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DOHaD (Barker-hipotézis): egy betegségorientált, korszakalkotó, brit eredetű teória, magyar gyökerekkel

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On the basis of comparative epidemiological statistical studies, the ’developmental origin of health and disease’ (DOHaD) theory was published in 1986, testifying the interrelation between certain perinatal events, like under-… Click to show full abstract

On the basis of comparative epidemiological statistical studies, the ’developmental origin of health and disease’ (DOHaD) theory was published in 1986, testifying the interrelation between certain perinatal events, like under- and overfeeding as well as infant mortality with cardiovascular lethality in adults (Barker DJ, Osmond C, Lancet, 1986; 137: 1077–1081) – and at present it is widely extended. The theory is rather similar to the hormonal imprinting concept, which had been published 6 years earlier (Csaba G, Biol Rev Cambr Philos Soc. 1980; 55: 47–63 and Horm Metab Res. 1984; 16: 329–335). This demonstrated the role of perinatal encounter with hormones or hormone-like molecules with adult’s endocrino-pathological events based on animal experiments. Barker hypothesized the role of hormonal imprinting in DOHaD (Phillips DI, Barker DJ, Osmond C, Acta Endocrinol (Copenh). 1993; 129: 134–138: „A possible explanation is that thyroid hormones present in the breast milk and absorbed by the suckling infant could, by the process of hormonal imprinting, permanently down-regulate the set point of thyroid homeostasis”, and this could have encouraged him to create the theory. Both theories suggest the relationship between the perinatal events and adult-age disease manifestation, however, in the case of faulty imprinting, perinatal disease does not have a role in the provocation by imprinters (only the encounter between the imprinter and the hormone receptor), but in the case of DOHaD, this seems to be involved in the process. The whole process points to the disturbance of epigenetic programming. On the basis of the present standpoint, DOHaD is valid in non-communicative diseases, however, considering the impact of faulty hormonal imprinting to the immune system, the extension to communicative diseases is expected and likely also the involvement of lifespan. Further critical developmental period is the adolescence (puberty), when similar reprogramming could be possible and also in certain cases (e.g., in the immune system) disease-causing reprogramming could occur during the whole life. The two concepts are not racing, but using different methods for verification supplement and support each other, by building up identical conclusions (faulty reprogramming) giving epigenetical explanation for numerous diseases. DOHaD and its antecedent, hormonal imprinting are not only theories, but realities, which are commendable to consider in diagnosis and therapy. Studying the tendencies of human creativeness, in all probability, the importance of DOHaD (and faulty imprinting) will be growing in the near and far future. Orv Hetil. 2020; 161(16): 603–609.

Keywords: hormonal imprinting; barker; disease; barker hipot; dohad barker

Journal Title: Orvosi Hetilap
Year Published: 2020

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