started at 2k daily too, went up to 4k after my labs came back low. now i’m wondering if the semaglutide changes the buildup math. if everything’s moving slower through my gut, does the vitamin D stay longer, absorb different, accumulate different than it would off-semaglutide? my prescriber said it wasn’t a concern but didn’t really explain why. everyone talks abt GLP-1s causing malabsorption but what if slower digestion actually means better absorption of fat-soluble stuff? that sounds backwards but i’m not sure it is. i’ve been logging it in careclinic alongside my labs every 8 wks. trying to track if my D levels are climbing different than they used to. but running on two-hour sleep windows so i can’t tell if i’m actually seeing a pattern or just seeing what i want to see. the mechanism probably exists. i just can’t hold it in my head yet to figure out if it matters.
the “slower digestion actually means better absorption” part is the piece i’d push back on a little. the logic tracks, longer transit time feels like it should mean more time to absorb things.
but for fat-soluble stuff like vitamin d, you also need bile to emulsify it properly. GLP-1s can impact gallbladder function and bile secretion, which isn’t talked about as much as the motility part.
so you could have two competing mechanisms: delayed emptying potentially increasing absorption time, while reduced bile flow
the “slower digestion actually means better absorption” part is the piece i’d push back on a little. the logic tracks, longer transit time for more contact makes sense on the surface.
but the confounder for fat-soluble vitamins like D is bile flow… GLP-1s can impact gallbladder function, which means you might have less bile to actually emulsify the fats the vitamin is carried in.
less bile could mean less absorption, even with the
The two-hour sleep windows are the louder variable here, not the transit time.
You’ve bundled two separate questions: transit time and absorption efficiency.
I hear you on trying to find a signal through the noise when you’re that sleep deprived. Before even getting to the GI transit question, I’d put a pin in the “running on two-hour sleep windows” part. From everything I’ve read and experienced, chronic sleep deprivation is its own metabolic state, not just a tiredness problem.
It keeps cortisol elevated and can create all sorts of weirdness that’s a much bigger metabolic input than a potential shift in vitamin D absorption. Your logic about slower transit and fat-soluble vitamins isn’t backwards at all, it’s a good question to ask. But the effect from that is likely so much smaller than the effect from the sleep deficit.
The thing that might help untangle this later is using the journal note in CareClinic next to each lab entry to log what your sleep was like that week. When you look back in a few months,