someone replied in a post of mine about an article in which it was suggested long cycle lengths for a change in one's set point. I have been pondering if such a thing is even possible and want to discuss it.


What would it take?
To increase msucel mass beyond what the body normaly wants to hold or drop fat bellow the same level one either has to constantly work to maintain this in a battle that would cause the body to respond by fighting even harder.. or one would have to somehow change the setpoint.


But how... this would seam to likly involve permanent increases in relating hormones or perhaps chances in the sensitivtly to those hormones.

Idealy it would be like adding a bowl to a scale and then hiting the Zero button to set it so that even with the bowl the scale reads zero. how this could be induced in the body I haven't a clue. it sounds almost like it would require some kind of suspensiong of the body's repsonce mechanisms while the increase in mass or decrease in fat was taking place at which point those repsonses would be allowed to resume without them senseing that a change had taken place..

A nice abstract idea but how can one use this and furthermore in the life of a bodybuidler would you wish to EVER let those responses resume?

I asked this question at hypertrophy-specific.com, and Lyle's view was that one can change the set point in only one direction. Decrease muscle to fat ratio. His view was that dopamine receptors recalibrate (at the neuron level) in the presence of excess food, much similar to the way drug addiction causes it to recalibrate. The drug addiction, BTW, causes an irreversible changes in the calibration (says Lyle). Absence of drug does not renormalize; absense of food (by the analogy) probably would not renormalize it either.

I would not be too surprised though, if one were to actually able to readjust the set-point. Human body has great adaptive powers, IMHO. For instance, if you examine long distance runners, the slow twitch to fast twitch muscle ratio seems to change over very long term (> 5 years). 6 months test shows that there is no short term change. In addition, if you look at various athletic activities, atheletes of one type of sport tend to have similar body types. Some might argue that illustrates only certain body types are good at that particular sport. I think otherwise -- such phenomenon illustrates gradual adaptation.

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What would cause human body to re-calibrate the set point (for more muscle / fat, long term? IMHO, the stimuli has to be such that it demonstrates

(1) fat store is unnecessary (in other words, no energy store needed).
It followss that the stimuli should NOT draw heavily on fat stores.
Stimuli provided by activies such as such as weight training
probably would be good. (Long distance running probably is not
good for this purpose).
This also implies that one's food has to be heavily composed of
carbs (probably low GI types).

(2) fat depletion has to be very gradual ("unnoticeable"), so that body
does not get into a shock mode. Rapid changes in body energy
store tells the body that it will go through times of starvation as
well as times of surplus -- this tells the body that fat storage is
necessary. In other words, very small caloric deficit per day.

(3) exercise must promote muscle build up.

(3) promotes more muscular body, while (2) shrinks the body down. By providing (2) and (3), you are telling your body to be able to deliver more kinetic power per unit of body weight. The only way for human body to do this is by losing body fat and increasing neuromuscular efficiency.

It's an interesting topic, but I think that it would take severe discipline to test out.
For instance, three years ago I began dieting down from a slightly overweight (for me) 190lbs (college...) to an emaciated 139 (I took it too far) over the course of about 1.5yrs. Now, I remained at around 140-50 for about 1.5yrs as well, with around 6-8%bf. I'm guessing that my setpoint is somewhere around 15-20%bf at 180lbs or so, based on how I was built as kid, an adolescent, and my experiences during early life.
During the 1.5yrs I spent around 140, I was suffering from constant fatigue, irritability, depression, complete obsession with food etc.. Basically, all signals pointed to low leptin, etc. I was diagnosed hypothyroid...it goes on and on.
Now, for reasons, many of which no one I knew understood, I was determined to remain hyper-lean. I ate very little, exercised a great deal, etc.
It was awful.
So what's my point? Well, if 1.5yrs won't alter setpoint, how the hell long will it take, and are you willing to endure the misery of attempting to force adjustment (I guess I've answered this one)?
I'm currently 176, bf around 8-9%, and I still have all the signs of low leptin (when eating below maintainance), though they I have learned ways to counteract them. So, in my experience, setpoint is determined by bf%, not weight.
So now we are looking at 2.5yrs of this (for me) low bf%, and there is absolutely no sign that my body is making any shift in altering setpoint.

