The way this works is that lipids in the adipocytes freeze a bit sooner than water, basically you can trigger an apoptosis pathway in the adipocyte before the freezing causes significant local damage to all the other tissues.
"Crystallization of cytoplasmic lipids within the adipocytes initiates a cascade of events, characterized by adipocyte apoptosis, panniculitis, and eventual loss of adipocytes. Clinically, this translates into an effective decrease in fat layer thickness"
The fat gradually "melts" away 2-3 months post treatment as the adipocytes undergo apoptosis, however, there are some rare case reports of the opposite happening, where the treatment site initiates an increase of fat mass via hyperplasia,. The main article is here..
Whats interesting is that the fat growth hyperplasia is restricted to the treatment area. If the patient had gained weight in a more evenly distributed pattern over his body, the doctors would accuse him of eating too much and exercising too little. Its things like this where hopefully intelligent people will start to wake up and realize that the CICO model of fat mass has to be wrong.
If we couldnt apply the CICO model here, why can we apply it in more generalized obesity?
The caveat is ofcourse that we cant apply the model of systemic hormonal control of fat in this situation either.
The only possible way to explain the localized growth of the fat is to look at localized factors, I.E. the tissue and cells there. The treatment had obviously caused some kind of change in the gene expression patterns of the cells in that area and/or initiated an adipogenesis program to the pre-adipocytes in that region.
Recall from my previous posts, that once a pre-adipocyte morphs into a mature adipocyte its guaranteed to store fat, regardless of food intake, exercise, insulin, leptin, etc once the activity of lipogenic enzymes increases and the cell surface gains significant caveolae, the jig is up.
The how and why of why the cryolipolysis causes this is a mystery at this point in time. The only clue seems to be that its more common in male patients, but the sample size might still be too small.
As an aside, it seems the incidence with which this happens may also be under-reported, the first paper estimated the cases to be 0.0051%. while a revision put the number closer to 0.47% or 2 in 422.
