Size at birth and cognitive ability in late life: A systematic review

Abstract

Introduction Recent evidence suggests that growth restriction in utero may lead to neurocognitive disorders in late life, either through impaired brain development or adverse metabolic programming. Methods Systematic review of literature investigating the relationship between size at birth and cognitive abilities in late life. The search, data extraction, and rating for the quality of reporting were conducted independently by two researchers. Results Of 533 selected studies, 11 were included in this systematic review and 10 of these were from high‐income setting. Of these 11 studies, eight indicated that lower birth weight is a risk factor for lower cognitive function in late life, at least in high‐income countries. The reported effect sizes were small and it was not possible to conduct meta‐analyses because of clinical heterogeneity Discussion A modest association of lower birth weight with lower cognitive abilities in late life is consistent with persisting effects of the prenatal environment on brain function. As with all observational studies, confounding is an alternative explanation. Further studies are required to elucidate the mechanisms.

Size at birth, lifecourse factors, and cognitive function in late life: findings from the MYsore study of Natal effects on Ageing and Health (MYNAH) cohort in South India

“…Findings from this study are consistent with some previous studies that have showed direct associations of birth weight with cognitive ability in childhood, adolescence, and young adulthood (Shenkin et al, 2004;Grove et al, 2017). The previous studies that have tested if body size at birth is associated with cognitive ability in late life have, however, produced contradictory findings (Grove et al, 2017;Krishna et al, 2019). Lower birth weight was associated with lower cognitive ability in three studies (Erickson et al, 2010;Costa et al, 2011;Raikkonen et al, 2013).…”

“…Direct comparisons of all measurements of size at birth with all reported cognitive outcomes in our study with those from the above-mentioned studies Birth size and cognition in late life 361 In this study, there was no evidence to support the DOHaD hypothesis that programming of cardiometabolic outcomes due to reduced prenatal growth and development had resulted in lower cognitive function in late life. None of the previously published twelve birth cohort studies (Krishna et al, 2019) were set up to explore the pathways of cognitive aging in a manner described in this study. However, similar to our study, the direct effects of birth size measures with late life cognition were independent of stroke and CHD (Raikkonen et al, 2013), diabetes and hypertension (Costa et al, 2011), and diabetes and CHD (Hyvarinen et al, 2009).…”

“…In addition to measurements of size at birth, indicators of SEP in early life and in mid-life were available for the MYNAH participants, which is unusual for cohorts of this age. Furthermore, unlike previous studies (reviewed in detail in Krishna et al, 2019) which were mostly limited to reporting associations of birth size with cognitive function, this study was specifically designed to explore the different DOHaD pathways of cognitive aging. Another strength of our study is the completeness of the data available for analyses: Birth weight (exposure) and cognition (outcomes) were available for all (n = 721), and diagnosis of cardiometabolic disorders was established in almost all of them (n = 716).…”

“…Birth weight and head circumference at birth are indicators of intrauterine growth and brain development, respectively (Epstein and Epstein, 1978;Gunnell, 2002). Larger birth weight, the most widely researched birth size measure, is associated with better cognitive function and higher intelligence from infancy through the third decade of life in several populations and countries independent of social background (Krishna et al, 2019;Shenkin et al, 2004;Grove et al, 2017). This association of birth weight with cognition occurs across the whole spectrum of birth weight rather than being confined to an extreme group.…”

Impact of In Utero Folate Exposure on DNA Methylation and Its Potential Relevance for Later‐Life Health—Evidence from Mouse Models Translated to Human Cohorts

“…[1] The majority of studies in the field have provided evidence for associations between early-life factors and cardiometabolic outcomes, [2,3] but the earlylife environment may also shape other health outcomes. [4][5][6] Currently, the mechanisms responsible for the observed relationships between early-life environment and later health outcomes are poorly understood. However, modulation of epigenetic marks, including DNA methylation, is a plausible mechanism mediating these relationships.…”