Friday, 22 January 2010

Don't fight it, if you like it.

I was listening to "Scream" by Timbaland in the car today and the first part of the title made me think of dieting. Sometimes our bodies fight our every effort to change our weight. This is a particular problem for people who are trying to lose weight. They feel cold, hungry & listless and they really want to EAT SOMETHING, damn it! It's because they are trying to change their set point weight. For information about set point weight, see Good Science: Dr. Leibel Explains Metabolic Slowdown with Weight Loss.

The problem with getting fat is that adipocytes (fat cells) can only hypertrophy (become larger in size) so much. When they reach a certain size, they secrete something (I don't know how this works so don't ask) that stimulates preadipocytes to become adipocytes. A larger number of something is called hyperplasia. Once adipocyte hyperplasia has occurred, we are stuck with them for life depending on what part of the body they've formed in. Visceral fat (the harmful fat around your internal organs) cannot be removed by liposuction. Only sub-cutaneous fat can. Losing weight & bodyfat results in adipocytes becoming smaller. However, the more of them there are, the smaller they have to become to achieve a given fat mass.

Adipocytes secrete leptin, the amount secreted reducing with reducing size. Leptin works by inhibiting the activity of neurons that contain neuropeptide Y (NPY) and agouti-related peptide (AgRP). Reducing serum leptin level acts on the hypothalamus, increasing our appetites and reducing our energy expenditures. When adipocytes become smaller than normal, leptin secretion reduces considerably and even though there are more of them, net serum leptin decreases and the end result is feeling cold, hungry & listless.

There's another problem that can occur with leptin. In the above example, there's a lack of leptin and the body doesn't work properly. This is analogous to type 1 diabetes. In some people, the hypothalamus becomes insensitive to leptin. Leptin resistance is analogous to type 2 diabetes in that the stuff's present at the correct level but it doesn't have the desired effect and the body doesn't work properly. The end result is also feeling cold, hungry & listless.

It's supposedly possible to restore the sensitivity of the hypothalamus to leptin, but that's for another blog post. So a fat person could say "I'm not fat, I'm hypothalamically-challenged!"


Dr.A said...

I've read 3 books on leptin, they all say something different and none of them make sense!

Nigel Kinbrum BSc(Hons)Eng said...

I've probably got it wrong as well! I saw a comment by Itsthewoo where she said that her serum leptin was really low after she lost ass-loads (!) of weight and that was causing her difficulties so she's been prescribed leptin.

However, a lot of fat people have normal serum leptin but still feel hungry, so they just keep eating. I think that "leptin resistance" explains that.

The problem is that there are loads of stimuli for appetite e.g. visual, smell/taste, peer pressure, emotional, habit etc and that makes it hard to work out what's going on.

Daniel Herman said...

If that's true though, it really does sound all doom and gloom for previous fatties like myself trying to get very lean (sub 10% is the ultimate goal, I've hit 11-12% at my leanest).

Since we've seen people like that become extraordinarily lean (John Stone, Built (IM forums)), I kind of refuse to believe that is true.

There simply must be something that can cause cell aptosis (I think that's the word) in fat cells whether it's a chemical or natural process. Since both of those individuals did not use steroids beyond HRT levels, I would imagine that there must be a natural process that accomplishes this somewhere. I mean the cells aren't immortal.

Nigel Kinbrum BSc(Hons)Eng said...

Hi Daniel.

I don't know John Stone but I know who Built is and she's certainly lean (I don't know how fat she was at her fattest). LCHF dieting suppresses appetite. Resistance training with weights also suppresses appetite.

Searching for "adipocyte apoptosis" yields a large number of studies, so there is hope. Leptin doesn't appear to be available on prescription in the UK but I don't know about elsewhere.

Getting below 10% BF is difficult. Is there a particular reason why you're trying to achieve this?


Daniel Herman said...

Hi Nigel,

I'm trying to do it just to prove that I can. I went from 260 at my heaviest around 21 yrs old to 155 by 22. At this point it's a given for me that I can easily maintain my weight around 170-180 with little difficulty, but one of my long term goals is still to lean out enough to have good definition. It's one of the things that drove me to lose weight after I initially got sick.

Also, I know myself and know that to maintain an exercise and nutrition routine, I need a goal. Whether that goal is fat loss, muscle gain, strength gain, etc.. it simply needs to be there or I won't eat healthy and exercise consistently.

Nigel Kinbrum BSc(Hons)Eng said...

Hi Daniel.

Well done so far and the very best of luck with your forthcoming fight. I've never had visible abs and my desire for food greatly exceeds my desire for visible abs. I'm not fighting it, 'cos I like it. See also More Evidence That Overweight is The Healthiest Weight


ProudDaddy said...

I've had interchanges with Carbsane about adipocyte number. She believes that it doesn't change during adulthood. My understanding is that at some threshold (about that of clinical obesity), hyperplasia occurs. Having a lot more fat cells might explain the undeniable metabolic differences between the formerly-obese and the never-obese, but I don't know how the mechanism can be explained without knowing the quantitative relationships between cell size and signalling outputs, and I wouldn't know where to start to find such curves. (Assuming a linear relationship wouldn't seem to explain much, since half as much from twice as many yields the same total.) So, I'm hoping both you and Evelyn can provide some insight.

Nigel Kinbrum said...

I'm on my Blackberry, so I'll keep it briefish.

I'm using Lyle McDonald's stock reply "it depends".
Some people don't have adipocyte hyperplasia and become diabetic when they continue to eat more than they burn. Others do, get fatter and don't become diabetic.

ProudDaddy said...

Thanks for the reply. What my comment was most concerced about was the difference in things like REE in the formerly-obese vs. the never-obese, so a few questions:

Do you still believe that hyperplasia occurs as we get fatter?

Do you have any info on the output curves of adipocyte hormones vs. cell size? (In vitro would be fine:-)

Nigel Kinbrum said...

STILL on BlackBerry.
Based on Itsthewoo's experience, I would say that a certain mass of fat results in more leptin secretion (and hence higher REE) with a smaller number of fuller adipocytes than a larger number of less full adipocytes.

I don't have any of the info you're after, but I haven't done a thorough search.

In conclusion, consistently eating more than you're burning is bad either because it makes you ill or because it messes up your RER & appetite - possibly for the rest of your life.