I understand that CHO elicitis insulin secretion, and that insulin inhibits lipolysis. But this leads me to a couple of questions for the nutritional experts among us:

1.) Does insulin supress oxidation of only STORED fat, or does it prevent consumed fat from being "burned" as well? IOW, if I eat a 300-calorie meal consisting of both carbs and fat at a time that my body's energy demand happens to be 300 calories, is the insulin secretion brought on by the carbs going to prevent the fat in the meal from being used as fuel?

2.) What is protein's effect on insulin? Many people advocate low-intensity cardio on an empty stomach so that insulin does not interfere with lipolysis, but they also recommend consumption of some protein to prevent muscle catabolism. Would the protein create any appreciable insulin response that might interfere with fat-burning?

THANKS GANG !!!

(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.

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.

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!!!!!!!!!!!!!!????????????

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

http://www.cuttingedgemuscle.com/Forum/sho...ghlight=protein

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.).

VC is most definantly corrent about this. It is my opinion that in most healthy people the majority of oraly ingested fat has to make at least one pass through your adipose tissue. This has to due with how fats are packaged up by the liver. of course not all of it depends on cyclomicron packaging. eating a tiny amount of fat probobly doesent have to go through the liver as it will go through the lymphatic system. Also eating a gross amount of fat will over load the livers packaging and delivery system and cause large increases in blood FFA. howver for the most part most fats need to probobly make at least one pass though your adipose tissue before they get a chance to be oxidized in tissue other than the liver.



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.

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?

Spook:

So does this mean that the adipose tissue can store fats even if a caloric deficit or energy need is present?

Also what leads you to "your opinion". I assume that there are others who do not believe this?



what about sucutaneous? Could the fact that insulin effects subcutaneous fat this be the reason why those last few layers or BF%'s are so hard to lose?

Wouldn't this allow one to overeat carbs and protein with minimal fats and still lose visceral fat?



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

yes fats can still be stored. jsut because the your caloric needs are not met does not mean the cellular machinary for fat storage shuts off. However during a deficet fats go in and then they go right back out of your adipose tissue. This is caused not by being in a deficiet but by the hormonal milleu associated with hypoglycemia. Namely decreased blood sugar, which is what the body recognizes as a deficet causes NE and corticosterone release.

well to my knowledge no one has ever studied whole body fat trafficing based on oral dose. I don't know if there are or are not people who agree with me. My reasoning is that most fat ingested orally gets packed in to TAG and clyclomicron in the liver. you need your fat to strip this coating off and then hydrolise the TAG to FFA and release it in to the blood stream. Granted some FFA is allways jsut released in to the blood stream but a good portion of it probobly has to make a pass through your fat cells in a healthy person.



absolutely. However it surely is not the sole factor. the more prominant reason in my opinion is at that body fat level it is nearly imposible to eliciet the hormonal response to hypoglycemia because leptin is nearly gone. So without drug intervention it is nearly impossible to shed those last few lbs of SAT. I don't think diet play much of a part in it at that point. With the exception that low fat is proobly better as at that fat level any fat will have a tendency to be stored instead of used.

As far as VAT goes yes you could lose it while over eating carbs and protein. 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. if you were eating mostly carbs and protein but under mantinance caloric level than you would probobly burn it off. Howver as VAT is hormonaly controlled, diet will play little part in removing it though the lower fat aproach is better. Its really the cotrisol and androgens that promote and sustain its growth. So to remove it you need lower androgens and cortisol.



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.

first its fat storage not lipogenesis. lipogenesis is the creation of fat from other substrate. yes we still care about GI. eating high GI foods will induce will send you over the edge in to hypoglycemia post meal by releasing to much insulin. So yes GI is still important. Low GI is still much better while dieting unless you are talking about exercise nutrition.



No one can anwser this. It depends on the amount of carbs you are consumin on a regular basis ( for GSI activity). as well as your training regimine. its to highly variable to anwser your question as worded.



The thermic effect of food (TEF) is not related to how difficult an item is to store. I don't think TEF is realy worth worying about one way or the other.



yes macros matter. I sugest you try this all sugar diet and see how well it works for you. not all macros are created equal. just look at all the research on fructose christ sake. People are going keto because for some people its better. There is no one best diet for everybody. Keto is far superior for obese people or those with signifigant fat to lose. See the obesity thread in general discussion as I explained this allready.



