of disrupted methylation previously observed in infants conceived at certain times of the year would then be prevented. In the longer term, we hope that the work described here will inform strategies for pre-conceptional supplementation in mothers that will lead directly to improved outcomes for infant growth and development, with life-long benefits for health and wellbeing.
One such possible mechanism involves a process known as methylation, which is one type of 'epigenetic' modification of the genome. Methylation requires a defined set of nutrients including folic acid and B-vitamins, both to provide the necessary chemical compounds, known as methyl groups, and to undertake the necessary metabolic conversions. Animal experiments have previously shown that supplementing the diets of female mice with these nutrients before they conceive has a profound effect on their offspring's appearance (e.g. changing their coat colour) and that these changes were associated with higher levels of methylation on their DNA. Until now it was unknown whether similar effects on offspring methylation occur in humans, but our group recently presented first-in-human evidence that they do. We have since followed up this work by looking at patterns of methylation across the genome. We found evidence of unusual or 'disrupted' methylation patterns associated with both maternal nutrient status and season of conception in certain types of genes, and notably in one gene (VTRNA2-1), where disrupted methylation has previously been linked with some forms of cancer and also with negative effects on the immune system.
With this grant we hope to extend this work in a number of ways. Firstly, we want to characterise these patterns of disruption more precisely by looking at a larger number of infants; interrogating key regions of the epigenome at high resolution using more advanced technologies; and looking for methylation effects all the year round. We hope this will provide further clues about the mechanisms underlying epigenomic disruption. Secondly, we want to investigate the effects of disrupted methylation in VTRNA2-1. Our Gambian research centre is a particularly good place to do this as we are able to link an individual's epigenetic information with medical records and other demographic data, and we can also conduct detailed laboratory investigations on blood cells in individuals known to have abberant methylation. These functional studies are an important part of the chain linking epigenetic effects to real, adverse health outcomes in people. Finally, with the help of advanced computer modelling, we will identify the specific combination of MD-related nutrients that may be causing the observed patterns of disrupted methylation. We will then develop a nutritional supplement to correct the observed suboptimal nutrient profile, and we will test its effectiveness in a randomised controlled trial. If effective, in future work we would seek to assess the effect on offspring methylation of giving this supplement to mothers-to-be. The hope is that the patterns of disrupted methylation previously observed in infants conceived at certain times of the year would then be prevented. In the longer term, we hope that the work described here will inform strategies for pre-conceptional supplementation in mothers that will lead directly to improved outcomes for infant growth and development, with life-long benefits for health and wellbeing.
Technical Summary
By exploiting a natural experiment in which rural Gambians consume different diets in dry and rainy seasons, we have recently obtained first-in-human evidence that maternal nutrient status at conception leads to sustained systemic alterations in DNA methylation of offspring. We further showed that conception in the dry season, with measured deficiencies in maternal methyl donor (MD) nutrients, preferentially disrupts the methylation of imprinted genes, allele-specifically expressed genes and metastable epialleles, leading to an excess of both hyper- and hypo-methylation and implying there will be variable developmental phenotypes. The gene with strongest evidence for disruption (VTRNA2-1) plays a central role in regulating RNA-dependent protein kinase (PKR); a pivotal antiviral protein with known tumour suppressor activity. We here seek funds to extend this work with the following aims: a) to fine map the patterns of epigenomic disruption within sensitive gene classes using refined methods (targeted capture and next generation bisulphite sequencing) on banked samples from a much larger cohort, to more precisely pinpoint conception months (and related exposures) associated with minimal and maximal disruption, and identify the most disrupted genes; b) to use a 'recall-by-epigenotype' design to study the functional consequences in T-cells and monocytes of disrupted methylation at VTRNA2-1 (expression by Northern blotting, PKR activation by Western blotting, and assessment of phosphorylation of eIF2a); c) to use in silico modelling of our MD metabolome data to identify key nutrient imbalances leading to disrupted methylation, use these insights to design supplements to optimise methylation pathways, and pilot these in non-pregnant women in anticipation of a large future RCT of pre-conceptional supplementation to prevent disrupted methylation. This work may have far-reaching implications for populations worldwide and across numerous physiological and disease endpoints.