So, I'm skeptical.

Tkarrde your experiance would only disprove that the set point could be altered by holding the body where YOU want it to be for an exrended period. I agree this is neither practicle nor is it likely to be very fruitfull.

before we go any further I need a little clairifacations, a set point for body fat is obvious but is there also a true set point for muscle mass? It would follow that the more muscle you have the more protein gets broken down during catabolism but gram per gram does it actually occur faster as total LBM increases upwards? Even if there is a set point for muscle mass and you could reset this one would still have to fight against atrophy so that part of my question is likly mute.

going back to the BF set point...

the dopamine concept is interesting, I wonder if it could be that supressing it or increasing it during dieting would have some effect on keeping results. I find it hard to believe that receptors cannot be 'resensitized' as if that were the case wouldn't sex have lot as satisfaction before we found a willing girl simply from masturbation raising the pleasure threshold?

the trouble is that while I can illustrate abstract models of how this could be possibly be accomplished i do not have a good grasp of what exactly is involved on a biological level.

We could start with leptin (why not) and theorize that taking some kind of synthetic leptin while dieting would allow one to reach a lowe body fat level without invoking a recoil response however without as much body fat ones leptin would drop after the diet anyway... it technically shouldn't be needed as much at this point but would the drop induce the body to go into a self preservation mode in which it tries to fatten up again?

Tkarrde

[you wrote]
> I'm currently 176, bf around 8-9%, and I still have all the signs of low
> leptin (when eating below maintainance), though they I have learned
> ways to counteract them. So, in my experience, setpoint is determined
> by bf%, not weight.

I was talking about setpoint of bf%, not that of body weight ... as it is more relevant to bb.

> So now we are looking at 2.5yrs of this (for me) low bf%, and there is
> absolutely no sign that my body is making any shift in altering
> setpoint.

I would be curious to know about the following (to make correlations against my "hypothesis"):
(1) your macronutrient percentages and the amount of caloric deficit per day and how long you have been at your diet (2) whether you are predominantly doing cardio or lifting and how long you have been doing it

> So, I'm skeptical.

Hey, my earlier optimistic view is just a guess. You and Lyle is more likely to be right.

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Supnut:

> . I find it hard to believe that receptors cannot be 'resensitized' as if that
> were the case wouldn't sex have lot as satisfaction before we found a
> willing girl simply from masturbation raising the pleasure threshold?

Lyle's point was that, once leptin level has hit a high level, our dopamine receptors get re-programmed to expect that level as being normal. We cannot "decrease" that expectation -- we cannot renormalize.

I think the weak point of Lyle's argument was his analogy to "drugs" and why drug users cannot renormalize their dopamine levels. Perhaps, with respect to dopamine levels, leptin has different effect than drugs on dopamine receptors and our "sensitivity" to leptin can be renormalized. Unfortuantely, real research results so far do not support the opposite view.

Can you tell me where to find Lyle's article on this?

http://www.hypertrophy-specific.com/cgi-bi...act=ST;f=3;t=79


Posts by Lyle, not "an article" ...

VirtualCyber,
1-this fluctuates, but basic breakdown is something like 35-40%P, 45-50%C, 15%F. Caloric deficit is likewise hard to determine. While at a bodyweight of 140 to 150, I was eating maintainance or slightly above (around 2800-3000cals--i'm active) and refeeding about 1-2times a week, thus allowing for my slow weight gain. Before that, to get to 139, I was eating about 1400cals a day (bad news). Currently, at 176, I'm eating apr. 2000-2400cals a day, and refeeding every 3-4days for 6hrs (still ironing the frequency out).

2-I lift and do HIIT, lifting 4days and doing HIIT 3 (save for present, for I am on a ONE cycle and have upped volume significantly in all respects). I had been lifting and running since commencing the weight loss 4yrs ago, though I really only added the HIIT about 3yrs ago.

That's an interesting theory, of Lyle's.

It is (almost) literally impossible for me to set myself as satiated. Aside from the ill-feel of my stomach bulging, I can eat and eat without end without my brain "telling" me that enough was had. When younger, quite skinny I was (Buchenwald-like bag-of-bones) and then when 18 I gained quite a bit of muscle (was at 220-230 solid). Come not long after that point I ballooned up to ~312 pounds---quite fat (although I had still a great deal of muscle).

