Low Birth Weight Is Associated With Higher Adult Total Cholesterol Concentration in Men

Davies, Anna A.; Smith, George Davey; Ben-Shlomo, Yoav; Litchfield, Paul

doi:10.1161/01.cir.0000140980.61294.4d

Cited by 64 publications

(65 citation statements)

References 22 publications

(30 reference statements)

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“…After excluding these subjects, mean birth weights were comparable to figures observed in the 1958 cohort (males: 3.43 kg versus 3.40 kg in the 1958 British cohort; females: 3.26 kg versus 3.26 kg). 12 Furthermore, birth weight category distributions and association between birth weight and adult height 11 were similar to those observed in the 1958 British cohort. 12,13 Therefore, the following results are for volunteers with birth weights between 800 and 5000 g. However, the results were similar when all of the data were included or participants with a high likelihood of having been born prematurely (birth weight Ͻ1500 g) were excluded.…”

Section: Validating Recalled Birth Weightssupporting

confidence: 55%

“…As reported previously, 11 comparison of birth weight distribution with the 1958 British cohort, a cohort with similar mean age but that only used birth weight derived from hospital records, 12 suggested that birth weights Ͻ800 g (6 participants, 0.02%) and Ͼ5000 g (163 participants, 0.6%) may have been misreported. After excluding these subjects, mean birth weights were comparable to figures observed in the 1958 cohort (males: 3.43 kg versus 3.40 kg in the 1958 British cohort; females: 3.26 kg versus 3.26 kg).…”

Section: Validating Recalled Birth Weightsmentioning

confidence: 73%

“…Study measurements have been described previously. 11 All of the participants completed a self-administered questionnaire in which birth weight, together with adult height and weight, were recalled as continuous variables and converted to metric units for analysis. Participants were also asked to select 1 of 4 options to indicate where the information about their birth weight came from: own memory, parent, hospital card, or other.…”

Section: Methodsmentioning

confidence: 99%

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Association Between Birth Weight and Blood Pressure Is Robust, Amplifies With Age, and May Be Underestimated

et al. 2006

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Abstract-Data on the early life origins of adult hypertension have been widely reported: however, recent research shows that the strength of association between small size at birth and higher blood pressure weakens as study size increases.In this article, we retest the association between birth weight and systolic blood pressure in a large cohort, examine whether age interacts with birth weight to predict blood pressure, and explore reasons why birth weight-blood pressure associations tend to weaken with increasing study size. Key Words: blood pressure Ⅲ epidemiology Ⅲ infant nutrition Ⅲ blood pressure determination T he "fetal origins" hypothesis suggests that "insults" at critical periods during fetal development can lead to permanent metabolic and structural changes in the fetus increasing the risk of many diseases in adulthood. 1 One key finding in support of this hypothesis is the observation, now replicated in many populations, that lower birth weight is associated with higher adult systolic blood pressure (SBP) 1,2 : an association observed independently of socioeconomic position. 3 Surprisingly, despite the wealth of literature in this field, the precise nature of the association between birth weight and blood pressure remains contentious.One important area of recent debate has focused on the strength of association between birth weight and blood pressure. In the most recent systematic review, Huxley et al 4 concluded that birth weight had little relevance in determining blood pressure levels in later life. This finding was at odds with previous systematic reviews, which have suggested that SBP decreases by between 2 and 4 mm Hg for each 1-kg increase in birth weight. 5,6 Central to the argument put forward by Huxley et al 4 was that after ordering studies by statistical size (derived from the inverse of the variance of the regression coefficient), a clear trend (PϽ0.0001) was observed toward weaker associations between birth weight and blood pressure in the larger studies. In small studies (typically with Ͻ1000 participants), a 1-kg increase in birth weight was associated with a 1.9 mm Hg decrease in SBP, whereas in large studies (typically with Ͼ3000 participants), SBP was reduced by only 0.6 mm Hg/kg. Huxley et al 4 suggested that this was evidence of publication bias, with smaller studies being more likely to be published if they found strong inverse birth weight-blood pressure associations. 7 The authors argued that because larger studies are known to be less prone to publication bias, a decrease of 0.6 mm Hg/kg was nearer to the true association. An additional contentious area in the literature has been the actual nature of the association between birth weight and blood pressure. Even within the large studies reviewed by Huxley et al, 4 the association was inconsistent, with some large studies reporting a perfectly linear association across the birth weight continuum 8 and others reporting a reverse J-shape pattern, whereby those individuals with the highest birth weight also tended toward slightly...

