Birth weight and prematurity with lung function at ~17.5 years: “Children of 1997” birth cohort

He, Baoting; Kwok, Man Ki; Yeung, Shiu Lun Au; Lin, Shi Lin; Leung, June Yue Yan; Hui, Lucas Chi Kwong; Li, Albert M.; Leung, Gabriel M.; Schooling, CM

doi:10.1038/s41598-019-56086-7

Cited by 14 publications

(9 citation statements)

References 68 publications

(58 reference statements)

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“…Similarly, a study from Hong Kong among 3030 children, showed that lower birth weight was associated with poorer lung function at 17.5 years of age, particularly in boys [ 39 ]. Furthermore, one case–control study from Finland that assessed lung function (z-scores) at the age of 22-years showed that young adults born with very low birth weight (< 1500 g) have reduced forced airflow regardless of a history of bronchopulmonary dysplasia [ 38 ].…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, one case–control study from Finland that assessed lung function (z-scores) at the age of 22-years showed that young adults born with very low birth weight (< 1500 g) have reduced forced airflow regardless of a history of bronchopulmonary dysplasia [ 38 ]. However, most of these studies are limited to a follow-up during childhood, adolescence or early adulthood [ 10 , 15 , 17 , 36 , 39 , 46 , 48 – 50 ], and some studies were restricted by small sample size [ 43 , 46 , 51 ], or lacking data on gestational age [ 18 , 52 ]. Nevertheless, the contradictory findings may even be due to heterogeneous methods applied or diverse confounders adjusted for.…”

Section: Discussionmentioning

confidence: 99%

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Can birth weight predict offspring’s lung function in adult age? Evidence from two Swedish birth cohorts

et al. 2022

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Background Associations between birth weight (BW) and adult lung function have been inconsistent and limited to early adulthood. We aimed to study this association in two population-based cohorts and explore if BW, adjusted for gestational age, predicts adult lung function. We also tested adult lung function impairment according to the mis-match hypothesis—small babies growing big as adults. Methods We included 3495 individuals (aged 46.4 ± 5.4 years) from the Malmo Preventive Project (MPP), Sweden, born between 1921 and 1949, and 1401 young to middle-aged individuals (aged 28.6 ± 6.7 years) from the Malmo Offspring Study (MOS) with complete data on BW and gestational age. Adult lung function (forced vital capacity [FVC], forced expiratory volume in one second [FEV1] and the FEV1/FVC-ratio) were analysed as level of impairment (z-score), using multiple linear and logistic regressions. Results BW (z-score) did not predict adult lung function in MPP, whereas BW was a significant (p = 0.003) predictor of FEV1 following full adjustment in MOS. For every additional unit increase in BW, children were 0.77 (95% CI 0.65–0.92) times less likely to have impaired adult lung function (FEV1). Moreover, adults born with lower BW (< 3510 g) showed improved lung function (FEV1 and FEV1/FVC in MOS and MPP, respectively) if they achieved higher adult body weight. Conclusions Adults born with lower birth weight, adjusted for gestational age, are more likely to have impaired lung function, seen in a younger birth cohort. Postnatal growth pattern may, however, compensate for low birth weight and contribute to better adult lung function.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Can birth weight predict offspring’s lung function in adult age? Evidence from two Swedish birth cohorts

et al. 2022

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“…On one hand, a lot of studies showed lung function impairment in preterm children (19)(20)(21). On the other hand, several studies observed inconsistent association between birth weight and FEV1/FVC (22,23). Kitchen et al (24) found that lung function was similar in very low birth weight children compared to normal weight birth ones at 8 years of age, despite very low birth weight children suffered more frequently from wheezing in the first 2 years of life.…”

