This is interesting
http://m.ajpendo.physiology.org/content/early/2013/11/13/ajpendo.00408.2013.abstract

Also, some very basic signal transduction of the mTOR pathway

I think I posted this site in another thread, but fuk it's great and belongs exactly here

http://themedicalbiochemistrypage.org/

This is very interesting imo

http://www.cell.com/abstract/S0092-8674(13)01485-2
http://www.sciencedaily.com/releases/2013/12/131219134453.htm

Basically, "A high-fat diet affects the molecular mechanism controlling the internal body clock that regulates metabolic functions in the liver"

"A high-fat diet reprograms the liver clock through two main mechanisms. One blocks normal cycles by impeding the clock regulator genes called CLOCK:BMAL1. The other initiates a new program of oscillations by activating genes that normally do not oscillate, principally through a factor called PPAR-gamma. Previously implicated in inflammatory responses and the formation of fatty tissue, this factor oscillates with a high-fat diet."

I guess to further edify because that could be vague if you didn't know about either of those mechanisms or their implications.. here's a couple quick reads:
On the Genes: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2040024/
http://www.ncbi.nlm.nih.gov/pubmed/9989497
http://www.ncbi.nlm.nih.gov/pubmed/11163178

On PPAR-gamma - http://themedicalbiochemistrypage.org/ppar.php#pparg

and to kind of summarize a key point that's pertinent to the original study I'm talking about anyway:
It, "is also involved in the maturation process from pre-adipocytes to mature adipocytes, increases lipogenesis in white adipose tissues, decreases the cell surface fatty acid transporter on muscle cells and increases glucose uptake in adipocytes (exclusively)."
also making a topic cause noone will read here lol. And I found it pretty cool

This post was edited by Balla on Dec 20 2013 10:24pm

Some reads/studies criticizing "set-point" theories and metabolic damage basically

http://www.beyonddiets.com/storage/References--Set%20Point.pdf

http://www.ncbi.nlm.nih.gov/pubmed/7883999

http://journals.cambridge.org/download.php?file=%2FPNS%2FPNS50_02%2FS0029665191000575a.pdf&code=298e9f3cdd451607388169c5ae3c5095

http://www.ncbi.nlm.nih.gov/pubmed/11063433

http://ajcn.nutrition.org/content/49/3/409.short

inb4 layne norton

Please send to layne norton

Hahaha i will send them

Lmfao.



inb4flamedandblocked

His response:

http://www.ncbi.nlm.nih.gov/pubmed/21677272

that's it

read it all, fail to see point.
the forces working against long term sustainable fat loss and the fail statistics are apparent, but how do they pertain to actual metabolic damage? Most factors can be summarized in low dopamine levels pushing people over the edge of binging, and there are a few ways to satiate them:

adding more fiber, drinking more water and doing more aerobics which facilitates larger serotonine levels mimicking dopamine satiety and lowering appetite (even after consuming back the same net calories lost from the activity).

So, metabolic dmg or not, low dopamine/high ghrelin are still going to be there whenever you reach a truly lean state. i do however agree with dispersing the kcal drops over a much larger time span to help adapt to diminishing dopamine levels via reverse dieting protocols, but you can fix your calories if too low at any given time and not have to wait xx time to "reverse the effect on ur metabolism".