Oh, sorry. I'm trying to build a working model of this whole thing, but have been struggling with substantial brain fog that in retrospect has roughly correlated with my fasting insulin and postprandial fatigue getting worse over the past few years...

Early in the year had a HOMA-IR(glucose, insulin) of 0.51(94mg/dl, 2.2 uIU/ml), more recently 1.2(105mg/dl, 4.6uIU/ml). OGTT at both timepoints showed a glucose drop below fasting, with reasonable insulin numbers, which I suspect is rapid gastric emptying that sometimes occurs in prediabetes/T2DM, and is often associated with largely the same set of postprandial fatigue/brainfog symptoms I get(going by Sigstad’s score criteria). Glucose peak likely occurred before 1h mark. On a glucose meter, my fasting glucose is consistently ~105, which very easily jumps to 150-170 even with a single sandwich or some lowish-glycemic-index buckwheat, and to 180-220 with what I'd consider "a normal meal".

I thought that impaired glucose tolerance was a consequence of impaired first-phase insulin secretion, which in turn strongly correlates with fasting insulin levels, which I thought was a function of insulin resistance... I don't know, I just hope so badly that treating this stuff will fix the brain fog that's been getting worse and worse for years now :(

About apnea, it's likely apnea->dysglycemia- glucose metabolism follows a diurnal cycle susceptible to disruption even by sleep restriction, and sleep disordered breathing as a spectrum causes abnormal autonomic tone, while much less of a case can be made for dysglycemia->apnea. Maybe damage to upper airway dilator muscle innervation, airway edema, or tongue base fat deposition... though most likely each of these would require anatomically compromised airway just like most cases do.