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Potential link between first-born children and health risks in adulthood

Sunday, November 14th, 2010

Each year, we hear that people are gaining weight and that chronic health problems like obesity, heart problems, and diabetes are on the rise.  It’s commonplace to ascribe these trends to personal lifestyle choices, such as the lack of exercise and diet, as well as the increasingly pervasive nature of fast food and processed, high-sugar foods.

However, there may be additional risk factors that are harder to control, such as genetics, and—as  a provocative new article in PLoS One (open access) suggests—birth order.  Specifically, first-born children might be more prone to these kinds of chronic health issues later in life:

Recent work has suggested that birth order may be a non-modifiable risk factor for obesity. Current evidence suggests that first-born infants grow faster than later-born infants. Dunger et al. suggest that the in-utero growth of first-born babies may be restrained as they have lower birth weight and accelerated post-natal catch-up growth, both of which are risk factors for obesity and cardiovascular and metabolic diseases, in adult life. However, whether first-born individuals have elevated metabolic risk in adulthood remains unknown. A recent study found that first-borns had a 4-fold risk of increased fat mass in early adulthood compared to later-borns. Neither of these studies evaluated the magnitude of metabolic risk induced by such greater weight and adiposity.

…Here we investigate the associations of birth-order with metabolic phenotype in early adulthood using data from a birth cohort of Brazilian young men. We tested two hypotheses. First, we wanted to confirm that first-born status was associated with low birth weight and faster infant growth. Second, we tested the hypothesis that metabolic risk was increased in first-borns compared to later-borns.

What did they find? What implications might their work have for public health given the kinds of global population changes we expect over coming decades?

Some results (excerpts):

  • After adjusting for family income, maternal education, household assets score and maternal smoking in pregnancy, first-borns had significantly lower mean birth weight.
  • First-borns also showed faster weight gains during infancy and had greater mean height and weight at 43 months.
  • This greater weight and height tracked into early adulthood, with first-borns being significantly taller and heavier than later-borns.
  • Total cholesterol and low-density lipoproteins were higher among first-borns.
  • Our analysis suggests that low birth weight does not itself explain the increased metabolic risk associated with birth order. Rather, rapid post-natal weight gain appears most important, although such rapid growth is itself a response to low birth weight. Broadly similar growth patterns have been linked to the occurrence of type 2 diabetes and coronary events in adults.

So why do these patterns happen?  Here is their hypothesis:

The lower birth weight of first-borns can be attributed to materno-fetal physiological interactions. Following implantation, cells from the outer layer of the blastocyst, known as trophoblast, invade the maternal endometrium and alter the structure of the arteries that transfer blood to the placenta. Such modification decreases maternal resistance and increases placental blood flow. These changes then impact on the placental dynamics of subsequent pregnancies, such that second-born neonates are well known to have higher average birth weight than first-borns. Dunger et al. suggested that first-born children have higher glucose levels compared to later-borns, an effect most likely due to the combined effect of insulin resistance due to the increased adiposity and to the possible in utero programming of the insulin glucose axis. Thus, the increased adult body weight and adiposity of first-borns is likely to be induced at least in part by the maternal constraint of intra-uterine growth. However, other mechanisms may also be important. There is preliminary evidence in animals and in humans, that the novel experience of the first pregnancy could raise the level of apprehension in primigravid women, thereby potentially affecting the growth of the foetus via modulation of the vascular and endocrine functions of the feto-placental unit. Maternal emotional stress is an established risk factor for low birth weight, intrauterine growth retardation, preterm delivery and still-birth. Specifically, circadian cortisol secretion pattern appears to be distinctive in primiparous women and an alteration of the hypothalamus-pituitary axis (HPA) function could modify maternal glucocorticoids levels and affect foetal development. Possible mechanisms for birth-order effects on foetal growth merit further research.

And what potential implications might this have for the health of the global human population as we approach 9 billion people on the planet by 2050 and move through demographic transitions, such as reduced family sizes (emphasis mine)?

Our findings contribute to understanding of the early origins of adult disease. Our data show that a demographic factor relevant to all human populations can generate variability in both early growth and later metabolic risk. These findings also have important implications for understanding the increasing prevalence of the metabolic syndrome worldwide, where many populations are undergoing demographic change in response to economic development. Globally, there is a trend towards lower fertility rate, such that increasing proportion of individuals will be first-borns. In Brazil, for example, the average number of children per women (total fertility rate) dropped from 6.0 in 1960 to 1.8 currently.

They conclude with several important qualifications:

[A] number of questions still merit attention. For example, studies should describe in more detail the growth patterns that appear to lead to elevate metabolic risk, and identify the optimal time periods for intervention. Studies should also clarify the relative contribution of different possible underlying mechanisms (growth patterns, psychological factors) to the effects that we observed in these samples. Third, more research is required to establish the magnitude of the effect, whether it is similar in men and women, and whether it amplifies with age, as adverse metabolic profile consolidates. In these samples of young adults, the magnitude of the effect was relatively small, but degenerative diseases are expressed primarily from middle age and early-life effects tend to become more important through adulthood.

Siervo, M., Horta, B., Stephan, B., Victora, C., & Wells, J. (2010). First-Borns Carry a Higher Metabolic Risk in Early Adulthood: Evidence from a Prospective Cohort Study PLoS ONE, 5 (11) DOI: 10.1371/journal.pone.0013907


Photo credit: portfolium

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