However now holding steady at around 200, I can't control my appetite as no matter what is done, never am I satisfied (when I trialed LeptiGen that helped, but in my circumstance any degree of aid is welcome as even that could not make away with cravings in full). At a steakhouse some weeks ago with a friend and his girl, I pounded down a good deal of food. My friend about 20 pounds more than me, was more than stuffed. I on the other hand could have, rather easily, made way in welcome for two or three rounds more of the same.

Perhaps that time then of obesity did "damage", along lines of Lyle's mention.

That's rather interesting. As I write this post, I'm early into my refeed. Having just had a few bowls of cinnamon toast crunch and then capn' crunch, I can share that I too have an insatiable appetite. As I've discussed before, my mind constantly wonders to food, so much so that while dieting it is at times the topics of my dreams, literally. I am rarely unaware of when next a meal is coming, and of what it will be. If something tastes good, as I find many cereals do, I can eat until uncomfortably full, simply because I so much enjoy the taste.
As a kid, this was often the case as well. If a box of pop tarts showed up in the house, I'd eat them within the day. The same with cereals, fruit snacks, sausage, etc.. I was usually quite thin, though I did undergo periods of adolescent 'chubbiness' which are typical for many, and somewhat traumatic for me (And most likely the root of my present obsession with remaining quite lean).

The best temporary solution I have found for blunting my hunger is copious amounts of diet soda; however I have for the most part learned to ignore my appetite, following the clock infinitely more often than my stomach would like. It seems that, for a variety of reasons, it is much harder for many to stay lean. The connection between satiety, appetite, and thoughts of food are clearly strong indicators of one's position in relation to one's setpoint.

I havent asked a question, but merely added my own experiences, brought to the fore while refeeding. I have a voracious appetite, and I wonder what degree of which can be attributed to/compounded by my having journeyed far below my setpoint for so long.
This reminds me of a study I once read...I'll try to find it and post it later

I am in the same boat as you guys, but the one time i could not eat until i knew i had enough , instead of just when that stranger called fullness told me to stop, was when i was depressed. My depression was definitely situational, as opposed to chemical, but i would only eat 2-3 spoonfulls of peanut butter the whole day and i would never think of food and i never thought of eating. Just a thought.

@ Tkarrde: I drink, on average, two liters of diet cola per day (in addition to E/C stacks and such). To no degree does resolution come.

To add to that I have noticed that when I have a breakup with a girlfriend my appetite for any kind of food practically dissapears. Also any kind of cravings for cheat foods go away. Why is this? Some sort of chemical release? This is extremely interesting to me.

Yes, indeed: Diet Cherry Coke, and Diet Pepsi, are key.
I want to clarify however. I said that consumption blunts my appetite. That was in incorrect way of stating the matter. Rather, I find myself reaching for the diet soda when, were I not conscious of dietary intake, I would in all probability reach for food. It fills the stomach. It does not satisfy cravings, let alone satiate appetite.
Point in case: Said consumption drops dramatically during a refeed, such to the point that I have consummed NO soda since 5p.m., when I would regularly have had 3-5.

That is the exact reason for my depression also, though i can say i will never be there again hopefully. Anyways if there was a way you could use those chemicals , or lack thereof, in regards to deiting , then you would certainly have something . I mean , never have i been disgusted at the thought of food, or maybne its just my mind was totally consumed by something else. Showering and teeth brushing also went away so who knows.

Blanit we have discovered something here! We should sell "depression caused by your girlfriend" in a bottle or something. Dieting problems for all solved! You heard it hear first remember that!

Then there is the fish oil theory ... Real research shows that those who consume fish (& thus fish oil) tend to have lower bf than those who do not. If I remember correctly, the research showed that the set points for two population groups (one eating lots of fish having lower bf) "seemed" to be different, even though they were from the same genetic pool.

Naturally, this makes one wonder if the bf set point can be altered over long term, via administration of either CLA or EFA. (BTW, CLA can cause fat cell apoptosis at very high dosage, in vitro).

