Carbs and Lipolysis

(1) It affects both. This means any fat you eat goes to where most of it likes to hang out (i.e., your waistline)

(2) Eating protein before exercise is good. It does not appreciably interfere with fat burning, even though it does cause some insulin response. It is worthwhile taking it for its muscle sparing effect. This point has been discussed at CEM forum.

It does not appreciably interfere with fat burning, even though it does cause some insulin response.

VC:
I have my doubts about this. Any studies/ info/ threads/ that I can take a look at?

Mad Amos, you have to consider the idea that fat doesn't require insulin in order to be stored. A caloric deficit also changes things a bit. A little bit of fat storage isn't always bad when dieting.

Posted by: @Logo

Mad Amos, you have to consider the idea that fat doesn't require insulin in order to be stored.  A caloric deficit also changes things a bit.  A little bit of fat storage isn't always bad when dieting.

i'd like to elaborate on that point. Not all insulin spikes are created equal. 1 gram of carb release insulin... but it's not enough to inhibit all fat burning... it largely depends on the degree. Lets not forget insulin's positive effect on leptin.

Once again, we should eat most of our carbs around our weight workouts b/c those are the time when nutrient partitioning is the greatest... so why not take advantage of this with cardio as well!!!!!!!!!!!!!!????????????

Posted by: @Lgoosey

It does not appreciably interfere with fat burning, even though it does cause some insulin response.

VC:
I have my doubts about this. Any studies/ info/ threads/ that I can take a look at?

Here ya go. The whole thread, not just the first post, is worth taking a look at.

All foods are glucogenic to certain extent. Someone said that protein is about 40% glucogenic (I am not sure about what kind of protein, or if it matters, or if this number is given to those in fasted state, etc.).

i'd like to elaborate on that point. Not all insulin spikes are created equal. 1 gram of carb release insulin... but it's not enough to inhibit all fat burning... it largely depends on the degree. Lets not forget insulin's positive effect on leptin.

I think we agree in theory. however one point to clear up. insulin alone dosent realy have any positive effects on leptin. However insulin and leptin act in the CNS and brain much the same way. So insulin can make up for low leptin or they can share there duties in the brain.

Also insulin does not effect lipolysis in visceral adipose tissue to any signifigant degree. This is one reason VAT tissue is so bad for you and is associated with morbidity, diabetes, high blood pressure, etc... VAT for the most part can not stop its lipolysis. Thus it is just constantly taking up cyclomicron packaged TAG and freeing it as FFA and dumping it back in to your blood stream which leads to insulin reistance. So you see insulins effects on lipolysis is sometimes desirable as eliminating it causes a host of problems.

So you see insulins effects on lipolysis is sometimes desirable as eliminating it causes a host of problems.

Several more good arguements against all-out ketogenic diets.

Wow...thanks guys!!!

A few more for y'all and then I'm done for a while (I PROMISE):

1.) If ASP doesn't need insulin for lipogenesis, and carbs are so beneficial, then ultimately do we still care about GI? It's obvious carbs don't make you fat, so why bother?

2.) Does glycogen repletion still occur in a deficit, and to what degree? To what degree does glycogen DEPLETION occur during a deficit?

3.) How does TEF factor in during a deficit? In other words, is it better to favor carbs and protein over fat because they're more "costly" to store and, therefore, we technically store less of them than we do fat?

4.) Does macro composition have ANY bearing on a deficit? It seems that (although I'm being feasesous here) one could eat pure sugar during a deficit and still lose fat. I see so many people going keto in conjunction with caloric deficit, and I just don't see the rationale. I mean, you're burning stored energy no matter what in this situation, right? Which brings me to my FINAL question...

5.) What exactly causes muscle catabolism during a diet? Is it a direct result of leptin reduction or are other mechanisms at work? Would there be any value in reducing the amount of deficit created by calorie restriction and increasing the amount provided by exercise as far as catabolism is concerned?

WHEW!!!

I'm trying to work out deficit amount, cardio schedule, meal timing, refeed schedule, macro composition, etc. and I want to manipulate them with an eye toward minimizing proteolysis (obviously). Any thoughts?

So you see insulins effects on lipolysis is sometimes desirable as eliminating it causes a host of problems.

Not disagreeing in the slightest bit but I am confused on how you can to this conclusion? what host of problems from elimating it?

Not disagreeing in the slightest bit but I am confused on how you can to this conclusion? what host of problems from elimating it?

The conclusion is easily reached if you have read the pertinant studies. Look at PPAR-gamma and RXR receptor blocker research. If you block either one alone then things improve. you get less adipose tissue mass and improved insulin resistance. however if you block both wich prevents fat storage to a signifigant effect then you induce insulin resistance and diabetes. you have to understand that your muscle is fully capable of doing your adipose tissues job. This is what happens in the obese and why obesity promotes diabetes (though it does not cause it, you still must be genetically predisposed). Storage of fat in your muscle cells called Intra-Myocellular Lipids IML is a very bad thing and induces insulin resistance and promotes diabetes by inhibiting PFK and shutting more carbs to the hexosamine pathway when its not apropriate to do so. This is why there are extremely lean people with TypeII diabetes as well as over weight ones. The lean type generaly posses a fat storage anomoly. And if you can't store it in fat then it gets stored in your skeletal muscle and thats just plain bad.