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.

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.

Sorry Spook...I definitely should have been clearer. Thanks for the response, though - I understand things a lot better than I did!

To clarify the above point: Let's first assume that one is consuming a diet relatively high in CHO. I suppose my question is does deficit caused by dietary restriction alone (irrespective of exercise) reduce glycogen, or does the body pull from glycogen stores to try to "make up" for the deficit? And then, if so, does the body then try to refill glycogen from consumed calories (i.e. food) even though one is pursuing a deficit, or do you just remain depleted until you run out?

Also, if one is consuming around 1 to 1.5g of protein per lb of bodyweight while eating at a deficit, will muscle catabolism still occur to any significant degree? Does eating every 3 hours have any beneficial impact on this or are there other strategies for controlling it?

THANKS!!!

As far as loosing VAT, it seems that keeping insulin high would supress cortisol and also not effect the lipolysis of VAT either. Not to mention the other anabolic benefits of higher insulin concentrations. Funny that I have been eating a good amount of calories and fewer yet large higher GI meals consisting of soley carbs and protein and have seen very positive effects. IMO This type of nutrional regiment(near maitenace cals// almost all carbs/protein) coupled with some sprints should work wonders for elminating VAT fat and then I have read that HIIT works well for the elimination of sub-q fat.

not necesarily. Insulin itself does not have a major impact on cortisol. Having to much insulin around will drive your blood sugar lower. This will in effect increase corticosterone production. Its not just Insulin either. you also have to contened with the portal vein glucosse sensor and the liver glucose sensor. I would think eating very slow digesting starches, with a very small amount of fat, and a tiny bit of fructose is the best way to go. This should keep blood sugar as level as possible which will keep corticosterone production as low as possible.

Also tacking some time to relax and cutting back on the stimulants could help as well.

The hepatoportal glucose sensor system is so often overlooked its just sad. It will get full treatment in leptin VI. It is teribly important. If you did not know there are direct afferent nerves that run from the portal vein to the adrenal medulla. There are also direct afferent nerve connection form the liver to the PVN. These two are how the body lets the brain no how much glucose is floating around as all the brain realy knows about is brain glucose and that is not generally reflective of blood glucose because the brain has to have it so tightly regulated that the two often do not coincide. fructose can send a very strong signal in the liver-PVN system. To much is very bad though which is why it should be a very small part of over all carb intake.

Spook
Interesting, The opposite of the above is spammed EVERYWHERE ....what about all the stuff concerning insulin spikes after workouts and insulin in the morning to keep rising cortisol levels at bay, etc etc.

Another off topic question to which you may be of help
When I do sprints, I like to allow a decent amount of rest and recovery between them and only go about 60 yards. Any thoughts on this and how/if I should restructure my approach?

I think insulin spikes first thing in the morning is a terible idea. Thats just going to shoot you right in to hypoglycemia till lunch time. Exercise nutrition is different. I do think an insulin spike is beneficial post or during exercise. However I think this has little to do with cortisol. Insulin is a potent vasodilator thus it enhances nutrient delivery to muscle during and post exercise and can thus work synergistically with the exercise induced increase in blood delivery to muscle. This is why I think its advantageous at this time not because of any anti cortisol phenomenon.

it is becoming ever more clear that in healthy people cortisol is not an endorince hormone at all. It exhibits much more of a paracrine effect. this is because 11Beta-HSD is present in numerous tissue and can either serve to activate or deactivate cortisol/coritosterone. This behavior of activation vs. deactivation differs tremendously between tissues and nutritional state.

Insulins postive effect in skeletal muscle, in terms of cortisol, has more to do with delivering excess nutrients and less to do with some how being antagonistic to cortisol.

For body comp the best thing to do is keep blood sugar as steady and level as possible. This keeps corticosterone + cortisol levels as low as possible. Which seems ideal. I would not look to knock out cortisol via supplments or durgs however as keeping it to low would cause problems. But modulation via blood sugar and stressor response (both immune/trauma and pshycological) seems to be what mother nature intended.

What method do you personally use to assess VAT levels?

