Sunday, 26 May 2013

Is it complex, or not? Make up your mind.

Often when reading papers on obesity, authors will quite commonly refer to body weight regulation as "complex". They will say things like, "bodyweight is regulated by a complex system of redundant networks".  etc blah blah

Usually, they will use this type of terminology only when referring to the difficulty of producing meaningful and sustained reductions in bodyweight. Although its also used to explain why bodyweight usually returns to normal after overfeeding studies.

And yet, the very same authors will quite facilely state that obesity is "caused" by over-eating and/or sedentary behavior.

So here we are presented with something of a paradox and contradiction, because, on the one-hand, bodyweight is supposed to be complex regulated system, but, it is easily manipulated by simple CICO, by simply having a bit extra on your dinner plate, or by simply missing your morning workout, you can apparently very easily change your bodyweight.

Nothing is more simple than overeating and being lazy. But apparently  these simple actions can very easily produce large and sustained perturbations in a complex and regulated system. I.E. bodyweight.

Now, how can bodyweight be a regulated, complex  and redundant system if it can be perturbed by such simple stimuli? Doesnt that sound contradictory? Isnt the point of a complex system is that its not easily perturbed? And protected from simple stimuli producing significant changes.

The only way to solve this contradiction is that, one of the premises is wrong. Either.....

1) bodyweight is a NOT a complex regulated system, but is a simple matter of CICO

2) overeating and laziness are not CAUSES of bodyweight changes, I.E. these simple stimuli are not capable of producing significant perturbations in the complex regulated system.

So please, obesity researchers, which is it? Complex or not? Either bodyweight is a complex regulated system or its a simple CICO program.

Can you make up your mind please?


There is a possible 3rd

3) only reductions in bodyweight are part of the complex regulated system, meanwhile increases in bodyweight are a simple CICO system. If this is true, then beware, because every time you overrate a measly 5 calories, those 5 calories become a permanent addition to bodyfat!

Wednesday, 15 May 2013

SCFA's inhibit insulin signalling in fat cells

I havent seen this study reported anywhere else in the blogosphere!

The gut microbiota suppresses insulin-mediated fat accumulation via the short-chain fatty acid receptor GPR43.

 Hence, this report also supports our results that suppression of adipose insulin signalling by GPR43 activation leads to prevention of obesity and improves systemic insulin sensitivity.

Look at how blasphemous this statement is, suppression of insulin signalling in adipose tissue prevents obesity.    lol  whha  ??!?!?!?!?!!!!?

Anyway, to cut a long story short, GPR43 is a receptor for short-chain fatty acids including acetate, and is expressed in various tissues including the adipocyte. There was some controversy surrounding the function of GPR43 in adipocytes because in vitro studies had shown that it promoted adipogenesis, but this research group claims to have shown that the in vitro observations of GPR43 do not match those of in vivo.

This study seems to support the nutrient partitioning idea, as GPR43 not only suppresses insulin signalling in adipocytes but improves systemic insulin signalling including in the muscle.

One observation I would like to make however, is that I have tried on numerous occasions high dose inulin for several days/weeks at a time but did not notice a reduction in fat mass.


Saturday, 11 May 2013

More on Fat Cell dynamics, - in response to weight loss/calorie restriction

cba today so ima just copy/paste

Adaptation of human adipose tissue to hypocaloric diet
  • In a study on type 2 diabetes patients submitted to 1-year dietary intervention combined with exercise, the authors stratified the adipocytes into four subfractions in respect to the cell size.16 At the end of intervention, the adipocyte size was reduced just in subfraction of ‘large’ adipocytes, while the other three remained unchanged.
  • investigations suggest that individuals with hypertrophic obesity—who are at higher metabolic risk6, 18, 19, 20—are more responsive to the adipocyte size-reducing effect of hypocaloric diets in comparison with those with small adipocytes, that is, with hyperplasic obesity.
  • In another study, using electron microscopy, the response was variable in a group of six patients submitted to 6 weeks’ LCD: in subjects with higher proportion of large adipocytes (hypertrophic obesity), the authors observed a shift from the fraction of large adipocytes towards the small ones, whereas in subjects with higher proportion of small adipocytes (hyperplasic obesity) no shift between the fractions occurred.
  • no reduction of adipocyte size in abdominal (but not in gluteal) SCAT was found after 20 weeks’ LCD in one study.15

  • insulin stimulation of de novo lipogenesis measured on isolated SCAT adipocytes was blunted after 4-weeks’ VLCD.10 However, in weight-maintenance phase, 1–3 years after initiation of the weight reducing program or after gastric banding, both, the basal- and insulin-stimulated, de novo lipogenesis measured on isolated adipocytes were increased when compared with the pre-diet condition.31

Prospective and controlled studies of the actions of insulin and catecholamine in fat cells of obese women following weight reduction.

  • Many of the adipocyte abnormalities associated with obesity improve after weight loss [1215]. Fat cell size decreases, as does basal lipolysis. Insulin and catecholamine actions are improved. However, it is not known if these actions completely return to normal. A full normalisation would suggest that the abnormalities are secondary to obesity. However, incomplete normalisation would suggest primary defects in adipocyte function that cannot be cured by weight loss
  • A prominent finding in this study was a decrease in fat cell volume below the control level in weight-reduced obese subjects. Since BMI, fat distribution and body fat content were similar in obese subjects and their controls, the results imply that adipose hyperplasia (at least in abdominal subcutaneous adipose tissue) is a major feature of weight-reduced obese subjects
  • This further strengthens the idea that insulin resistance is secondary to obesity, whereas adipose hypercellularity and low adipose lipolytic rates may be primary factors in obesity.
  • In conclusion, adipose tissue hyperplasia (many small fat cells) is present in the weight-reduced state and probably explains the low rates of adipocyte lipolysis in this condition. However, adipocyte insulin resistance is a secondary and fully reversible phenomenon in obesity.

You cant select a random obese person from the population then tell him "fat mass is only about CICO", because you have no idea of the amount of fat cell hyperplasia they are suffering from. The more fat cells you have, the fatter youll be, BY DEFAULT.

Why am I posting this? Because I want it to be apparent that people suffering from significant hyperplasia will be unable to resolve their dysfunctional metabolism with diet and exercise alone, despite what you may hear from high standing medical doctors and bloggers. More likely we will need pharmaceutical intervention or in the worst case scenario, surgery.

How can you tell if your suffering from hyperplasia? Well, while I dont have references to back up these claims, I have several ideas. Firstly, the ease with which you rebound weight gain after weight loss will signify hyperplasia. Also the degree to which you are metabolically healthy despite significant increases in weight will signify significant hyperplasia. If you was very heavy but with no clear signs of diabetes = significant hyperplasia.

Also, just look at your fat tissue, is it very "lumpy" with lots of partitions? or is it very roundish and circular? The former = hyperplasia. See pictures in this post for example. The guy in the left most likely has significantly more hyperplasia than the right.