Friday, 6 February 2015

the "master" gene

I was reading through JJ's tweets other day and came across this

despite it being quite disturbing, something out of a horror movie, reading the ensuing discussion was fascinating. This article explains what is going on.

Basically, there is a gene they refer to as "eyeless" and when activated, this gene sets off cascade of signalling that results in the growth of an eye at that location.

The reason I found this so interesting is because we have also seen here on this blog another candidate for a "master" gene. PPAR-γ.    Just as activating "eyeless" caused eye growth in strange places of the body, substantial evidence indicates that activating PPAR-γ causes adipocyte appearance.

My guess is, it probably didn't how much the fly ate and exercised, once the eyeless gene was on, the eye WAS GOING TO GROW, regardless.

At this point im fairly sure that the cause of obesity is refined carbs promoting hyperglycemia and hyperinsulinemia.  These 2 in turn promote epigenetic changes to adipose tissue aswell as the recruitment of adipose tissue progenitor cells ( preadipocytes ) Once a preadipocyte turns into a mature adipocyte, its going to store (alot) fat, everything else is irrelevant.

I also found this interesting post on t-nation, where he explains that people who respond poorly to resistance training do so because of genetics and poor recruitment of muscle progenitors ( satellite cells ).  This could potentially be similar to the reason some people are resistant to obesity, i.e. failure to recruit progenitor cells in adipose tissue.


  1. I endorse this blog entry.

    Sounds legit.

  2. I clicked on my bookmark to your blog by mistake (not that it's ever a mistake to go to your blog). I was intending to go to Woo's blog, so reading this as a Woo post was very strange. As many would agree, the "style" is so different.

    But what struck me was the use of the phrase "resistant to obesity" in the last sentence. Woo uses this phrase as well.

    As a person who has never been obese, just modestly overweight at worst, I tend not to think of myself as "resistant to obesity." I think of heavier people as "prone to obesity."

    I wonder how this semantic difference influences obesity research, if at all. The phrase "resistant to obesity" implies that in our "obesigenic" environment, getting fatter is the norm. Thus, deviation from the norm on the thinner side is "resistant." In this sense, "obesigenic" means equally "too much carbohydrate" to LCHF devotees as "too many calories" means to the mainstream view.

    I realize this off-topic to a very interesting and pointed post, but there it is.

    By the way, great to see a new post after a month of drought.

    1. its the "is the glass half full or half empty" type of argument.

      proneness is probably a better way to phrase it simply because cells *react* to environment. either you react to your environment because you have the receptors for it, or you dont have the receptors therefore dont react.

      the "too many calories" view however is nothing to do with a perspective but instead is born purely from inability for abstract thinking, logical reasoning etc. stupid ppl basically. they latch on to what they see and what makes "intuitive" sense and try to find reasons/data which fit those intuitions.

      I.E. fat cells store "calories" and obese ppl "eat alot" -> therefore ppl eating too many calories causes obesity.

      despite the fact this has been dis-proven in so many ways, many ppl still believe it.

      the reason obese ppl eat more than thin people is because they have high energy expenditure due to having more body mass.

  3. "people who respond poorly to resistance training do so because of genetics and poor recruitment of muscle progenitors ( satellite cells )."

    It is possible that the mechanism of this as well as proneness to adiposity, at least in men, involves androgens, i.e. androgen deficit.
    Clin Endocrinol (Oxf). 2010 Feb;72(2):176-88
    Effects of androgens on adipocyte differentiation and adipose tissue explant metabolism in men and women.