Also, stimulants...I was unclear on this; what is their impact on VAT?

Like Spook stated, it's probably the indicators of blood glucose levels that regulate cortisol levels in this manner. Am I correct here?

This statement seems to be in opposition to the use of suppliments such as Fl7 and Ab-Solved. Just how low cortisol levels are we talking and would the use of said suppliments bring levels this low?

I look how far my stomach sticks out. I myself have well above average test and estrogen levels. On the high end of the bell curve. You can not see VAT. it is directly behind your ab muscle near your organs. Thus it has little impact on what you see in the mirror. I think the best way of trying to figure out how much VAT you posses is to look at you profile. Stand up stright and and turn sideways and look in the mirror. If your stomach sticks out or protrudes at the point where the abs meet the pecs then you probobly have excess vat. This is called a distended stomach and is seen in those malnurished children on those TV comercials. There distended stomach is generaly caused by a lack of Vitamin A that potentiates storage in VAT. This distended stomach or tortise shell look can also be seen in the more recent pro BB'ers. Like Mr. Coleman. His stomach has that big tortise shell apearance. However in the pro BB'ers its probobly caused by using to much GH which leads to organ groth and pushes there stomach out.

VAT is basically Beer gut fat. For example im myself, I can see my abs at about 13% BF. However my stomach protrudes and has a rounded apearence even at low levels of BF. Ironically I never even though about using absolved. untill B5150 noticed such a large reduction in waist line measurements. I then tried it out and noticed the results myself. my waist shrunk but my apearence did not improve much. So it seems I am the ideal cantidate for Absolved as I have well above average T levels and I probobly have excess cortisol because of my insomnia.

Also I feel I should say for bias reasons that I recieve absolutely no money from Avant for FL7 or Absolved sales. So don't think I am pimping it because I have a vested interest. This product was designed before I joined avant and thus I recieve no money for its sale. So you can rule out any bias on my part. I jsut think its a damn good product for people like myself.



stimulants increase VAT.

http://www.ncbi.nlm.nih.gov/entrez/query.f...6&dopt=Abstract

here is a brand spacking new study on it. Stimulants make your PVN super sensitive to activating the adrenals. One thing not mentioned in that study is there is a thing called the basal sympathetic nodule located at the base of your brain. It has direct connection to the PVN and delivers NE to the PVN. This is nodule is the fight or flight center of the brain and can be inervated by amphetamines and particularly the combo of yohimbine + ephedrine.

BUMP for Spook's reply on the above.

Also Spook, you said you don't advocate a breakfast insulin spike. Does this mean keep breakfast low in overall CHO or just make sure the GI of your breakfast is low? As an example, I like to have a bowl of All-Bran mixed with oat bran, fresh fruit, whey powder, and plain FF yogurt. I may even have a light english muffin with peanut butter. Although this equates to a relatively high CHO load, the GI is very low. Is this acceptable?

Not really. FL7/Absolved modulate local cortisol. not corticosterone production at the adrenals. What I ment when I said looking to knock out corisol was trying to prevent corticosterone production at the adrenals. That would cause problems. Modulating active/inactive bia 7-oxo-DHEA on the other hand will have little effect on blood corticosterone levels (unless used oraly). In other words its tissue specific not whole body reduction.

avoiding the liver while dieting is a good idea especially while dieting. You will be hypoglycemic much of the day thus your body wants to make corticosterone. This would jsut be exacerbated by oral 7-keto use. However when eating near or above mantinance you will not be hypoglycemic most of the day thus lovering in the liver is not such a big deal.

I think this is why FL-7 is recomended for anti-fat gain during bulking and why Absolved is better when dieting. Both are superior to oral however.

yes though not even close to the degree of exercise use of muscle glycogen. Though liver glycogen will be reduced more by diet than exercise. So it depends on which glycogen your talking about. Either way calroic restriction or exercise will reduce glycogen stores.



yes it pulls from the stores. In the abscence of insulin the pacreatic beta cells (that cause insulin secretion) stop secreting GABA. The two go hand in hand. When the pacreas secretes insulin it also secretes GABA. GABA acts to stop the alpha pacreatic cells from secreting glucogon. Thus when blood sugar is low GABA's inhibition is removed and glucagon secretion comences. This results in mobilization of both skeletal muscle and liver glycogen stores in an atempt to "make up" for the blood sugar deficiet.



