Fecal glucocorticoid metabolite and T3 profiles of orphaned elephants differ from non-orphaned elephants in Zambia

Many times, members have mentioned issues in their early lives. In this paper, these are referred to as early-life adverse events (ELAEs).

I note that diogenes several times referred to issues such as stress in early life as being causative, or at least contributory, to thyroid issues.

It is, in my view, entirely reasonable to look for links between elephants and humans. We have a lot in common. 

Fecal glucocorticoid metabolite and T3 profiles of orphaned elephants differ from non-orphaned elephants in Zambia

Daniella E Chusyd  1 , Janine L Brown  2 , Steve Paris  2 , Nicole Boisseau  2 , Webster Mwaanga  3 , Moses Kasongo  3 , Lisa Olivier  3 , Stephanie L Dickinson  4 , Bailey Ortyl  4 , Tessa Steiniche  1 , Steven N Austad  5   6 , David B Allison  4   5 , Michael D Wasserman  7

    PMID: 40196305 PMCID: PMC11974515 DOI: 10.7717/peerj.19122

Abstract

Background: 

Elephants provide valuable insight into how early-life adverse events (ELAEs) associate with animal health and welfare because they can live to advanced ages, display extensive cognitive and memory capabilities, and rely heavily on social bonds. Although it is known that African savanna elephants that experienced ELAEs, such as being orphaned due to human activities, have altered behavioral outcomes, little is known regarding the physiological consequences associated with those stressors.

Methods: 

We compared fecal glucocorticoid (fGCM) and thyroid (fT3) metabolites as well as body condition scores (BCS) in rescued and rehabilitated orphaned (early-dry season: n = 20; late-dry season: n = 21 elephants) African savanna elephants in Kafue National Park, Zambia to age- and sex-matched wild non-orphaned controls groups (early-dry season: n = 57; late-dry season: n = 22 elephants) during the early- (May/June) and late- (September/October) dry seasons, respectively. Age and sex were known for orphans. For non-orphan controls, age was estimated based on dung diameter, and sex was determined based on external genitalia. Hormone concentrations were compared between groups by age class to account for developmental and nutritional transitions experienced in early life. Given that environmental stressors (e.g., availability of food and water sources) change over the course of the dry season, early- and late-dry seasons were separated in the analyses.

Results: 

fGCM concentrations were higher in orphans at younger ages than non-orphaned controls of any age. This may be due to the younger orphans being temporally closer to the traumatic event and thus not having had sufficient time to establish meaningful social bonds that could buffer the negative outcomes associated with ELAEs. Alternatively, orphans could have acclimated to living under human care, resulting in fGCM concentrations that were not different from wild controls at older ages. Orphans also had significantly higher mean fT3 concentrations than non-orphans, suggesting increased caloric intake during rehabilitation. There was no difference in BCS between orphan and non-orphan elephants at any age or time period, possibly reflecting the limitations associated with BCS assessments in younger elephants.

Conclusions: 

Together, these results provide insight into possible physiological responses underlying ELAEs and/or living under human care, including alterations in fGCM and fT3 concentrations, particularly in younger orphans. While these hormonal changes suggest a physiological response to trauma, the support of social bonds and acclimation to human care may mitigate long-term stress effects, highlighting the critical role of social integration in elephant rehabilitation and conservation efforts.

Keywords: African savanna elephants; Early life adversity; Stress; Thyroid hormone. 

https://pubmed.ncbi.nlm.nih.gov/40196305/

Open access here:

https://pmc.ncbi.nlm.nih.gov/articles/PMC11974515/

What happens to T3?

If you are familiar with thyroid hormones, you will probably be aware that the interaction of the T3 hormone (tri-iodo-thyronine) with the T3 receptor is how it has its effects on cells.

We need enough T3 - much of which will be transported into our cells from the bloodstream. (Some might be formed by de-iodinating T4 within cells. But I'm desperately trying to simplify this to the extreme!)

The diagram below illustrates T3 (whether supplied to the cell as T3 or converted within the cell) to the T3 receptors in the nucleus. 

We often see descriptions of T3 (and many other substances) reaching their receptors as if a key is being put into a lock. And that makes it very clear that only the specific substance can actually properly activate the receptor. Other substances could potentially block a receptor, or act rather like the the proper substance - but often with less (or more) stimulation of the receptor.

For example:

• Blocking TSH-receptor antibodies prevent the usual TSH stimulating the thyroid gland to produce and release thyroid hormone.
• Stimulating TSH-receptor antibodies act more powerfully than the usual TSH thus stimulating the thyroid gland to produce and release excess thyroid hormone. Which is the fundamental issue in Graves disease.

But what is almost never discussed is what happens to the T3 when it has locked into the receptor. How long does it remain there? What eventually makes the receptor releasee it? Why doesn't that T3 molecule immediately re-attach to that same receptor? Or, if that receptor has become exhausted, why does it not attach to another T3 receptor?

Or does the T3 attach to several T3 receptors in succession?

I find it difficult to see how to combine the processes that would appear obvious with the extremely tight requirement for T3.

If one T3 molecule can attach to multiple receptors, what controls the total number?

Does the T3 molecule released by the T3 receptor get expelled from the cell?

Does the T3 molecule get degraded in some way? Or converted into T2? In which case we need to go through the same questions regarding T2 and T2 receptors!