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IGF-1 production is stimulated by GH, hence why individuals seeking to increase their IGF-1 levels inject GH to facilitate its production in the liver

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elegantly demonstrated that neural stem cell secretomes inhibit microglial activation via BDNF/VEGF signaling, but their work neglected gastrointestinal dysbiosis, overlooking the bidirectional crosstalk now recognized as central to ASD pathophysiology [42]

The result is a peptide that retains and enhances the cognitive/neuroprotective properties of the ACTH fragment without triggering cortisol release