Planned Impact
We are optimistic that our proposed research can have a very high level of impact with potential implications for future children worldwide. Our current analyses (summarised in the Case for Support) strongly suggest that we have serendipitously discovered a link between pre- and peri-conceptional environmental exposures (with diet being the leading candidate) and instability in the normal processes of DNA methylation leading to epigenetic errors. Such errors are known to lead to many pathologic syndromes arising from developmental defects and these are likely to be the tip of an iceberg. If, as our data suggest, a mother's nutritional status at conception can cause a permanent disruption of methylation at differentially methylated regions in imprinted genes, allele-specifically expressed genes and metastable epialleles, then there is a very high likelihood that these could be linked to a wide range of 'disordered' phenotypes. The fact that our most susceptible candidate gene is a tumour suppressor gene that also plays a central role in regulating immunometabolism provides an indication of the potential significance of our work. The implications are that by correcting a woman's methyl donor status prior to conception we could greatly reduce epigenetic instability and avoid a large proportion of methylation errors. It is conceivable that such errors contribute to a wide range of avoidable pathologies, sub-clinical syndromes and disease susceptibility traits. For instance, imprinted genes play an active role in fetal and placental development and imprinting errors are already known to cause a host of developmental abnormalities. We speculate that they may influence traits such as intra-uterine growth retardation (IUGR) and pre-term birth (PTB) that, whilst less severe for the individual, represent enormous burdens of disease on a worldwide basis.
Who will benefit from this research? a) Parents worldwide who are planning a family. Note that folic acid is already widely promoted and there are many supplement formulations marketed to mothers-to-be, but our data suggest that folic acid alone is not sufficient and other supplements are purely empirical and lack an evidence base; b) Governments and their health systems. Although is is premature to make such claims it is not inconceivable that reducing epigenetic errors by improving mothers' preconceptional nutritional status could reduce the prevalence of a wide range of diseases that affect the health, wealth and well-being of populations.
How will they benefit from this research? Our ultimate vision is to be able to formulate appropriate foods and/or supplements to optimise the metabolic machinery necessary for appropriate DNA methylation during early embryonic and fetal development. These could be promoted to mothers-to-be through multiple routes; either commercially or non-commercial. There is a strong chance that a 'one-size-fits-all' solution may not work and that supplements would need to be targeted by country, population groups, ethnicity, etc or even formulated for each woman. Our in silico modelling of nutrient effects on methyl donor pathways will be important in inserting this question and in designing a range of supplements to suit different population groups.
Who will benefit from this research? a) Parents worldwide who are planning a family. Note that folic acid is already widely promoted and there are many supplement formulations marketed to mothers-to-be, but our data suggest that folic acid alone is not sufficient and other supplements are purely empirical and lack an evidence base; b) Governments and their health systems. Although is is premature to make such claims it is not inconceivable that reducing epigenetic errors by improving mothers' preconceptional nutritional status could reduce the prevalence of a wide range of diseases that affect the health, wealth and well-being of populations.
How will they benefit from this research? Our ultimate vision is to be able to formulate appropriate foods and/or supplements to optimise the metabolic machinery necessary for appropriate DNA methylation during early embryonic and fetal development. These could be promoted to mothers-to-be through multiple routes; either commercially or non-commercial. There is a strong chance that a 'one-size-fits-all' solution may not work and that supplements would need to be targeted by country, population groups, ethnicity, etc or even formulated for each woman. Our in silico modelling of nutrient effects on methyl donor pathways will be important in inserting this question and in designing a range of supplements to suit different population groups.
Organisations
- MRC Unit the Gambia (Lead Research Organisation)
- Charité - University of Medicine Berlin (Collaboration)
- University College London (Collaboration)
- QUEEN'S UNIVERSITY BELFAST (Collaboration)
- UNIVERSITY OF CAMBRIDGE (Collaboration)
- University of East Anglia (Collaboration)
- QUEEN MARY UNIVERSITY OF LONDON (Collaboration)
- International Agency for Research on Cancer (IARC) (Collaboration)
- H3Africa (Collaboration)
- University of the Gambia (Collaboration)
- UNIVERSITY OF LEEDS (Collaboration)
- University of Bristol (Collaboration)
- The University of Texas Medical Branch at Galveston (Project Partner)
- Harvard University (Project Partner)
- University of Cambridge (Project Partner)
- University of British Columbia (Project Partner)
- Cornell University (Project Partner)
People |
ORCID iD |
Publications
Antoun E
(2022)
DNA methylation signatures associated with cardiometabolic risk factors in children from India and The Gambia: results from the EMPHASIS study.
in Clinical epigenetics
Bhutta ZA
(2017)
Delivering an action agenda for nutrition interventions addressing adolescent girls and young women: priorities for implementation and research.
in Annals of the New York Academy of Sciences
Candler T
(2021)
DNA methylation at a nutritionally sensitive region of the PAX8 gene is associated with thyroid volume and function in Gambian children.