5.) What exactly causes muscle catabolism during a diet? Is it a direct result of leptin reduction or are other mechanisms at work? Would there be any value in reducing the amount of deficit created by calorie restriction and increasing the amount provided by exercise as far as catabolism is concerned?

It can be caused by the very fact that your in a dificet if protein intake is not adequate because protolysis will increase to provide aminos as substrate for oxidation. However if one is consuming adequate protein then it is mostly caused by the hormonal milleu. Namely increased cortisol and reduced sex hormones.

Posted by: @Spook

VAT is controlled by androgens and cortisol for the most part. If you were over eating strictly carbs and protein and you lowered your androgen levels and inhibited local (not plasma) cortisol then the fat in your fat would most likely redistribute to SAT.  Its really the cotrisol and androgens that promote and sustain its growth. So to remove it you need lower androgens and cortisol.

Hmmm....care to elaborate more on this?

For instance, what type of effect would the use of systematic androgens and a local or systematic cortisol-suppressant (ie Ab-Solved/FL7) have on this process?

Hmmm....care to elaborate more on this?

For instance, what type of effect would the use of systematic androgens and a local or systematic cortisol-suppressant (ie Ab-Solved/FL7) have on this process?

I will go over the different fat cell types in Leptin VI. There are actually three different classfications realy. SAT, VAT, and deep layer SAT.

Men store more fat in VAT and deep layer SAT than women do. Most somen store there fat in SAT, pretty exclusively. Women afflicted with PCOS of course also store more fat in VAT like men do because of increased androgens and increased cortisol production. PCOS women resemble the symptoms of adrinal hyperplasia which is just an over active adrenal gland.

VAT is basically unregulated fat cells. They are what happens when fat cells just stop listening to your body. They show near non stop lipolysis that is not attenuated by insulin. They primarily use ASP as a means of storing fat. They release a huge amount of angiotensinogen (leads to high blood pressure and promotes more VAT). They release a huge amount of TNF-alpha and IL-6 and IL-1beta. The primary signal for VAT recurtment and growth is cortisol, angiotensinogen, and androgens. Vat mostly undergoes apoptosis.

SAT is basically the oppisite. It blunts lipolysis in the presence of insulin. It uses both ASP and FAT(CD/36) for FFA uptake. It does not release that many cytokines comparatively with the exception of leptin. SAT releases much more leptin than VAT (one of the many reasons women have higher levels of leptin). Its primary recurtment signal is PPAR-gamma. Sat mostly returns to being pre-adipocytes instead of going in to apoptosis.

Androgens promote VAT growth by several means. The most important is probobly increasing 11Beta-HSD1 production in pre-VAT cells. in VAT cells 11beta-HSD1 activates inactive cortisol (note in other tissue this is the oppisite). angiotensinogen converts to angiotensin II (RAS is completely expressed in VAT and pre-VAT cells) angiotensin II directly inhibits recurtment in vitro but in-vio its prodifferentiation because is creates a protein that primes the pump for cortisol based recrutment. cortisol in SAT is lipolytic, its pro-storage in VAT.

So anyone tacking androgens has an increased risk for VAT growth. the T/E ratio seems to be irelevant for this. Its pure T level that seems to be important. Thus anyone with naturally high levels of T or useing systemic androgens is at an increased risk of VAT growth. This can be seen easily in rat research. Male rats develop VAT, females dont. But females given test develop VAT. So this agress with the PCOS patients.

Increased cortisol is also of importance. And this is local cortisol. As par stated. Blood levels mean F*** all. as VAT cells are completely capable of activating inactive cortisol on there own and do not need the liver. So its totaly corticosterone + cortisol that impacts VAT.

systemic use of androgens is going to put one at increased risk. the usage of FL7/Ab-solved (FL7 is probobly better) would be of much benefit during this time to prevent VAT growth by lowering local cortisol. oral would not be ideal as it would inhibit coritosterone to cortisol conversion. This seems advantageous on the surface but less plasma cortisol will just increase corticosterone production thus the absolute level of corticoserone + cortisol will increase leading to more VAT.

Other things that can effect this are stressors and simulants. Rats given a singal dose os amptheamine show an alteration in DBH receptors in the PVN. this caused a super-sensitive induction of the hyptophalamic-pituitary-adrenal axis. Basically stimulants alter the PVNs mode of operation. It made it trigger happy for activatiing the adrenals even when there is realy no need. This effect lasted 3 weeks. It may have lasted even longer but that was the duration of the study at which point they killed the rats to examine there brains. So stimulants can increase ones basal corticosterone + cortisol levels.

If absolved truely is eliminating VAT(and I believe it is). Then this is truely wonderfull. VAT is the fat that is associated with morbidity, impotence, heart failure, high blood pressure, etc.... This is because of whats called the portal vein theory. As stated above VAT pumps out massive amounts of FFA and cytokines. Because of VAT's location (your midsection behind your ab muscles) it dumps all of this right in to your liver. This leads to a change in your whole bodies physiology. The fact that it can't keep its fat stored causes blood FFA levels to increase leading to insulin resistance. To much TNF-alpha exacerbates this. The excess production of IL-6 and IL-1 beta is assocated with heat disease. Its basically syndrome X/metabolic syndrome. Its bad news. So this makes Ab-Solved a possible life saving supplement for anyone that stores a good chunk of fat in VAT like myself.