The competition for nutrients that arises when pregnancy coincides with continuing or incomplete growth in young adolescent girls increases the risk of preterm delivery and low birthweight with negative after-effects for mother and child extending beyond the perinatal period. Sheep paradigms involving nutritional management of weight and adiposity in young biologically immature adolescents have allowed the consequences of differential maternal growth status to be explored. Although nutrient reserves at conception play a modest role, it is the dietary manipulation of the maternal growth trajectory thereafter which has the most negative impact on pregnancy outcome. Overnourishing adolescents to promote rapid maternal growth is particularly detrimental as placental growth, uteroplacental blood-flows and fetal nutrient delivery are perturbed leading to a high incidence of fetal growth-restriction and premature delivery of low birthweight lambs, whereas in undernourished adolescents further maternal growth is prevented and depletion of the maternal body results in a small reduction in birthweight independent of placental size. Maternal and placental endocrine systems are differentially altered in both paradigms with downstream effects on fetal endocrine systems, organ development and body composition. Approaches to reverse these effects have been explored, predominantly targeting placental growth or function. After birth, growth-restricted offspring born to overnourished adolescents and fed to appetite have an altered metabolic phenotype which persists into adulthood whereas offspring of undernourished adolescents are largely unaffected. This body of work using ovine paradigms has public health implications for nutritional advice offered to young adolescents before and during pregnancy, and their offspring thereafter.
Clare F Hodkinson, Ellen E A Simpson, John H Beattie, Jacqueline M O'Connor, David J Campbell, J J Strain and Julie M W Wallace
A reciprocal relationship between the endocrine and immune system has been demonstrated under pathophysiological conditions. However, few studies have assessed the relationship between thyroid hormones and immune function in apparently healthy individuals. Therefore, to clarify our understanding of normal physiological endocrine–immune interactions this study aimed to examine the interrelationships between thyroid hormones and immunity in healthy individuals. Total triiodothyronine (T3), total thyroxine (T4) and markers of immune status were assessed in 93 free-living and apparently healthy individuals aged 55–70 years. T3 and T4 concentrations were determined by commercially available kits. Immune status was assessed using flow cytometry and biochemical markers. Statistical analysis was performed by partial correlation, controlling for age. Thyroid hormone concentration was positively associated with markers of inflammation (P≤0.05), natural killer-like T cells (P≤0.001), expression of interleukin-6 (IL6) by activated monocytes (P≤0.05); percentage expression of memory T-lymphocytes (P≤0.01), memory T-helper lymphocytes (P≤0.05) and memory T-cytotoxic lymphocytes (P≤0.05), and higher IL2 receptor density on CD3+T-lymphocytes (P≤0.05). Thyroid hormone concentration was inversely associated with early lymphocyte apoptosis (P≤0.05) and the ratio of naïve- to memory T-cytotoxic lymphocytes (P≤0.05). The current study provides preliminary evidence of a role for T3 and T4, within normal physiological ranges, in the maintenance of lymphocyte subpopulations, and in mediating the inflammatory response. In conclusion, these findings highlight the potential implications of altered thyroid function in older individuals and the importance of future research examining thyroid–immune interactions.