in Science advances
Candler T
(2019)
Epigenetic regulation of POMC; implications for nutritional programming, obesity and metabolic disease
in Frontiers in Neuroendocrinology
Corbin L
(2018)
Formalising recall by genotype as an efficient approach to detailed phenotyping and causal inference
in Nature Communications
Derakhshan M
(2022)
Tissue- and ethnicity-independent hypervariable DNA methylation states show evidence of establishment in the early human embryo.
in Nucleic acids research
Derakhshan M
(2024)
Metastable epialleles in humans.
in Trends in genetics : TIG
Dopico XC
(2015)
Widespread seasonal gene expression reveals annual differences in human immunity and physiology.
in Nature communications
Eriksen K
(2017)
Influence of intergenerational in utero parental energy and nutrient restriction on offspring growth in rural Gambia
in The FASEB Journal
Description | FANUS Council |
Geographic Reach | Africa |
Policy Influence Type | Participation in a guidance/advisory committee |
Impact | FANUS is the overall supervisory body for all African Nutrition Societies |
URL | https://www.fanus.org/ |
Description | IUNS Council |
Geographic Reach | Multiple continents/international |
Policy Influence Type | Participation in a guidance/advisory committee |
Impact | IUNS is the governing body for all National Nutrition Societies and thereby influences governance and outputs |
URL | https://iuns.org/ |
Description | Epigenetic mechanisms linking maternal pre-conceptional micronutrient supplementation with offspring health in India and The Gambia |
Amount | £486,087 (GBP) |
Funding ID | MR/N006208/1 |
Organisation | Medical Research Council (MRC) |
Sector | Public |
Country | United Kingdom |
Start | 06/2015 |
End | 06/2018 |
Description | Inter-generational risk factors for obesity: a path to prevention in LMICs based on a modifiable epigenetic signature in the POMC gene |
Amount | £244,447 (GBP) |
Funding ID | MR/S006516/1 |
Organisation | Medical Research Council (MRC) |
Sector | Public |
Country | United Kingdom |
Start | 03/2019 |
End | 09/2021 |
Description | LPS Enhancement |
Amount | £475,000 (GBP) |
Organisation | Medical Research Council (MRC) |
Sector | Public |
Country | United Kingdom |
Start | 12/2021 |
End | 03/2022 |
Description | Newton Fund MRC Joint Research Programme: Women's and Children's Health |
Amount | £928,853 (GBP) |
Organisation | Medical Research Council (MRC) |
Sector | Public |
Country | United Kingdom |
Start | 06/2015 |
End | 06/2018 |
Description | Nutrition and the epigenome: early environmental factors influencing human developmental programming |
Amount | £2,127,410 (GBP) |
Funding ID | MR/T032863/1 |
Organisation | Medical Research Council (MRC) |
Sector | Public |
Country | United Kingdom |
Start | 09/2020 |
End | 09/2025 |
Description | Nutrition-sensitive epigenetic mechanisms in the early human embryo - developing insights from stem cell and organoid models |
Amount | £99,355 (GBP) |
Funding ID | MR/V005820/1 |
Organisation | Medical Research Council (MRC) |
Sector | Public |
Country | United Kingdom |
Start | 03/2021 |
End | 04/2023 |
Description | Unsolicited approach |
Amount | $350,000 (USD) |
Organisation | Bill and Melinda Gates Foundation |
Sector | Charity/Non Profit |
Country | United States |
Start | 05/2015 |
End | 06/2017 |
Title | West Kiang DSS |
Description | Demographic Surveilance System for West Kiang Region |
Type Of Material | Biological samples |
Year Produced | 2015 |
Provided To Others? | Yes |
Impact | Forms the platform for all studies we conduct and creates novel research findings through secondary analyses. |
Title | Submission of epigenomic data to public databases |
Description | We upload all our epigenetic analyses to public databases |
Type Of Material | Database/Collection of data |
Year Produced | 2016 |
Provided To Others? | Yes |
Impact | Not yet known |
Description | ALSPAC |
Organisation | University of Bristol |
Department | Avon Longitudinal Study of Parents and Children (ALSPAC) |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | We are collaborating with the Bristol ALSPAC team in order to 'clone and adapt' their advanced processes for use in WABR. |
Collaborator Contribution | The ALSPAC team are advising us on optimising the set up of 'externalising' our West African BioResource to international collaborators. |
Impact | Work in progress - none yet. |
Start Year | 2018 |
Description | Aflatoxin studies |
Organisation | International Agency for Research on Cancer (IARC) |
Country | France |
Sector | Academic/University |
PI Contribution | Provision of study site and samples |
Collaborator Contribution | IARC - epigenetic analysis UoL/QUB - aflatoxin analyses |
Impact | None yet |
Start Year | 2011 |
Description | Aflatoxin studies |
Organisation | Queen's University Belfast |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | Provision of study site and samples |
Collaborator Contribution | IARC - epigenetic analysis UoL/QUB - aflatoxin analyses |
Impact | None yet |
Start Year | 2011 |
