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OBJETIVO: Avaliar os efeitos do consumo da semente de linhaça durante a lactação sobre o peso corporal, indicadores hematológicos e massa de gordura visceral dos filhotes de ratas na idade adulta. MÉTODOS: Foram utilizadas 16 ratas Wistar que, após o parto, foram divididas em dois grupos que receberam, durante a lactação, as seguintes dietas: grupo-controle (GC), ração à base de caseína, e grupo linhaça (GL), ração à base de caseína contendo 25% de semente de linhaça. Ao desmame, os filhotes machos passaram a receber ração comercial até a idade adulta, quando foram sacrificados aos 170 dias de vida para coleta de sangue e avaliação da massa de gordura visceral. RESULTADOS: Foi encontrado menor peso corporal da prole do GL (GL = 42,69±3,06 g; GC = 47,31±4,72 g; p = 0,036) ao desmame. Aos 170 dias de idade foram observados menores valores na hemoglobina do GL (GL = 12,30±1,28 g/dL; GC = 13,88±0,91 g/dL; p = 0,02). Não foram verificadas diferenças estatísticas na massa de gordura visceral entre os grupos. CONCLUSÕES: O consumo materno da ração à base de semente de linhaça durante a lactação promoveu menor peso ao desmame e níveis menores de hemoglobina na idade adulta quando comparados ao GC.OBJECTIVE: To investigate the effects of maternal flaxseed consumption during lactation on the body weight, hematological indicators and visceral fat mass of male offspring in adulthood. METHODS: Sixteen female Wistar rats were divided into two groups after giving birth. During lactation the control group (CG) was fed a casein-based diet and the flaxseed group (FG) was fed a casein-based diet containing 25% flaxseed. After weaning, male offspring were fed on commercial chow until adulthood and euthanized at 170 days for blood collection and visceral fat mass assessment. RESULTS: Offspring of rats in the FG had lower body weight (FG = 42.69±3.06 g; CG = 47.31±4.72 g; p = 0.036) at weaning. At 170 days, lower hemoglobin levels were observed in the FG (FG = 12.30±1.28 g/dL; CG = 13.88±0.91 g/dL; p = 0.02). There was no statistically significant difference in visceral fat mass between groups. CONCLUSIONS: Maternal consumption of a flaxseed-based diet during lactation resulted in lower body weight at weaning and lower hemoglobin levels in adulthood, when compared with the control group.

OBJETIVO: Apresentar um novo ramo da ciência, denominado origens desenvolvimentistas da saúde e doença (DOHaD), abordando conceitos, métodos de estudo, aspectos éticos e perspectivas para essa área do conhecimento. FONTES DOS DADOS: Revisão não sistemática da literatura biomédica, com o intuito de obter referências históricas e atualizadas relacionadas com o tema em discussão. SÍNTESE DOS DADOS: Estudos recentes demonstram associações entre agravos ocorridos em fases iniciais do desenvolvimento somático e a amplificação do risco para doenças crônicas ao longo da vida, tais como obesidade, diabetes e doenças cardiovasculares. Diferentes modelos foram propostos na tentativa de melhor explicar essas associações, como a teoria do fenótipo poupador, a programação, as respostas adaptativas preditivas e o conceito de concordância ou contraste. Alguns dos possíveis mecanismos envolvidos nesses processos são: efeitos do ambiente sobre a expressão gênica, através de mecanismos epigenéticos; efeitos de sinais hormonais transmitidos ao feto através da placenta ou ao recém-nascido através da lactação. CONCLUSÕES: O DOHaD agrega informações advindas de várias áreas do conhecimento, propondo novas metodologias de investigação no sentido de esclarecer a influência de eventos adversos ocorridos em fases precoces do desenvolvimento humano sobre o padrão de saúde e doença ao longo da vida. Esse novo campo da ciência propõe novos modelos de causalidade e mecanismos envolvidos no surgimento e desenvolvimento de doenças crônicas. Os resultados dessas investigações poderão resultar em impacto significativo na prevenção de doenças crônicas, bem como na promoção de saúde em diferentes fases da vida.OBJECTIVE: To present a new branch of scientific knowledge, known as the developmental origins of health and disease (DOHaD), covering its concepts, study methods and ethical considerations in addition to the prospects for this area of knowledge. SOURCES: A non-systematic review of the biomedical literature intended to identify historical and current references related to the subject under discussion. SUMMARY OF THE FINDINGS: Recent studies demonstrate associations between aggressions suffered during the initial phases of somatic development and amplified risk of chronic diseases throughout life, such as obesity, diabetes and cardiovascular diseases. A variety of models have been proposed in attempts to better explain these associations, such as the thrifty phenotype, programming and predictive adaptive response theories and the concept of match or mismatch. Some of the mechanisms possibly involved in these processes are: effects of the environment on gene expression, through epigenetic mechanisms; effects of hormonal signals transmitted to the fetus via the placenta or the newborn via lactation. CONCLUSIONS: DOHaD draws together information originating from many different areas of knowledge, proposing new investigative methodologies to elucidate the influence of adverse events that occur during early phases of human development on the pattern of health and disease throughout life. This new scientific field proposes new models of causality and of the mechanisms involved in the emergence and development of chronic diseases. The results of these investigations may result in a significant impact on the prevention of chronic diseases, and also on health promotion in different phases of life.

Abstract Objective: To discuss the recent literature on paternal obesity, focusing on the possible mechanisms of transmission of the phenotypes from the father to the children. Sources: A non-systematic review in the PubMed database found few publications in which paternal obesity was implicated in the adverse transmission of characteristics to offspring. Specific articles on epigenetics were also evaluated. As the subject is recent and still controversial, all articles were considered regardless of year of publication. Summary of findings: Studies in humans and animals have established that paternal obesity impairs their hormones, metabolism, and sperm function, which can be transmitted to their offspring. In humans, paternal obesity results in insulin resistance/type 2 diabetes and increased levels of cortisol in umbilical cord blood, which increases the risk factors for cardiovascular disease. Notably, there is an association between body fat in parents and the prevalence of obesity in their daughters. In animals, paternal obesity led to offspring alterations on glucose-insulin homeostasis, hepatic lipogenesis, hypothalamus/feeding behavior, kidney of the offspring; it also impairs the reproductive potential of male offspring with sperm oxidative stress and mitochondrial dysfunction. An explanation for these observations (human and animal) is epigenetics, considered the primary tool for the transmission of phenotypes from the father to offspring, such as DNA methylation, histone modifications, and non-coding RNA. Conclusions: Paternal obesity can induce programmed phenotypes in offspring through epigenetics. Therefore, it can be considered a public health problem, affecting the children's future life.