It tries to replete but this depends on length and quantity of carbs consumed. you see normaly in the fed state transport of glucose in to muscle cells is the rate limiting step in glycogen formation. Howver when fasted glucogon lowers the activity of glycogen synthase I (GSI). at this point GSI becomes rate limitng. Thus when dieting GSI is the rate limiting step in glycogen formation. So initially if you eat a some carbs most of it will be used as fuel and not be used to replenish glycogen. however if you keep injesting carbs then eventually GSI will be upregulated again and more carbs will go to glycogen formation. This description depends on numerous factors however.

Not all carbs are created equaly. for example injesting a small amount of fructose will lead to preferantial refilling of liver glycogen when consumed with starches. This is because of the special way in which fructose is metabolized. It skips PFK which is the rate limiting step in glucose metabolism in some instances. it can then trick your liver in to thinking you have lots of glucose so it will cause the starches to be shuttled to liver glycogen. This is the same reason to much fructose is bad when hypercaloric. In that case the last thing you want to do is trick your liver in to thiinking you have lots of glucose because then it just over activates the lipogenic enzymes. But a little fructose while dieting is beneficial for lean people because of this trickery. Also acetate can effect this as well.



yes becase of increased cortisol and decreased sex hormones. Additionaly activation of AMPK will slow whole body protein synthesis and results in muscle catabolism.



yes eating more frequently has a host of benefits. It keeps blood sugar more level. it keeps you in the fed state more hours of the day even when in a deficit.



jsut low in GI. I think carbs should be a large portion of breakfast I just don't think slamming down some malto or dextrose is a good idea. Eating some oatmeal with a little fruit and some table sugar is my personal choice. This provides slow digesting starches, some fructose, and some quick digesting glucose to raise your blood sugar levels initially but keep them elevated till lunch.

My research on GABA supplementation in humans has shown that a GABA deficiency is common whenever vitamin B-6, manganse, taurine is lacking. The enzyme GA decarboxylase, forms GABA from Glutamic Acid. GABA can stimulate Prolactin release in humans also. Calcium and calmodulin can decrease excess GA in the brain which leads to increased GABA production. 3 grams/day of oral GABA supps in men are effective at reducing elevated BP through the calcium-channel blocker mechansims of GABA. Many studies in experimental animals show that GABA can signifigantly decrease insulin induced hyperphagia. (Tews et al., 1984). However, it seems that GABA supplements of 1-3 gram/day do stimulate glucagon release from the pancreas. Adding sodium chloride to GA (MSG for example) and also to GABA causes increased sodium excretion and increased urination.

L-alanine, the "non-essential" amino acid, comes from pyruvate conversion and also via the breakdown of carnosine which results in the production of Histidine/Alanine. Pantothenic Acid is crucial for this to occur. Isoleucine stimulates the release of alanine from muscle also. Post-exercise ketosis is also inhibited by alanine as the liver quickly converts alanine to usuable glucose. Alanine stimulates glucagon secretion also while being directly correlated with blood glucose levels in fasting states. Alanine inhibits ketogenesis in humans by a direct effect on the liver independent of insulin (Nosadini et al., 1981).
Alanine elevates pyruvate levels in men, but not in women. Conversely, Lactose is elevated in women by alanine but not in men. Alanine decreases cholesterol levels in men, but not in women. Hopefully my post is at least semi-related to this thread as hypoglycemia/glucagon/carbs and lipolysis were being discussed...

A paper you may want to pick up:

http://www.ncbi.nlm.nih.gov:80/entrez/quer...7&dopt=Abstract

Here's the most current model of what happens with dietary fat.
Coming out of the small intestine, you've got chlymicrons entering the lymphatic system, eventually they reach the microcirculation of the adipose tissue. This means that ALL ingested dietary fat, except for short and medium chain triglycerides, will go through fat cells first, no matter what else you're doing. This is simply how dietary fat is handled.

At that level, they are acted upon by LPL (lipoprotein lipase), releasing free fatty acids.

As well, the fat cell is hydrolyzing stored triglyceride at some rate (set by activity of hormone sensitivity lipase) also releasing fatty acids.

