- We are generally aware and concerned about circadian disruption issues in teens and of insulin resistance in teens.
- Two studies suggest we may be missing the boat by not including more focus on pre-pubertal children and early-puberty.
- Related to this is another post about various aspects of melatonin and circadian factors in fertility and gestation.
Light Exposure and Circadian Effects in Puberty:
In early and mid-puberty, in the evening, there is greater suppression of melatonin by low and moderate intensity light exposure – compared to teens in the late and post-pubertal stage.
- “The pre- to mid-pubertal group showed significantly greater melatonin suppression to 15 lux (9.2 ± 20.5%), 150 lux (26.0 ± 17.7%), and 500 lux (36.9 ± 11.4%) during evening light exposure compared to the late- to post-pubertal group (-5.3 ± 17.7%, 12.5 ± 17.3%, and 23.9 ± 21.7%, respectively; p < .05). No significant differences were seen between developmental groups in morning melatonin suppression.”
- These results indicate support for a greater sensitivity to evening light in early pubertal children.
- The increased sensitivity to light in younger adolescents suggests that exposure to evening light could be particularly disruptive to sleep regulation for this group.”
Increased sensitivity of the circadian system to light in early/mid puberty.
J Clin Endocrinol Metab. 2015 Aug 24:jc20152775. Crowley SJ1, Cain SW2, et. al.
See page Sleep, Light, Circadian
The Known Increase in Insulin Resistance Seen in Teens Actually Begins About Age 7
Insulin resistance has been found to start to rise from about age 7, and increase into puberty.
Insulin resistance is known to be higher during puberty in both sexes, but the time frame of the onset of this was not known. This study was done to look at that, and showed the rise in insulin resistance did not start with the start of puberty, but at about age 7.
“Age Before Stage: Insulin Resistance Rises Before the Onset of Puberty” LINK
The link is to the full text, with tables to show the info more clearly. Here are some quotes. I know it is “a bit” dense, but some people love the details.
“The IR of early adolescence is usually attributed to puberty, but our data suggest that it emerges well before the rise in LH that initiates puberty and before any discernible physical changes. The prepubertal increase in IR was partially accounted for by increases in adiposity, with percent fat alone explaining 25 and 30% of the variation in IR in boys and girls, respectively. Type 2 diabetes is increasingly common in childhood, and the majority of diabetic children are female (23), consistent with their greater adiposity and IR. However, even when accounting for increases in percent fat, IGF-1, and age, over half of the total variance in IR remained unexplained (model 6).
We are unsure why insulin demand should begin to rise from as early as 7 years, although three observations are noteworthy. First, adiposity starts to rise around the same age, and fat is known to reduce insulin action. Second, serum IGF-1 rises progressively as puberty approaches, and the growth hormone/IGF axis is known to be associated with IR (24). In the current study, IGF-1 contributed an additional 3% to the variance of IR in both sexes, after accounting for the effects of adiposity and age. The higher IGF-1 levels in girls may relate to their greater adiposity, or may reflect the fact that low levels of estrogen produced prepubertally in girls could have a sensitizing effect on growth hormone, thereby increasing both IGF-1 and IR. Alternatively, since both insulin and IGF-1 belong to the same proinsulin superfamily, girls could be more “IGF-1 resistant” in the same way that they are more insulin resistant.
Third, adrenarche occurs around 6–8 years. Adrenarche precedes activation of the gonadal axis and is characterized by an abrupt rise in the adrenal androgen dehydroepiandrosterone (25). Although speculative, it is possible that dehydroepiandrosterone (sulfate) is responsible for the age-dependent rise in IR either directly or indirectly by promoting fat accumulation. Adrenarche has been linked before to IR in girls (3), though not in boys (26).”
“In summary, IR is already rising from 7 years of age in contemporary boys and girls, ∼3–4 years before pubertal onset, however it is defined. The rise can partly be explained by the accumulation of fat, and to a lesser extent by rising IGF-1. There remains an age-related, but unexplained, residual that might be ascribed to the rise in adrenal hormones. The demography of childhood diabetes is changing, and prepubertal IR may be important.”
