Birth Size and Brain Function 75 Years Later

Muller, Majon; Sigurðsson, Sigurður; Kjartansson, Ólafur; Jónsson, Pálmi V.; García, Melissa; Bonsdorff, Mikaela von; Gunnarsdóttir, Ingibjörg; Þórsdóttir, Inga; Harris, Tamara B.; Buchem, Mark A. van; Gudnason, Vilmundur; Launer, Lenore J.

doi:10.1542/peds.2014-1108

Cited by 50 publications

(55 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Additional results from that cohort have shown that the associations between cortical thickness and intelligence in old age are strongly related to intelligence in childhood, suggesting that relationships found in aging reflect lifelong patterns (8). Finally, birth size is related to total brain size (adjusting for head size) and to cognitive function, particularly in those with lower education, in late life (9), and childhood socioeconomic status has been linked to the volume of the hippocampus in older people (10). Thus, there are clear trends in the literature to suggest that both genes and early-life variables are related to late-life brain structure and cognitive aging.…”

mentioning

confidence: 80%

Early life sets the stage for aging

Jagust

2016

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Although many people would agree with the proposition that factors in early life can have profound consequences for a person's health and well-being in later life, the extent of this relationship and the mechanisms that underlie it are debatable. This is especially true when considering how childhood and even gestation might affect outcomes seven or eight decades later. We know that aging is associated with great variability in cognitive and physical health, yet attempts to explain this variability have largely been limited to a few genetic factors and a host of exposures measured in mid-and late-life. Increasing attention, however, is being drawn to the ways in which development and aging may be linked. In PNAS, Walhovd et al.(1) provide novel observations on how early-life events are related to pervasive lifelong effects on brain and cognition.Cognitive abilities in older people are highly variable between individuals but tend to be consistent across cognitive domains within individuals (2). Put simply, some people do better than others in general; those with preserved memory also tend to show preservation in language, perceptual speed, and visuospatial ability. This finding is consistent with studies of intelligence through the lifespan, with a general intelligence factor, or g, explaining considerable variance across many different cognitive abilities. The source of this age-related variability is often ascribed to clinical and preclinical age-related brain disease along with "brain aging," a poorly understood process that affects multiple neural systems (3). Both genes and the environment drive these processes, and their effects on behavior and cognition may be mediated by another factor, defined as "brain reserve." Brain reserve is a construct that cannot be directly measured; its presence is inferred through the observation that individuals show different behavioral responses to similar levels of brain pathology (4). One of the proxy variables used to assess brain reserve has been educational attainment, with the supposition that those with more education have been endowed with greater neural resources to withstand the effects of neurological disease (Fig. 1). Although reserve may encompass dynamic or plastic responses to aging and disease, here we are discussing what are presumably static processes present throughout much of life.This model has been tested by measuring the effects of Alzheimer's disease (AD) brain pathology. Convincing data across different cohorts have shown that higher levels of education are not associated with differential neuropathology, but are associated with less dementia risk and less-severe cognitive change in the face of such pathology (5). These data have been widely interpreted as the effects of brain reserve, measured as educational attainment, limiting the behavioral effects of age-related neuropathology. However, this model is unsatisfying because it is devoid of underlying neural mechanisms with limited understanding of the environmental and genetic factors that might un...

show abstract

mentioning

confidence: 80%

Early life sets the stage for aging

Jagust

2016

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

show abstract

“…Low PI, defined as the lowest tertile (<24.3kg/m 3 ), indicates having soft tissue mass below normal for the stage of skeletal development, in other words it measures thinness at birth [13]. We previously found low PI, but not small birth weight and short birth length, was associated with smaller relative TB brain volume (Table 2)[9]. Therefore in these analyses we focus on PI as the indicator of birth size.…”

Section: Methodsmentioning

confidence: 99%

“…Moving further back in life, the “fetal origins of adult disease” hypothesis proposes that an unfavorable intrauterine environment, suggested by small birth size, may induce permanent changes in fetal organs [6,7], that in combination with effects of environmental exposures during childhood and adult life may condition the later risk of disease, particularly cardiovascular diseases [8]. Based on data from the AGES-Reykjavik Study, we have recently reported that small birth size, as defined by a lower Ponderal Index (PI), was associated with smaller brain volumes and reduced cognitive function at old age [9], which is consistent with the fetal origins of disease. We further extend these findings by investigating whether small birth size modulates the association of CVRF and late-life brain atrophy, as an indicator of diffuse pathology in the brain.…”

