With cryolipolysis, if fat cells are killed and are gone for good, what's the cause of paradoxical adipose hyperplasia?

nobody knows exactly why this happens, thats why it's a "paradox" that it grows instead of gest killed.  Best, Dr. Emer.

Dear lemonnn:This is an excellent question which at this time can not be answered definitively.  It appears that this paradoxical response to cryolipolysis occurs primarily if not exclusively with individuals who undergo treatment when they are markedly overweight. We are born with a given number of fat cells (about 30 billion), which stays the same throughout our lifetime, with the exception of the obese, who make more new adipocytes, presumably to accommodate the larger amount of fat that must be stored. If these individuals undergo cryolipolysis, their fat cells may respond to being chilled by increasing their number rather than shifting into the end stage of their life cycle, programmed cell death.This side effect is very rare, and Zeltiq has offered liposuction to any patient who has experienced it without charge to the patient. If candidates for CoolSculpting are chosen appropriately, perhaps it would not occur at all.To be conservative. I always recommend to my patients that they not gain weight in the months after CoolSculpting. All the best,   Dr. Clark

The mechanism of PAH is basically unknown and instead of apoptosis, fat cells enlarge . Currently statics are it is 1 in every 20,000 cases, it occurs 2-3 months post treatment.
The pathogenesis of this phenomenon is unknown. Hypothesized causes include: (1) hypertrophy of a subset of pre-existing mature adipocytes that survive cryolipolysis (fat is capable of hypertrophy in response to metabolic and hormonal changes, without necessarily creating new cells); (2) recruitment of the abundant, existing pre-adipocyte and/or adipose tissue stem cell population, induced by cytokines associated with the healing phase after cryolipolysis (e.g. by ILGF-1 and other signals); (3) stimulated uptake and differentiation of circulating stem cells into fat; (4) induced changes in local expression of receptors associated with adipocyte metabolism; and (5) induction of both adipocyte and fibrous tissue hypertrophy in response to hypoxia. Many stimuli are known to increase fat tissue including glucocorticoids, loss of sympathetic innervation, and hypoxia.