Dante:
I have never been overweight in my life and I could out eat most people I know and never feel full, so I don't think that a previous weight problem would do it (IMHO). This does not change no matter what I do, how I eat, what i weigh, how much BF I am carrying, etc.

When dieting, I can blunt my hunger by spreading my theromgenics rather than taking them in a large dose (thank you for that advice Dante), but that is blunt, not dissipate.

Thank God I am not the only one with a coke, I mean a Diet Coke problem!

Indeed !

@ Icequeen,

Two boxes, equal in size----one houses a refrigerator and one covers nothing. Are they then the same?----Or for another example, the hearts of one and then another may both beat slow, but for one this could owe cause to athletic proclivities and in the other, weakness.

So, the equality of appetite for two people, could owe due to causes as different. Whether that's the case here, of course, is something else

Note, I should however that my appetite has always been rather voracious, but never to this extent as I've been often to find myself in craving.

LOL@ the Cola quip. I've run through, at times before, four two-liter bottles of diet cola in a day. Were it not for the Aspartame, I'd probably be a normal, and decent human being. But they'll take just as what's offered.
Blood&Iron posted an intresting abstract, long not ago, as with regards to Aspartame and Leptin (in rats, at least). Let me find it.

Here:

http://www.mindandmuscle.net/avantforum/in...e3a3765f335c67f

wow... lots of interesting stuff in this thread guys.

virtual, can you point me to some more info on your CLA quote about fat cell apoptosis?

Dante do you smoke cigarettes?

Just a thought. I noticed when I quit smoking that I could feel more satiety than I did while i smoked. I could almost actually feel the nutrients being utilized in a way that was foreign(although the foreing thing was really the smokes). On the other hand I feel when you smoke that smoking a cigarette is the only way I can quit eating, sometimes...

I also eat a crapload of fiber. Just today I had five cups of broccoli before I even ate my chicken and salad...

Im starting to wonder if there isnt an opportunity for some mental magic here as well...

I don't smoke, so no, the answer. However, I'm rather fond of Nicorrete, a liking which I should make more foreign come soon, before liking makes itself synonymous with addiction (it tends to 'balance' me---likely due to a Dopamine issue as may I have--don't know).

I too, make welcome for a generous helping of fiber as may come from natural peanut butter, oat flakes and flax seeds (I've been overly fond, lately, of Optimum Complete Protein Diet [strawberry] mixed with pb--I can barely control myself, and at times, I don't).

With regards to fiber, I eat quite a bit of it, but find that it doesnt always curb appetite. For instance, when sourced from sweet potatoes or veggies, it does little. But after some oat bran, it does seem to work rather well.
For a nice aspartame/fiber combo, check out All-Bran Extra Fiber cereal-something on the order of 50cals, 7grams carb, 14grams fiber per 1/2cup. Sweetened only w/ nutrasweet.

all bran is amazing stuff.

Yes Dante, I would highly suggest you turn to some other forms of "normalizing" than nicotine. Being a slave to the machine so to speak, I can say that anyone using it for too long will eventually find themselves stuck with it as an undesirable bed partner...

As for your all's appetite, I am intrigued and find a challenge in compiling a regimen to combat cravings. But Im also confused because it seems that some of you dont necessarily wish to seek out refuge. Rather it almost seems as if you look at it as an asset, but I might be dead wrong and pickingup sarcasm on your parts.

I for instance, have always battled with being overweight. There have been times i have eaten uncontrollably(besides the natural occurence involved with ingestion of cannabis) and yet I have found that I can force the process to a halt. It is quite often my food choices rather than the overall amount of consumption that has lead to my weight fluctuations. Even then I dont think that I have made as many bad choices as mch as something genetic doesnt seem to want me to say farewell to my pooch. Perhaps something Ericksonian in nature could provide understanding of this dilemma. I wonder what would happen if we were to ask our unconscious minds, what having extra fat supplies allows us to experience that we feel would be neglected should we lose it? It seems to me that if buddhist monks can survive extreme cold in noting but a fine silk robe, that we might be able to tap into our own mental resources to bring about physical change on this plane, but we first must be made to feel comfortable.