Section: Introductionmentioning

confidence: 99%

Late-life brain volume: a life-course approach. The AGES-Reykjavik study

Muller

Sigurðsson

Kjartansson

et al. 2016

Neurobiology of Aging

Self Cite

View full text Add to dashboard Cite

Background The “fetal-origins-of-adult-disease” hypothesis proposes that an unfavorable intrauterine environment, estimated from small birth size, may induce permanent changes in fetal organs, including the brain. These changes in combination with effects of (cardiovascular) exposures during adult life may condition the later risk of brain atrophy. We investigated the combined effect of small birth size and mid-life cardiovascular risk on late-life brain volumes. Methods and Findings Archived birth records of weight and height were abstracted for 1348 participants of the AGES-Reykjavik (2002-2006) population-based cohort, who participated jn the original cohort of the Reykjavik Study (RS; baseline 1967). Mid-life cardiovascular risk factors (CVRF) were collected in the RS. As a part of the late-life AGES-Reykjavik exam a brain MRI was acquired and from it, volumes of total brain (TB), gray matter, white matter, and white matter lesions were estimated. Adjusting for intracranial volume, demographics, and education showed small birth size (low Ponderal Index (PI)) and increased mid-life cardiovascular risk had an additive effect on having smaller late-life brain volumes. Compared with the reference group (high PI/absence of mid-life CVRF), participants with lower PI/presence of mid-life CVRF (BMI>25kg/m2, hypertension, diabetes, ‘ever smokers’) had smaller TB volume later in life; B (95%CI) were -10.9mL (-21.0; -0.9), -10.9mL (-20.4; -1.4), -20.9mL (-46.9; 5.2), and -10.8mL (-19.3; -2.2) respectively. Conclusions These results suggest that exposure to an unfavorable intrauterine environment contributes to the trajectory towards smaller brain volume, adding to the atrophy that may be associated with mid-life cardiovascular risk.

show abstract

“…15 However, recent findings in other conditions suggest that there may be more plasticity to epigenetic changes and these might be modifiable. 16,17 Therefore, programs may modify the influences of stress and weathering. communication, August 12, 2014).…”

Section: Health Inequity In the United States As A Source Of Poor Ptbmentioning

confidence: 99%

Fighting for the Next Generation: US Prematurity in 2030

et al. 2014

View full text Add to dashboard Cite

Preterm birth (PTB) is a serious problem, with >450 000 neonates born prematurely in the United States every year. Beginning in 1980, the United States experienced a nearly 3-decade rise in the PTB rate, peaking in 2006 at 12.8%. PTB has declined for 7 consecutive years to 11.4% in 2013, but it still accounts for 1 in 9 neonates born every year. In addition to elevated neonatal and infant mortality among those born preterm, many who survive will have lifelong morbidities and disabilities. Because of the burden of morbidity, disability, and mortality for PTB, as well as its impact more broadly on society, including excess annual costs estimated to be at least $26.2 billion by a committee for the Institute of Medicine, the March of Dimes initiated the Prematurity Campaign in 2003. In 2008 the March of Dimes established a goal of reducing the US PTB rate to 9.6% by 2020. However, the United States ranks extremely poorly for PTB rates among Very High Human Development Index (VHHDI) countries, subjecting untold numbers of neonates to unnecessary morbidity and mortality. Therefore, the March of Dimes proposes an aspirational goal of 5.5% for the 2030 US PTB rate, which would put the United States in the top 4 (10%) of 39 VHHDI countries. This 5.5% PTB rate is being achieved in VHHDI countries and by women from diverse settings receiving optimal care. This goal can be reached and will ensure a better start in life for many more neonates in the next generation.

show abstract

Birth Size and Brain Function 75 Years Later

Cited by 50 publications

References 40 publications

Early life sets the stage for aging

Early life sets the stage for aging

Late-life brain volume: a life-course approach. The AGES-Reykjavik study

Fighting for the Next Generation: US Prematurity in 2030

Contact Info

Product

Resources

About