It looks like these fatty acids from both sources (dietary ingested fat AND bodyfat) are going into a common pool of fatty acids (note, this is functionally identical to how both dietary and endogenously derived amino acids enter a free pool).

Depending on hormones, fatty acids from that pool are being reesterified in the fat cell via ASP.

Schematically it might look like this

ASP <-
Fat cell <-> Free fatty acid pool <-> dietary fatty acids
HSL -> <- LPL

Blood flow is moving perpendicularly (say from bottom to top) through the system.

The rate of adipose blood flow will affect how quickly (or not) fatty acids are removed from this common free pool. With good blood flow (i.e. during the fasting state or exercise), there will be a net removal of fatty acids (i.e.fatty acids escape to be used by other tissues for energy). With poor blood flow (after a meal, stubborn bodyfat), more will be re-esterified and yo'ull get net storage.

It's the net effect, storage vs. oxidation that affects whether you gain or lose fat.

In a caloric deficit (no matter what the macronutrient intake), you spend more time in the fasting (post-prandial) state over a 24 hour period. That includes between meals (b/c they are smaller) and while you're sleeping.

In a calorie surplus (no matter what hte macronutrient intake), you spend less time in the fasting state over a 24 hour period.

This is also why, generally speaking, shuffling around fats and carbs has no real impact on things, at least not within an identical calorie intake. As you eat more carbs, you lower fat intake so even though you burn less fat, the difference may be identical to a diet where you're eating less carbs and more fat.

That is, what matters at the end of the day is fat balance (fat oxidation - fat intake). Under most circumstances, fat balance will be identical to calorie balance. A positive calorie balance will turn up as a postive fat balance (fat gained) and vice versa.

Raising the seminal question: why bother with one diet vs. another?

Becuase there are other factors including adherence, maintaining training intensity, food preferences and others that go into a diet. If you can't stick to a high-carb/low-fat diet (b/c you're hungry or whatever), it doesn't matter if it should generate the same fat loss at a given calorie level: if you eat more, you'll lose less fat.

Lyle

This may be so on paper but in my experience the breakdown and timing has a huge influence on my progress or lack thereof.

Lyle probably doesn't need me to defend his position, but ...

there is a study which shows that, over a short term, you are right (as between keto-like diet and carb based diet), because of other factors, that Lyle mentioned above. The same study also shows, over long term, the diet type doesn't make any much difference, under identical caloric conditions.

thanks lyle that was indeed an interesting read.

Agreed...


But now, what I'm trying to understand-- based on what Lyle's just presented and what has already been discussed/covered @ length-- is how this all works out in vivo-- especially in ectos. For example: take myself (endo-meso) and my younger brother(very ecto-meso). Almost all the men on my mom's side of the families are Ectos, and all the men on my dad's side are Endos, so I guess we 'split the difference.' Anyways, my diet probably resembles something along the lines of a 50/35/15 C/P/F; he eats much closer to a 70/10/20. My intake is clean, veggie and whole-foods heavy, and generally low GI, whereas he combines fats and high GI carbs constantly in conjunction with a very low protein intake. We're both very active/athletic, but I've never understood how his body can oxidize (or if it's not oxidizing, it sure is 'effacing') this level of dietary fat intake in lieu of his constant carb-consumption and continually agonized insulin state, wheras I--when I was younger-- ballooned up pretty rapidly with a similar macro-nutrient intake, weight it took me years to lose. Is it an issue of 'good' vs. 'bad' (as Lyle put it) 'blood-flow?' (as in partioning?). I just still fail to see how how certain individuals manage to maintain a 'fat balance' under these types of conditions (and I know we all know the type of person I'm talking about...) when it just doesn't seem like their metabolism could possibly 'handle' all this substrate excess. IMO it seems like there's also a highly individualized and highly intricate process which dietary fat goes through post-digestion, and I still fail to see how total 'calorie-balance' (even when you take into account sleep/fasted times) reconciles some of these discrepancies...

I would agree with that from a diet only perspective at least in the lean. In obese people do you not think the low carb aproach is superior?Particularly for its reduction in leptin and insulin, all while aclimating the brain to use ketones instead of glucose. Reseting the BBB GLUT1 content.

