Peter "Big Cat" Van Mol - The Physiology Of Fat Loss - A 4 Part Series!

**webmaster** · 03-03-2004, 04:30 PM

The first article is related to lipolysis and non-shivering thermogenisis. To not complicate things too much, I will stick to discussing only the local effects on fat cells and their adjacent nerves in this first instalment.

http://www.bodybuilding.com/fun/losefatnow.htm

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ShaneG85 · 03-03-2004, 06:08 PM

Does Big Cat have any competition pictures up? In a very old article, he said he wanted to work his way up in weight and be, i believe, 215-217 on stage.

Shane

Jimmy_magix · 03-04-2004, 07:47 AM

I think he has decided not to compete, I read an update on his progress and he has been through some really tough times.

Big Cat · 03-04-2004, 03:39 PM

It was 225-228 and no, I never did make it. Since then my competition days are over, and I must admit the theoretical aspect of it all is taking priority over the hard slavery in the gym. I currently maintain 215 at about 8-10% body-fat.

I guess common sense crept in that i shouldn't work my ass off and settle for top 5 at a national show in a country with only 10 million inhabitants, If I can bring in several international titles a year as a trainer. This year I have Philiep van Nuffel competing in world championships, and I'm helping Ivan Nicholov prepare for the Musclemania superbody.

Thanx for the interest in my physique

but I think my mind will probably be speaking for me from now on.

Jimmy_magix · 03-05-2004, 03:01 AM

Quote:

Originally posted by Big Cat
Thanx for the interest in my physique but I think my mind will probably be speaking for me from now on.

and a very clever mind it is too! Im always amazed at the depth of your articles. I cant wait for the other two articles on fat loss. Pretty hard to understand for a Philosophy and English degree student, but I have managed to with the pen and paper you recommended! Thank you very much for allowing me the greater understanding of physiology. Ill stop now because it sounds too much like I'm kissing ass

JT

Big Cat · 03-05-2004, 01:39 PM

Actually its more than 4 parts. I just sent the first 4 parts in so far.
There will be 5 theoretical parts, and then hopefully 3 or more practical parts with in depth discussions of various products based on the theoretical part.

Big Cat · 03-05-2004, 01:43 PM

And being a philosophy student doesn't mean anything in this regard. I love philosophy. And throughout my high school years I sucked at science and was convinced I would study psychology (which I initially tried). Now we are a molecular biology degree and two years of biomedical and biopharmaceutical technique farther ...

So don't give up just yet, your interest can drive you to learn most anything.

03-09-2004, 05:24 PM

Not to nitpick, but I got the wrong impression about the mechanism of SOCS3 from your article.

SOCS3 is turned on by IL-6 downstream signaling, yes, but it acts to shut off IL-6 effects in the cell. It does not offer an additive effect to IL-6 signaling - it is there for allosteric feedback. SOCS3 is also stimulated by other cytokines/growth factors such as insulin-like growth factor (IGF-1) and growth hormone (GH). I haven't seen that it is turned on by insulin itself, but I am unsure if insulin can stimulate the IGF-1 receptor or not. There are different isoforms.

IL-6 is also one of the cytokines heavily upregulated during a heart attack. I'm not sure if increasing IL-6 systemically would be a very good idea.

Sorry, didn't mean to be pissy - just thought I'd mention it. I'm working on a PhD in biochemistry and my thesis is heavily dependent on cytokine and inflammatory pathways. If you would like references for the above information, you may email me at signecarlson@hotmail.com.

Thanks.

03-10-2004, 04:56 AM

Quote:

Originally posted by Unregistered
Not to nitpick, but I got the wrong impression about the mechanism of SOCS3 from your article.

SOCS3 is turned on by IL-6 downstream signaling, yes, but it acts to shut off IL-6 effects in the cell. It does not offer an additive effect to IL-6 signaling - it is there for allosteric feedback. SOCS3 is also stimulated by other cytokines/growth factors such as insulin-like growth factor (IGF-1) and growth hormone (GH). I haven't seen that it is turned on by insulin itself, but I am unsure if insulin can stimulate the IGF-1 receptor or not. There are different isoforms.

Not at all, you are quite correct. SOCS3 is in principle a negative feedback regulator for most things that activate it. Insulin, IGF-1 and leptin all use similar cascades that use SOCS3 as negative feedback, reducing respective insulin/leptin/IGF-1 sensitivity. The downregulation of IL-6 as a results leads to less SOCS3 activation, which then leads to more IL-6 and more SOCS3. But since IL-6 in this instance is activated by Src, which is also activated by PKA which is not downregulated, IL-6 to some extent remains upregulated leading to a long term significant increase in insulin sensitivity.

Very interesting that you brought this up, since I was not aware that GH activates SOCS3 directly. Do you have any data that corroborates this ?

Quote:

IL-6 is also one of the cytokines heavily upregulated during a heart attack. I'm not sure if increasing IL-6 systemically would be a very good idea.

Since IL-6, especially in this instance, is upragulated by increased sympathetic activity, I do not find it odd that it is higher during cardiac arrest. This is also the reason most drugs that increase sympathetic activity are not recommended to the elderly or to heart patients. I see no causality in this though.

Quote:

Sorry, didn't mean to be pissy - just thought I'd mention it. I'm working on a PhD in biochemistry and my thesis is heavily dependent on cytokine and inflammatory pathways. If you would like references for the above information, you may email me at signecarlson@hotmail.com.

Not at all, its nice when someone takes an interest in the details and adresses them. Most people I end up discussing this with, like company owners and supplement developers don't know the first thing about physiology and biochemistry, so this is enlightening to say the least.

The same offer is extended, if you ever want to talk, feel free to email me.

Thanks. [/B][/QUOTE]

twistedneck · 03-10-2004, 06:19 PM

OMG, I've read all 4 parts several times now and still can't grasp enough.

I am however, taking my Vit. A ED at 10,000iu and eliminating supplemental zinc and Vit. E.

Keep up the good work Big Cat, looking forward to the next installments. TW.

twistedneck · 03-13-2004, 10:17 AM

Quote:

Testosterone and trenbolone are the two most potent drugs in this regard, and they are highly synergistic in this regard as well. Testosterone blocks the cortisol receptor, whereas trenbolone may reduce receptor number and may reduce size of the adrenal gland long term.

Usually in a diet we try to make use of cortisol without letting it get out of hand.

Big Cat, what does this mean for someone who uses oral or depo cortisol here and there for huge performance gains on races longer than 1 hr? (three or four times / year max, usually oral short acting but sometimes inj. long acting, boy does that help pain and make you fly!).