Dr. Rusch and colleagues1 propose that improving sleep quality may be a good way to reduce depression and post-traumatic arousal symptoms, and that it increases the IGF-1 concentrations. We have some concerns about this study arising from our own related animal model research.
The expression of IGF-1 increased when the brain undergoes internal and external environmental stimulation.2 This research result has been verified by our work and that of Dr. Rusch. Our research discovered that the expression of IGF-1 receptor did not increase simultaneously with that of IGF-1, but slightly lowered instead, as assessed by immunohistochemistry and the QRTPCR method. This indicates that they are not related, although IGF-1 has protective effects on stress. Thus, it is concluded that IGF-1 receptor may limit the positive role of IGF-1 to a certain extent, and may be involved in the pathophysiological process of PTSD in cognitive function changes. All we know is that a decreased level of insulin-like growth factor may promote development of cognitive dysfunction,3 and that IGF-1 is involved in regulating hippocampal neurogenesis, forming abnormal neural network, and affecting the excitability of hippocampal neurons.4 Dr. Rusch's paper tends to make readers believe that the increase of IGF-1 has an effect on the improvement of patients' cognitive function; however this remains unknown and requires verification by further research.
The authors have indicated no financial conflicts of interest.
Dong Y, Zhang G. Does increased IGF-1 concentration have a clear positive significance in reducing depression and posttraumatic arousal symptoms? J Clin Sleep Med 2015;11(10):1243.
Rusch HL, Guardado P, Baxter T, Mysliwiec V, Gill JM, authors. Improved sleep quality is associated with reductions in depression and PTSD arousal symptoms and increases in IGF-1 concentrations. J Clin Sleep Med. 2015;11:615–23. [PubMed]
Schober ME, Block B, Beachy JC, et al., authors. Early and sustained increase in the expression of hippocampal IGF-1, but not EPO, in a developmental rodent model of traumatic brain injury. J Neurotrauma. 2010;27:2011–20. [PubMed]
Holly JM, Perks CM, authors. Insulin-like growth factor physiology: what we have learned from human studies. Endocrinol Metab Clin North Am. 2012;41:249–63. [PubMed]
Gao L, Blair LA, Salinas GD, et al., authors. Insulin-like growth factor-1 modulation of CaV1.3 calcium channels depends on Ca2+ release from IP3-sensitive stores and calcium/calmodulin kinase II phosphorylation of the alpha1 subunit EF hand. J Neurosci. 2006;26:6259–68. [PubMed]