Agreed. The AKR1C1 finding underlines that fat tissue isn’t one uniform “storage tank.” Different depots can have different local hormone metabolism and signaling, so a systemic calorie deficit doesn’t necessarily translate into fat loss from the affected regions in lipedema.
Your point about localized insulin resistance fits well with this. The carbohydrate–insulin model makes more sense when applied at tissue level—where specific depots may have altered insulin/estrogen sensitivity and behave differently than the rest of the body.
Also worth mentioning: I know Norwegian researchers who have been looking into lipedema and insulin resistance, but the work isn’t published yet.
Agreed. The AKR1C1 finding underlines that fat tissue isn’t one uniform “storage tank.” Different depots can have different local hormone metabolism and signaling, so a systemic calorie deficit doesn’t necessarily translate into fat loss from the affected regions in lipedema.
Your point about localized insulin resistance fits well with this. The carbohydrate–insulin model makes more sense when applied at tissue level—where specific depots may have altered insulin/estrogen sensitivity and behave differently than the rest of the body.
Also worth mentioning: I know Norwegian researchers who have been looking into lipedema and insulin resistance, but the work isn’t published yet.