What is wrong with obesity research

This paper in Nature Communications 14-3-3ζ Coordinates Adipogenesis of Visceral Fat has garnered some attention in the popular press. It is also a perfect example of what is wrong with the way modern obesity research is conducted and reported. This paper finds a protein that regulates adipogenesis or fat cell production. I haven’t gone into details of the results but let’s just assume that it is correct. The problem is that the authors and the press then make the statement that this provides a possible drug target for obesity. Why is this a problem? Well consider the analogy with a car. The gas tank represents the adipocytes, – it is the store of energy. Now, you find a “gene” that shrinks the gas tank and then publish in Nature Automobiles and the press release states that that you have found a potential treatment for car obesity. If it is really true that the car (mouse) still takes in the same amount of petrol (food) as before, then where did this excess energy go? The laws of thermodynamics must still hold. The only possibilities are that your gas mileage went down (energy expenditure increased) or the energy is being stored in some other auxiliary gas tank (liver?). A confounding problem is that rodents have very high metabolic rates compared to humans. They must eat a significant fraction of their body weight each day just to stay alive. Deprive a mouse or rat of food for a few days and it will expire. The amount of energy going into fat storage per day is a small amount by comparison. It is difficult to measure food intake precisely enough to resolve whether or not two rats are eating the same thing and most molecular biology labs are not equipped to make these precise measurements nor understand that they are necessary. One rat needs to only eat more by a small amount to gain more weight. If two cars (mice) grow at different weights then the only two possible explanations is that they have different energy expenditures or they are eating different amounts. Targeting the gas tank (adipocytes) simply does not make sense as a treatment of obesity. It might be interesting from the point of view of understanding development or even cancer but not weight gain. I have argued in the past that if you find that you have too much gas in the car then the most logical thing to do is to put less gas in the car, not to drive faster so you burn up the gas. If you are really interested in understanding obesity, you should try to understand appetite and satiety because that has the highest leverage for affecting body weight.

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3 thoughts on “What is wrong with obesity research

  1. this is a slightkly different issue or take, but i know when at times i have lost alot of weight going down to like 125 to 135 lbs —i should be betweren 140 and maybe 150 ) due to pneumonia, and starving (hiking and living off the land) in mexico and the himalayas, my appetite went way down too for a fairly long time —till i slowing regained it. one can;t or want to accomodate more gasoline—–this is also why people may use surgical removal oof fat as well, or even try using tighter fitting clothes. also i think fat cells sort of have their own minds—they send out ‘i’m hungry’ signals and also want to multiply and grow a la capitalism (piketty).

    i have no idea if that drug idea would work and its possible for some people it may work.

    but my problem with obesity and other health research is its part of the ‘pop the pill’ aproach to.improviing life. alot of poor proplr i know are on ‘meds’; poor kids are diagnosed with adhd; that muslim sop killer in tennessee was on meds, as was the batman shooter, the columbine kids etc. If you have probklenms—-economic, social—its often seen as desirable an d profitable to just essentially put you dope (and some just go and there k2, heroin, alochol , tobacco themselves—–i can get all of them within 2 or 3 blocks or have them delivred here —i hhad to tell peoople i know not to do tjhat here and i have nowe banned them since i am trying get away from this scene with little success–like trying to lose weight ).

    also pill promoters often live in basically affluent areas, so in a sense they are analogous to welathy drug dealers. many universities have had scandals since ‘pharma’ was sponsoring shodddy research, writers up the results, gettinfg a prof to sign it in exchange for alot of money. There are maybe too many incentives to change this system—JHU has a big clinical trial thng so heroin addicts can get their fix in exchange for a weeks being a guijnea pig. ‘its all good’.

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  2. ps this is essentiallly analogous to a lotka-volterra predator/prey model, which was also used by goodwin and p samuelson to formalize marxist dynamics. L-v i think was essentialy shown by S Smale in the 70’s essentially can simulate pretty much everything—its universal, like the turing maschine .

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  3. A simpler argument against the mechanism in this paper (as a target for reducing obesity): We already have a way to reduce the amount of energy that can be stored in adipose cells, it is called being diabetic. Reducing the number of adipose cells and reducing the amount of energy that each can store probably aren’t very different, especially in terms of the symptoms they will cause. Unless appetite and satiety are somehow regulated on a per adipose cell level, in which case intake could decrease for one but not the other.

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