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Section: Validating Recalled Birth Weightssupporting

confidence: 55%

Section: Validating Recalled Birth Weightsmentioning

confidence: 73%

Section: Methodsmentioning

confidence: 99%

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Association Between Birth Weight and Blood Pressure Is Robust, Amplifies With Age, and May Be Underestimated

et al. 2006

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“…Perhaps the best example of this association is the link between intrauterine growth restriction (IUGR) and the metabolic syndrome in adulthood, expressed in terms of insulin resistance (1,2), type 2 diabetes (1), hypertension (3,4), an altered lipid profile (5,6), obesity (7)(8)(9)(10), and cardiovascular disease (11,12). The thrifty phenotype hypothesis of Hales and Barker (13) proposes that low birth weight and associated long-term insulin resistance are adaptive if food supplies are scarce and likely to remain so over time.…”

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confidence: 99%

Preliminary evidence for an impulsivity-based thrifty eating phenotype

et al. 2012

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IntroductIon: Low birth weight is associated with obesity and an increased risk for metabolic/cardiovascular diseases in later life. results: The results of the snack delay test, which encompassed four distinct trials, indicated that the gender × intrauterine growth restriction (IUGR) × trial interaction was a predictor of the ability to delay the food reward (P = 0.002). among children with normal birth weights, girls showed a greater ability to delay food rewards than did boys (P = 0.014).In contrast, among children with IUGR, there was no such differential ability between girls and boys. Furthermore, in girls, impulsive responding predicted both increased consumption of palatable fat (P = 0.007) and higher BMIs (P = 0.020) at 48 mo of age, although there was no such association with BMI at 36 mo. dIscussIon: In girls, the quality of fetal growth may contribute to impulsive eating, which may promote an increased intake of fats and consequently higher BMIs. as with the original thrifty phenotype, such a mechanism would be adaptive when food supplies are sparse, but would be problematic in societies with ample access to calorically rich foods. Methods: We examined whether the quality of intrauterine growth programs obesogenic eating behaviors, by investigating (i) the relationship between birth weight and impulsive eating in 3-year-old children (using the snack delay test), and (ii) whether impulsive eating predicts fat intake and/or BMI at 4 years of age (using a laboratory-based test meal).

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“…Além disso, em achados subseqüentes, esses e outros pesquisadores demonstraram que o baixo peso ao nascer se associava a um padrão alterado de lipídeos plasmáti-cos 12 , redução da densidade óssea 13 , respostas ao estresse diferenciadas 14 , artérias menos elásticas 15 , padrões de secreção hormonal específicos 16,17 e maior incidência de depressão 18,19 . Essas observações geraram a "hipótese do fenótipo poupador" (thrifty phenotype hypothesis), a qual propõe que o feto é capaz de se adaptar a um ambiente intra-uterino adverso otimizando o uso de suprimentos energéticos reduzidos, no sentido de garantir sua sobrevivência.…”

Section: Modelos Causaisunclassified

Developmental Origins of Health and Disease (DOHaD)

2006

Early Human Development

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ResumoObjetivo: 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.J Pediatr (Rio J). 2007;83(6):494-504: DOHaD, programação, hipótese de Barker. AbstractObjective: 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 influe...

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Low Birth Weight Is Associated With Higher Adult Total Cholesterol Concentration in Men

Cited by 64 publications

References 22 publications

Association Between Birth Weight and Blood Pressure Is Robust, Amplifies With Age, and May Be Underestimated

Association Between Birth Weight and Blood Pressure Is Robust, Amplifies With Age, and May Be Underestimated

Preliminary evidence for an impulsivity-based thrifty eating phenotype

Developmental Origins of Health and Disease (DOHaD)

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