Network-Like Facets of Neuroendocrine Aging in the Human: Specific Disruption of Feedback and Feedforward Linkages Within the Aging Somatotropic ...

Full title, since it didn't fit: Network-Like Facets of Neuroendocrine Aging in the Human: Specific Disruption of Feedback and Feedforward Linkages Within the Aging Somatotropic, Gonadotropic, and Corticotropic Axes in Men and Women

Summary: Lots of facts about growth hormone, leutinising hormone, follicle-stimulating hormone and gonadotropin-releasing hormone, with very little cohesion.

Interestingness: 3

Paper by Johannes D Veldhuis in the Journal of Anti-Aging Medicine, Volume 3, Issue 3, Spring 2000.


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This is another long review paper by Veldhuis mainly about growth hormone (GH) and its friends, even though its supposedly about the interaction between different hormonal axes. It has 266 references. It's too much information to summarise. I'll jot some notes. A lot of the same information as in Veldhuis's previous paper is covered as well as in all the other GH papers. I'll skip bits that I think are repeated. A lot of the graphs presented don't look very convincing. They tend to have around 10 people per group, so the curves look like they could change easily.

Newer data says more GH secreted by women than men, and decline with aging is half as slow.
Secretion pulses more irregular and lower in older people for GH, leutinising hormone (LH), insulin and prolactin. Follicle-stimulating hormone (FSH) secretion pulse and base go up.
Intra-venous gonadotropin releasing hormone (GnRH) pulses normalised LH secretion in older men.

Inferenced mechanisms mentioned:

• Lower endogenous growth hormone-releasing hormone (GHRH) secretion and/or lower growth hormone releasing peptide (GHRP) effect could explain loss of GH secretory pulse.
• Evidence for too much somatostatin and GHRH deficiency. Neither alone enough.
• Partial GnRH deficiency and Leydig-cell steroidogenic defect both exist, and the latter is not fixed by external GnRH.

They do some computer models of the GnRH-LH-T axis and from those they like the following hypotheses for the loss of synchrony between LH and T release in older men:

• Lower feed-forward drive of T synthesis by Leydig cells.
• Same, plus lowered negative-feedback by T of GnRH and LH release.

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Abstract follows:

The present update highlights the impact of age on dynamic regulatory changes arising singly and multiply within several prototypical neuroendocrine axes in the human. A neuroendocrine axis is viewed here as a homeostatic unit maintained by multivalent interactions or network-like integration among CNS-hypothalamic, pituitary, and target-tissue sites; for example, the GHRH/somatostatin-GH-IGF-I, GnRH-LH-sex-steroid and CRH/AVP-ACTH-cortisol feedback-controlled axes. Homeostatic control is driven by (time-lagged) interglandular signaling and dose-sensitive interfaces. According to this broader perspective, a neuroendocrine system operates as an interdependent ensemble of reciprocally communicating control nodes. This dynamic precept provides a foundation for identifying among the earliest vivid features of signaling disruption within the somatotropic, gonadotropic, and corticotropic (as well as insulinotropic) axes in healthy aging men and women. Internodal linkages likely deteriorate further in the face of acute or chronic illness, medication use, systemic stress and/or hospitalization, resulting at times in overt failure of neuroglandular output. This extended concept offers a notion of neuroendocrine axis frailty as a precursor to frank endocrinesystem disability in aging. Such a framework also confers the expectation that pluri- or multiaxis disruption (e.g., combined somatotropic and gonadal) would further adversely impact homeostatic vigor in aging individuals.