Description | Aflatoxin studies |
Organisation | University of Leeds |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | Provision of study site and samples |
Collaborator Contribution | IARC - epigenetic analysis UoL/QUB - aflatoxin analyses |
Impact | None yet |
Start Year | 2011 |
Description | African Partnership for Chronic Disease / H3Africa |
Organisation | H3Africa |
Country | South Africa |
Sector | Charity/Non Profit |
PI Contribution | Participation in Research partnership to assess the burden and aetiology of non-communicable diseases (NCDs) in sub-Saharan Africa (SSA), with a focus on genetic epidemiology |
Collaborator Contribution | Coordination of research projects across multiple sites, provision of a platform for interventional research in NCDs, ensureing that African populations benefit from the ongoing advances in genomics. |
Impact | None yet |
Start Year | 2012 |
Description | African Partnership for Chronic Disease / H3Africa |
Organisation | University of Cambridge |
Department | Department of Public Health and Primary Care |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | Participation in Research partnership to assess the burden and aetiology of non-communicable diseases (NCDs) in sub-Saharan Africa (SSA), with a focus on genetic epidemiology |
Collaborator Contribution | Coordination of research projects across multiple sites, provision of a platform for interventional research in NCDs, ensureing that African populations benefit from the ongoing advances in genomics. |
Impact | None yet |
Start Year | 2012 |
Description | African Partnership for Chronic Disease / H3Africa |
Organisation | University of the Gambia |
Country | Gambia |
Sector | Academic/University |
PI Contribution | Participation in Research partnership to assess the burden and aetiology of non-communicable diseases (NCDs) in sub-Saharan Africa (SSA), with a focus on genetic epidemiology |
Collaborator Contribution | Coordination of research projects across multiple sites, provision of a platform for interventional research in NCDs, ensureing that African populations benefit from the ongoing advances in genomics. |
Impact | None yet |
Start Year | 2012 |
Description | DEEP - Diverse Epigenetic Epidemiology Partnership |
Organisation | University of Bristol |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | Co-applicants with Drs Hannah Elliott and Josine Min at Bristol and Prof Giriraj Chandak at CCMB Hyderabad |
Collaborator Contribution | Contribution of conceptual inputs, epigenetic data and bioinformatics. |
Impact | https://www.deep-epigenetics.org |
Start Year | 2024 |
Description | Epigenetics and telomere length |
Organisation | University College London |
Department | Institute of Child Health |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | We provide the research setting and samples and hypotheses. |
Collaborator Contribution | Dr Jess Buxton brings expertise and methods training. |
Impact | None yet. |
Start Year | 2015 |
Description | Harnessing DNA methylation variation between populations to understand disease discordance across ancestries (MR/X021599/1) |
Organisation | University of Bristol |
Department | MRC Integrative Epidemiology Unit |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | Provision of samples, data and analysis |
Collaborator Contribution | Generated grant idea and obtained funding |
Impact | none yet |
Start Year | 2023 |
Description | Maternal nutrition and offspring miRNAs |
Organisation | Queen Mary University of London |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | We provide the research setting, samples and manpower. We sought and successfully achieved additional funds from the Bill Melinda Gates Foundation to support this work. |
Collaborator Contribution | Dr Sarah Finer at QMUL brings expertise in miRNA programming an training in lab methods. |
Impact | None yet. |
Start Year | 2015 |
Description | POMC collaboration |
Organisation | Charité - University of Medicine Berlin |
Country | Germany |
Sector | Academic/University |
PI Contribution | Provision of SoC data to add to analysis and publications |
Collaborator Contribution | Comparative data and analysis on POMC methylation and obesity |
Impact | Publications have been listed |
Start Year | 2016 |
Description | Research partnership with University of East Anglia |
Organisation | University of East Anglia |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | We benefit from that expertise in placental epigenetic from our collaborator Dr David Monk and his student Rebecca Sainty |
Collaborator Contribution | Methods for placental cell separation |
Impact | In progress |
Start Year | 2022 |
Description | University of Cambridge |
Organisation | University of Cambridge |
Country | United Kingdom |
Sector | Academic/University |
PI Contribution | Insights from our nutritional epigenetics research in a human population in The Gambia are helping to drive several potential research projects with the Department of Genetics at Cambridge |
