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Centrally, semaglutide engages brainstem vomiting centres: it can access circumventricular regions like the area postrema and activate GLP-1 receptors in the dorsal vagal complex (area postrema and nucleus tractus solitarius), directly stimulating nausea and emesis pathways [60,61,62]
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Unlike SGLT2 inhibitors, GLP-1 medications do not cause the glucosuria that promotes fungal growth
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They work better together: Combined, NAD+ and Sermorelin target different systems simultaneously, which is why many patients eventually use both
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