I do think one thing throws a wrench in the works of this proposition even for those who are lean. I agree with all things being equal that diet modification alone in lean people will have little impact (except protein intake, and quality of nutrients). However since we poses the ability through supplementation and drugs to alter various protein and enzyme activity does that not change the rules? I think it does. For example a PPAR-gamma inhibitor. would that not change the rules of shuffling carbs and protein. when utilizing such a tool would that not shift the ideal toward higher carb lower fat? I think it would. Thats just one example of many. For someone not utilizing supplements or drugs I agree with whats said but don't you think the ability to alter such enzymes makes macronutrient selection more important. Like an adipsin inhibitor as another example.

How so? That is, what differences are you comparing (macro/timing) and what differences are you seeing? And in what time frame?

Lyle

A few things.
Some research (by Blundell) has identified high and low fat phenotypes, taht is people who seem to adapt to fat intakes to a better or worse degree. High fat phenotypes seem to maintain leanness even in the face of a high fat intake. Unfortunately, so far it's only cross sectional, hard to say if it's a diet effect or a gene effect. And the mechanisms are unknown.

A secondary factor might be NEAT (non-exercise adpative thermogenesis). In response to overfeeding, some people increase spontaneous activity to a far greater degree than others. In one study, folks were overfed 1000 cal/day; NEAT and fat gain was measured. Some people increased NEAT by nearly 700 cal/day storing very little fat; others increased it almost not at all, storing nearly the entire excess of calories.

Studies examining metabolic rate adjustment to dieting show similar differences, some people's bodies drop metabolic rate harder and faster than others. ONe study found that the folks who best increased metabolic rate to overfeeding dropped it the least with starvation and vice versa. Basically, some people are genetically more blessed than others.

Basically, there can be differences on the output side of the energy balance (and maybe fat balance equation). But this is a genetic effect (especially NEAT), not subject to dietary modification as far as I can tell. Folks who stay lean easily (even in the face of apparent food consumption):

a. tend to fidget and move around constantly, burning off a metric assload of calories
b. don't eat as much as you think: their appetite tends to downregulate more effectively and they balance out days of relative overfeeding with underfeeding.

These effects are probably interelated (think sensitivity to insulin, leptin, etc at the brain) but they are still genetic. It's also possible that they partition calories differently (or better), more to muscle and less to fat or what have you. That's also genetic, a function of neurochemistry and there are also issues of hormones (testosterone, cortisol), insulin sensitivity, etc.

Basically, when you compare two individuals, it's not uncommon to see differences in how nutrients are utilized: one may increase NEAT or partition calories to muscle better than another, and that can explain the discrepancy (twin studies bear this out, genetic twins gain and lose much more like each other than like other sets of twins).

I guess the issue is whether varying diet compositino is going to affect results in one individual. That is, given a low fat vs. low carb diet (with identical protein intake) will a given individual see drastically superior results. I suppose it's not out of the realm of possibility (esp. considering the high fat phenotype work that's starting to appear) but I don't think the data to support it is very strong.

Body composition cahgnes (partitioning) are controlled to a great degree (something like 75-80%) by internal factors, the primary correlate being bodyfat percentage. That leaves a rather small percentage to be affected by diet or training or what have you (drugs work best).

Lyle

Yes. I was thinking primarily in term of naturals. Of course, drugs alter all of this. But with drugs you're stepping outside of normal metabolism and biochemistry so you'd expect the rules to change.

And of course, implicit in what I wrote (hopefully anyhow) i taht protein intake is adequate. Most of hte studies that folks trot out finding that macro composition drastically affects things are comparing studies of low to high (I'd say adequat to inadequate protein). Of course the higher protein intake is going to be better from a LBM mainteannce standpoint and all the rest. I don't even consider low protein diets in such discussions; they are too retarded to even consider.

Stated a little bit more explicitly, my feeling is that

a. given an identical caloric intake that is neither too low nor too high as this will skew results: excessively low caloric intake will cause greater LBM loss no matter what you do and excessively high intakes cause excessive fat gain

b. adequate protein

c. adequate essential fatty acids

The macro composition of the diet will have a minimal, if any, impact on the rate or composition of what is lost or gained. Again, this assumes naturals, some type of non-retarded training structure and all the rest of it. Drugs or shitty training are going to affect all of the above.