Collaborator Contribution | Interaction with students and PIs within the secondment host department (Dept of Genetics) have generated ideas for further work including pilot studies examining potential mechanisms underpinning our observations in The Gambia. We are currently conducting cell model experiments to investigate a key metastable epiallele with a potential causal link to pancreatic genesis and Type 1 Diabetes in humans. |
Impact | Work is ongoing and will come to fruition in 2022/23 |
Start Year | 2021 |
Description | BBC documentary |
Form Of Engagement Activity | A broadcast e.g. TV/radio/film/podcast (other than news/press) |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Media (as a channel to the public) |
Results and Impact | We featured prominently in the BBC 2 documentary: 'Countdown to Life: The Extraordinary Making of You' |
Year(s) Of Engagement Activity | 2015 |
URL | http://www.bbc.co.uk/programmes/b06crff1 |
Description | ING website |
Form Of Engagement Activity | A magazine, newsletter or online publication |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Other academic audiences (collaborators, peers etc.) |
Results and Impact | ING now has it's own website, where key news items are posted regularly. The website is a vital point of information to ING's research activities. |
Year(s) Of Engagement Activity | 2012 |
Description | International press coverage |
Form Of Engagement Activity | A press release, press conference or response to a media enquiry/interview |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Media (as a channel to the public) |
Results and Impact | Following a press release we achieved worldwide media coverage for our latest epigenetic studies. |
Year(s) Of Engagement Activity | 2015 |
URL | http://ing.mrc.ac.uk/home/news/ |
Description | MRC Centenary Events @ UCL |
Form Of Engagement Activity | Participation in an open day or visit at my research institution |
Part Of Official Scheme? | Yes |
Type Of Presentation | Keynote/Invited Speaker |
Geographic Reach | Local |
Primary Audience | Public/other audiences |
Results and Impact | 500 attendees across a wide range of the public plus other academics Wider interest and knowledge of MRC activities |
Year(s) Of Engagement Activity | 2013 |
Description | MRC Festival |
Form Of Engagement Activity | Participation in an open day or visit at my research institution |
Part Of Official Scheme? | No |
Geographic Reach | Local |
Primary Audience | Policymakers/politicians |
Results and Impact | MRC Festival is an Annual Showcase of MRC Unit The Gambia's activities |
Year(s) Of Engagement Activity | 2016 |
Description | MRC UCL Open Day |
Form Of Engagement Activity | Participation in an open day or visit at my research institution |
Part Of Official Scheme? | No |
Geographic Reach | Local |
Primary Audience | Public/other audiences |
Results and Impact | ING participated in the UCL Centenary event, targeted at the general public but also including scientists from other MRC Units and groups in London. ING contribution included a formal lecture by Prof Prentice plus stands and exhibitions highlighting our work in Keneba. Publicity in local London area. |
Year(s) Of Engagement Activity | 2013 |
Description | Open Day (Gambia) |
Form Of Engagement Activity | Participation in an open day or visit at my research institution |
Part Of Official Scheme? | No |
Geographic Reach | Local |
Primary Audience | Study participants or study members |
Results and Impact | Open Day in Keneba |
Year(s) Of Engagement Activity | 2016 |
Description | Open days |
Form Of Engagement Activity | Participation in an open day or visit at my research institution |
Part Of Official Scheme? | Yes |
Geographic Reach | National |
Primary Audience | Participants in your research and patient groups |
Results and Impact | Open day Continued good relations with surrounding villagers who participate in our research |
Year(s) Of Engagement Activity | 2007,2008,2013,2014 |
Description | Podcast |
Form Of Engagement Activity | A press release, press conference or response to a media enquiry/interview |
Part Of Official Scheme? | Yes |
Geographic Reach | International |
Primary Audience | Participants in your research and patient groups |
Results and Impact | Contribution to podcast Multiple |
Year(s) Of Engagement Activity | 2009,2014 |
Description | Public lecture |
Form Of Engagement Activity | A formal working group, expert panel or dialogue |
Part Of Official Scheme? | Yes |
Geographic Reach | Local |
Primary Audience | Public/other audiences |
Results and Impact | Open Lecture to general audience including politicians Improved profile |
Year(s) Of Engagement Activity | 2008,2013 |
Description | Radio interview |
Form Of Engagement Activity | A press release, press conference or response to a media enquiry/interview |
Part Of Official Scheme? | No |
Geographic Reach | International |
Primary Audience | Public/other audiences |
Results and Impact | BBC World Service interview None. |
Year(s) Of Engagement Activity | 2009,2014 |