Diabetes Care. 2012 Mar; 35(3): 536–541. doi: 10.2337/dc11-1281
Age Before Stage: Insulin Resistance Rises Before the Onset of Puberty
A 9-year longitudinal study (EarlyBird 26)
Alison N. Jeffery, PHD, Brad S. Metcalf, MSC, Joanne Hosking, PHD, Adam J. Streeter, MSC, Linda D. Voss, PHD, and Terence J. Wilkin, MD
Is There An Intergenerational Metabolic and Circadian “Hit” from Circadian Disruption in the Mother?
There is some evidence and theory suggesting an inter-generation effect of circadian disruption in the mother during gestation, resulting in both metabolic and circadian problems in offspring.
Things are clearly changing generation by generation in terms of worsening metabolic health. There has been a lot of effort to try to figure out what is causing this, which is likely to be many things, with a different mix of factors in different people.
If it were to be true that a disrupted circadian milieu in the pregnant mother resulted in the child having an impaired circadian rhythm system, that could amplify the other factors that are tending to increase insulin resistance in youth and younger adults. One could imagine how this could worsen over subsequent generations.
Hum Reprod Update. 2014 Mar-Apr;20(2):293-307. doi: 10.1093/humupd/dmt054. Melatonin and stable circadian rhythms optimize maternal, placental and fetal physiology.
Reiter RJ1, Tan DX, Korkmaz A, Rosales-Corral SA. Free Full Text LINK
Of the many sections in this review, one is “Programming fetal circadian rhythmicity”. Of that section, a small portion is this:
“There is now general agreement that maternal circadian rhythms are influential in the entrainment and programming of fetal and newborn circadian rhythms (Fig. 5), but what rhythms are affected may be species specific. While information in this field is still rudimentary, evidence has shown that disturbances of the fetal circadian system, regardless of the cause of those perturbations, have long-term consequences in the offspring. As an example, women who engage in shift work during pregnancy have an increased incidence of spontaneous abortions, premature deliveries and low birthweight infants (Zhu et al., 2004). Shift work greatly alters the melatonin cycle, the sleep/wake rhythm and feeding times which also could be instrumental in contributing to these complications. Exposure of rats to simulated shift work caused increased hyperleptinemia and adiposity of the offspring at 3 months after birth and altered glucose tolerance and insulin resistance, reminiscent of that seen in metabolic syndrome, when the offspring were 1 year of age (Varcoe et al., 2011). Clearly, the impact of a disturbed light:dark cycle in late pregnancy and during the perinatal period may have major effects on subsequent behavioral and metabolic functions (Ferreira et al., 2012). Given the remarkable rise in the diagnosis of metabolic syndrome, obesity, attention deficit-hyperactivity disorder, autism spectrum disorders, etc., it may be worthwhile to be more attentive to the light:dark environment during pregnancy (Hardeland et al., 2012). This is especially true since the frequency of these conditions has run in parallel with excessive use of light at night, a change that is difficult to avoid in current societies.
Offspring that are delivered prematurely are not exposed to a normal maternal melatonin rhythm that they would be if they were still in utero and they do not generate a melatonin rhythm on their own (Kennaway et al., 1992). Thus, preterm infants are deprived of exposure to the melatonin cycle during a critical interval of their development. How or whether the lack of exposure to this rhythm in these premature infants has consequences on any aspect of development remains unexamined. This problem could be potentially partially rectified if premature infants would be breast fed since a melatonin rhythm normally exists in human breast milk, with higher levels at night than during the day (Illnerova et al., 1993). This still would require, however, that the mother be in darkness for several hours before and at the time of night-time breast feeding and also the much lower levels of melatonin in the breast milk (relative to those in the blood) may render these concentrations insignificant in terms of programming the SCN of the newborn.”
Clearly, as the above authors say, “information in this field is still rudimentary”. The implications of all this are staggering, more attention to these topics is urgently needed.
See this post for a wider discussion of the topic of circadian effects and melatonin in fertility and gestation. Circadian Health and Fertility