Fat Handbags Have Already been Stopped

Continuing on from yesterday's post and the noteworthy attempt of 'obesity' promoters to decry any possibility of blocking a cell that has already been blocked. Looking back at research indicating the maturation process of our fat handbag adipose cells, can be stimulated to completion by a hormone called Adamts1.

Sentiments expressed by Dr. Brian Feldman-part of the research team concerned-about the purported implausibility of slowing fatty tissue genesis was backed up and emphasised by an NHS website,

The coverage by the Mail Online was generally accurate, highlighting the important fact that this research has not necessarily identified a target for anti-obesity treatment options.

"The important fact" eh? Why would that be either? Important to whom? It's not even about expectation management. If you say, eventually it seems like they'll be a means of stopping adipose tissue from increasing, you can go on to say, but not for a while yet if you want.

It's the enthusiasm for shutting that avenue down that is a red light.

If one steps back from puberty, it could be seen purely as an increase body mass. In healthy cells; bone, muscle and FAT [etc.,]. By dint of that, blocking or slowing puberty effectively does the same for adipose as part of that repression,

Initiating the treatment early for a child who experiences gender dysphoria has greatest effect; the body of the patient is less developed and later, the need for surgery such as mastectomy or “reduction thyroid chondroplasty and voice modification therapy” is avoided.

Avoid mastectomy? Okay, this is the brotherhood of wikistan, I haven't looked further into it yet, still, I think we can confidently state the human breast has fatty tissue.

Puberty blockers supposedly work by suppressing the release of chemicals that launch the process of puberty into effect. They are released from the pituitary gland. Incidentally, one of these hormones is called "follicle-stimulating hormone" or (FSH), yes, that relates to the troublesome, poly-cystic ovary, follicles. This could go to explain why PCOS can now seemingly be diagnosed without the presence of challenging follicles.

I'm not here to recommend nor decry puberty-blocking, initially a treatment for precocious puberty. This is really about being told what isn't supposed to be possible or likely, when it has already happened however imperfectly.

Even if it hadn't, it would hardly be an outlandish possibility to be able to modify the extent/speed of one cells proliferation, given the body already does this. If you've ever dieted for any period, you'll know that it can speed up your body's capacity to gain weight like no-ones business. How can that happen if gain is all one speed?

And where you can slow, you can look to stop, or at least slow even further. So if any 'obesity' wallahs are struggling with this concept, why don't they mosey on over to those working in the area of arresting puberty and ask them for a clue?

It slightly recalls the suggestion that "weight loss" is supposed to be hard, when the body already goes down (and up) in weight, daily, with consummate ease. One might humbly imagine attempts to figure out the ways it manages this impossibility/immorality/unlifestyle generated action. Only for that also to be mysterious improbable.

As I've repeatedly stressed (oops), "obesity science" doesn't actually have to reverse weight. It can merely settle for subduing replication of cells. The spluttering response...

'If you block fat formation, extra calories have to go somewhere in the body, and sending them somewhere else outside fat cells could be more detrimental to metabolism.

...when confronted with this notion fails to grasp-stopping a person's weight/fat mass where it is. Which is the norm for most people fat to thin alike, it's homoeostasis, all you're doing is seeking to help that along. When it comes to blocking fat, of course we are talking about the activity that promotes its genesis /proliferation.

We are talking here about outliers who are enduring aggressive symptoms that include/lead to swift unending gain. 

And blocking or suppressing adipose cells can equally have an affect on other metabolic features including hunger and appetite. Because fat cells are "metabolically active" sending as well as receiving messages.

You may be asking why in the midst of a supposed adipocalypse of urgent proportions, is there this continual urge to deny possibility of the obvious target to save us from this impending hellacious fate? In favour of such cutting the sugar in soft drinks.....no less....