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The reasons could have been multipronged ranging from toxic accumulation of folate and B12 in patients of diabetic nephropathy with low GFR or competitive inhibition of TMP and TPP transport at the level of RFC1 transporter by high dose folate at key sites such as the kidney and vascular cells thus adversely affecting sharing of thiamine between tissues rich in thiamine and those deficient in it [183]
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Its a naturally occurring compound in your body that plays a big role in how your body uses fat for energy
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Given the coupling between copper and energy status (e.g copper is a cofactor at Complex IV of the ETC) and how intensely metabolically active neurons are, it seems like short-term IP GHK-cu in the brain is acting analogously to the copper ionophore elesclomol in Tregs
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