As far as obese and low carb vs. high carb, I'll just note that there may be other reasons (outside of body comp changes) to pick one diet over another (body comp is one rather narrow issue to focus on). Health issues are one (more and more studies are finding that a subset of obese individuals has a worsening of blood lipids and other factors on high-carb diets); decreasing leptin, insulin, TNF-alpha is another potential issue (tho leptin will drop profoundly on any calorically restricted diet, with less of an impact of macro intake). Adherence is yet another (b/c if you can't stick to a diet, for whatever reason, it won't work no matter what theoretical arguments you make for it).

Then again, I think it's a matter of degrees (and your definitino of low-carb). I find most high carb diet interpretations to be fundamentally retarded. A diet of 60/30/10 (c:p:f) is unbalanced, too little dietary fat and few would need that many carbs unless they were involved in massive volumes of high intensity activity, had superior insulin sensitivity and picked carbs fairly low on the GI. Pro athletes with genetic gifts basically.

Studies looking at helath risk are finding that moderate fat (25-35% diets) give better results than either extreme (too low or too high). Studies looking at protein intake find both better LBM maintenance, better hunger blunting and better blood glucose maintenance at 25% compared to lower. So we've already got 25-35% fat and 25% protein. So at most yo'ure looking at maybe 40-50% carbs within that context.

My 'ideal' high-carb/low-fat diet is 25-30% protein, 40-50% carbs and 25-30% fat or so (the numbers are actually based on bodyweight since percentages are meaningless). More than sufficient to sustain all but hte highest intensity activities and even moderately insulin resistant folks should do ok on it. They can probably get away with higher GI crap since carbs are being lowered.

EVen for obese and relatively insulin resistant folks, I think that should work fine. For extremely insulin resistant folks, a further reduction in carbs may be necessary.

Lyle

Could the success of one type of diet vs. another at all be influenced by what the dieter likes/believes will work better (beyond just being able to "stick to" one diet over another)? Could it be that, with less stress/greater feeling of well being/etc, one might garner varying results (even if those results are small) on different macronutrient ratios?

That's a good point, and IMO I think you're absolutely right on this. Considering that there are so many factors-- activity levels, insulin sensitivity, leptin etc.-- that are essentially 'interrelated' with one's diet and it's effects on health, body comp and what-have-you, there is really no ideal diet. There are better foods-- eating a salmon steak beats scarfing a Whopper calorie-for-calorie and in terms of macronutrient benefits pretty much hands down, but what works for some may not work for others, especially when it comes down to things like overall CHO intake. I mean, I think its obvious that some people are better suited to lower-carb intakes, whereas there are others-- particularly a lot of intense/endurance athletes-- who thrive on high-carb diets.

Based on what mechanism?

I mean yeah, belief in a given approach is good from an adherence standpoint. Face facts, almost any diet works as long as you stick with it. Most diet books spend 50+ pages selling the diet (which cna typically be summed up in 1-2 pages) because belief tends to make people stick to it; as long as it's not fundamentally retarded, it should work.

I don't see how belief is going to affect things outside of that.

Lyle

I know we often talk about set-points in regards to cutting, as the 'leanest' our bodies want us to be. But, when looking at phenomena like NEAT, it almost seems like certain individuals have an ingrained 'ceiling'-set-point (for lack of a better description) on their phenotype that keeps them below a certain bf%. I may be completely reaching on this one, but is it possible that leptin or some other physiological process could actually act to 'plateau' bf% in certain lean individuals? I mean, could it potentially work both ways in regards to an individual's tendency to display different forms of adaptive thermogenesis?

could the 'thrifty' gene actually 'fight' fight gain in certain individuals?

A recent study is informative in this regards: it looked at metabolic adapation to overfeeding and starvation in the same individuals and compared the response. It found that the people who showed the greatest increase in metabolic rate in response to overfeeding showed the least drop in metabolic rate to starvation. And vice versa. Obviously, the first would tend to resist obesity (and lose weight if they managed to get fat). The second group would have a propensity to get and stay obese (they have a harder time dieting). It's semi analogous to diet resistant and diet induced obesity genotype mice.

