In this study, we found that in vitro exposure to IL-1 was sufficient to induce pT H 17 cells, driving an increase in CD38-expressing cells, whereas in vivo targeting CD38 consistently decreased cortical IL-1 in the AD brain, suggesting that CD38 treatment could lead to IL-1-mediated modulation of T H 17 cell pathogenicity
Compared to other secretagogues, it appears to show limited activity toward prolactin or cortisol pathways
The only problem is that, in most cases, science is not nearly as convinced
The FDA has also flagged safety concerns regarding certain bulk substances used in compounding, as well as broader compounding risks
However, it is important to note that these observations come exclusively from animal studies and that safety data in humans remain very limited