Section: Discussionmentioning

confidence: 99%

Pulmonary Outcomes in Children Born Extremely and Very Preterm at 11 Years of Age

et al. 2021

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Background: There is increasing evidence of prematurity being a risk factor for long-term respiratory outcomes regardless the presence of bronchopulmonary dysplasia (BPD).Aim: To assess the effect of prematurity on respiratory outcomes in children born ≤32 weeks of gestational age at 11 years of age.Materials and Methods: Fifty five ex-preterm children (≤ 32 weeks of gestational age), born in Chieti between January 1, 2006 and December 31, 2007, performed lung function and diffusing capacity test (DLCO) at 11 years of age. Furthermore, allergy evaluation by skin prick test (SPT), eosinophil blood count and assessment of eosinophilic airways inflammation by exhaled nitric oxide (FeNO) were performed. The ex-preterm group was compared to an age- and sex-matched group of term children.Results: No difference for atopic and respiratory medical history was found between ex-preterm children and term controls, except for preschool wheezing that resulted more frequent in ex-preterm children. No difference neither in school-aged asthma frequency nor in lung function assessment at 11 years of age was found between the two groups. Lower DLCO values in ex-preterm children compared to term controls regardless the presence of BPD were found; furthermore, we showed a positive association between DLCO and gestational age. Eosinophil blood count, positive SPTs and FeNO values were similar between the two groups.Conclusions: Diffusing lung capacity was decreased in ex-preterm children at 11 years of age in the absence of lung function impairment and eosinophil airway inflammation, suggesting a non-eosinophilic pattern underlying pulmonary alterations. It could be desirable to include the diffusing capacity assessment in follow-up evaluation of all ex-preterm children.

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“…Conversely, the positive influence of angiogenesis on alveolar growth and regeneration is of great therapeutic importance (181,183). Structural alveolar and vascular changes during lung development could account for the functional alterations that were reported after IUGR in epidemiological studies: several cohort studies have shown that school-children born IUGR have a significantly lower FEV1 and airway resistance as well as a higher susceptibility to airway infections, independent of catch-up growth (184)(185)(186)(187)(188)(189). Moreover, in long-term follow-up studies it was shown that a low birthweight decreases lung function in adulthood, with a reduction of lung capacity and elasticity, resembling a COPD phenotype (9,190).…”

Section: The Adverse Effects Of Iugr On Pulmonary Structure and Functionmentioning

confidence: 99%

Perinatal Nutritional and Metabolic Pathways: Early Origins of Chronic Lung Diseases

et al. 2021

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Lung development is not completed at birth, but expands beyond infancy, rendering the lung highly susceptible to injury. Exposure to various influences during a critical window of organ growth can interfere with the finely-tuned process of development and induce pathological processes with aberrant alveolarization and long-term structural and functional sequelae. This concept of developmental origins of chronic disease has been coined as perinatal programming. Some adverse perinatal factors, including prematurity along with respiratory support, are well-recognized to induce bronchopulmonary dysplasia (BPD), a neonatal chronic lung disease that is characterized by arrest of alveolar and microvascular formation as well as lung matrix remodeling. While the pathogenesis of various experimental models focus on oxygen toxicity, mechanical ventilation and inflammation, the role of nutrition before and after birth remain poorly investigated. There is accumulating clinical and experimental evidence that intrauterine growth restriction (IUGR) as a consequence of limited nutritive supply due to placental insufficiency or maternal malnutrition is a major risk factor for BPD and impaired lung function later in life. In contrast, a surplus of nutrition with perinatal maternal obesity, accelerated postnatal weight gain and early childhood obesity is associated with wheezing and adverse clinical course of chronic lung diseases, such as asthma. While the link between perinatal nutrition and lung health has been described, the underlying mechanisms remain poorly understood. There are initial data showing that inflammatory and nutrient sensing processes are involved in programming of alveolarization, pulmonary angiogenesis, and composition of extracellular matrix. Here, we provide a comprehensive overview of the current knowledge regarding the impact of perinatal metabolism and nutrition on the lung and beyond the cardiopulmonary system as well as possible mechanisms determining the individual susceptibility to CLD early in life. We aim to emphasize the importance of unraveling the mechanisms of perinatal metabolic programming to develop novel preventive and therapeutic avenues.

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Birth weight and prematurity with lung function at ~17.5 years: “Children of 1997” birth cohort

Cited by 14 publications

References 68 publications

Can birth weight predict offspring’s lung function in adult age? Evidence from two Swedish birth cohorts

Can birth weight predict offspring’s lung function in adult age? Evidence from two Swedish birth cohorts

Pulmonary Outcomes in Children Born Extremely and Very Preterm at 11 Years of Age

Perinatal Nutritional and Metabolic Pathways: Early Origins of Chronic Lung Diseases

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