The study described such individuals as either being.

spendthrift phenotype (large increase to overfeeding/small drop to underfeeding). These would be your classic ectomorphs who have tons of trouble gaining weight no matter what they do but can lose weight very easily.

thrifty phenotype (small increase to overfeeding/large drop during underfeeding). this would be your classic endomorph who puts on fat readily and has trouble losing it.

http://www.ncbi.nlm.nih.gov:80/entrez/quer...9&dopt=Abstract

The mechanisms at work are still being debated. I suspect leptin sensitivity as being a key aspect. One of the followup NEAT studies found no relationship between leptin levels and the NEAT response but hormone levels and actual brain response (a function of hormone levels and sensitivity) wasn't measured.

So, yes, I think yo'ure correct in principle. I suspect that the thrifty phenotype is the more common one, as it makes the most sense from an evolutionary standpoint. The folks who are/stay naturally lean/skinny are definitely in the minority.

I suppose the more interesting question is:
a. what's the mechanism behind it
b. can we mimic/alter it in any way

As above, I suspect leptin sensitivity (and sensitivity to other hormones, thyroid, insulin, catecholamines, everything involved in the metabolic rate response to food intake) as being the primary mechanism.

At this point, I'm not sure 'b' is in our grasp outside of pharmacological interventions.

Lyle

It would make sense from an evolutionary standpoint if you could make a connection between the two phenotypes and their genetic history. It would make sense that a people from a more seasonal climate (extremes of plenty and scarcity) would tend to store more energy and those from a more tropical climate (very little change in food supply) would merely expend more energy.

Spook -
This may not mean much in the grand scheme of this thread, but I just wanted to throw this out.
The distended stomach is primarily caused by a lack of albumin, which then causes loss of osmotic pressure and leads to severe edema in the stomach. I do not think anyone on this forum will be affected by this, but I just wanted to make that point.

The information on this board continues to blow my mind. Awesome work by everyone here

you are correct I was thinking of two different examples. I did not mean "there" in that sentance to refer to the malnurished kids.

kwashiorkor is the name of that disease

I'm not sure. I was thinking stress might play a role or maybe some other mental components. It just seems like the mind can be so powerful in other aspects of the body (though I guess like you mention it would more be from an adherence stand point). Also, I know that everything else may suggest that all diets are equall provided they stay within the basic guidelines set above, however some people do seem to do better on a given type of diet over another. It might seem to be just based on what one can stick to but with how anal many bb'ers are it just doesn't seem as though that is really the issue. But to answer the "by what mechanism" question; basically I have NO idea , that's why I was throwing it out there for you to shoot down - haha.

Yeah, that's my hunch. If you look at animals that evolved under tropical (no seasonal food availability) conditions, you don't tend to see the major thrifty gene types of adaptation; I suspect it's the same for humans. There was simply never any real need to evolve mechanisms to ensure easy bodyfat storage and hard loss for survival.

Lyle

Well, I certainly don't disagree with you about stress (which is why I remain convinced that the folks who are obessing about the minutiae of their diet, none of which can have more than a miniscular effect, are doing more harm than good) but I'm not convinced that choice of diet (or beleif) is going to significantly going to affect that.

I guess if someone is going to do a diet that they didn't believe in, I'd question it on more fundamantal grounds: like why are they being retards? Doing something you don't believe in on some level would suggest a real lack of brainpower; I doubt many would do it if they didn't believe in it on some level.

I suspect the reason folks do better or worse on a given diet has more to do with issues I mentioned previously: food preferences (which affects adherence), genetic issues (insulin sensitivity, maybe ability to alter nutrient or calore burning), training volumes/intensity, food choices, etc.

Lyle

Lyle,

It seems fairly obvious from what you've said that the choice of diet ultimately matters very little and that all of the varied and sundry minutae amount to a hill of beans in the great scheme of things. What things can we manipulate, then, that actually will have a real and quantifiable impact? I'm not speaking of AAS, prohormones, or anything else remotely pharmacological. I mean basic dietary manipulations (repartitioning strategies, etc.) that will actually amount to something regardless of the choice of diet or even one's relative level of leaness. What are your thoughts?