I still have stretch marks from my remarkable weightloss of ten years ago. I lived off of nothing but fish, spaghetti(with tomato juice), iced tea(my blood must have been 50% iced tea) and fruit juice for five months and lost 70 pounds. Ofcourse that was before I knew how to make sound decisions regarding protein loss versus fat loss. The interesting thing was, instead of putting the weight right back on, I kept losing, watching another twenty pounds come off as I began to eat normally once again.

As far as set point is concerned, I have always fluctuated around 235-250. But when I stay busy in the gym, and eat right(not to the extreme, just no junk crap), I can easily maintain 205, with the bf staying lower than when I am 235. When I allow little debbie and hostess, along with fast food back into my life, it slowly makes its way back up to 235 where it likes to stay at.

NightOp

There has been a couple of solid papers on CLA's beneficial effect on fat reduction. I don't have link to them at the moment. There are additional posts at elitefitness forum and at HST forum.

Here are some abstracts for CLA and apoptosis. Alas, all experiments were on mice, lol, so, its unfortunate:

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(1) Conjugated linoleic acid (CLA), body fat, and apoptosis.

Miner JL, Cederberg CA, Nielsen MK, Chen X, Baile CA.

Animal Science Department, University of Nebraska, Lincoln 68583-0908, USA. jminer1@unl.edu

OBJECTIVE: The objective of the study was to determine if consumption of conjugated linoleic acid (CLA) by mice could induce apoptosis in adipose tissue. Other objectives were to determine the influence of feeding mice CLA for < or =2 weeks on body fat, energy expenditure, and feed intake. RESEARCH METHODS AND PROCEDURES: A mixture of CLA isomers (predominantly c9,t11 and t10,c12) was included in the AIN-93G diet at 0, 1, and 2%, and fed to mice for 12 days (Trial 1), or was included at 2% and fed to mice for 0, 5, and 14 days (Trial 2). Feed intake was measured daily and energy expenditure was determined by direct calorimetry on day 9 in Trial 1. Retroperitoneal fat pads were analyzed for apoptosis by determination of DNA fragmentation. RESULTS: Dietary CLA reduced feed intake by 10% to 12% (p < 0.01), but either did not influence or did not increase energy expenditure as indicated by heat loss. Body weight was not influenced by consumption of CLA in Trial 1 but was increased (p < 0.01) by CLA in Trial 2. Weights of retroperitoneal, epididymal, and brown adipose tissues were lower (p < 0.01) in animals fed CLA, although liver weight was increased (p < 0.10; Trial 1) or not changed (Trial 2). Analysis of retroperitoneal fat pad DNA from both trials indicated that apoptosis was increased (p < 0.01) by CLA consumption. DISCUSSION: These results are interpreted to indicate that CLA consumption causes apoptosis in white adipose tissue. This effect occurs within 5 days of consuming a diet that contains CLA.

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(2) Conjugated linoleic acid suppresses triglyceride accumulation and induces apoptosis in 3T3-L1 preadipocytes.

Evans M, Geigerman C, Cook J, Curtis L, Kuebler B, McIntosh M.

Department of Nutrition and Foodservice Systems, University of North Carolina-Greensboro, 27402-6170, USA.

Four sets of experiments were conducted to examine the influence of conjugated linoleic acid (CLA) isomers during proliferation and differentiation of cultures of 3T3-L1 preadipocytes using physiological culturing conditions. Cultures treated with either albumin [bovine serum albumin (BSA) vehicle] or linoleic acid (LA) served as controls. For the proliferation study (Expt.1), cells were cultured in media containing a crude mixture of CLA isomers or pure LA at 0, 10, 50, or 200 microM for 4 d. Preadipocyte proliferation (cell number, 3H-thymidine incorporation into DNA) decreased as the level of CLA increased in the cultures. In contrast, LA had no impact on DNA synthesis. In Experiment 2a, postconfluent cultures were grown in media containing a crude mixture of CLA isomers or LA at 0, 10, 50, or 200 microM for the next 6 d. Postconfluent cultures supplemented with 50-200 microM CLA had less triglyceride (TG) and were smaller in size than cultures supplemented with similar amounts of LA. In Experiment 2b, postconfluent cultures supplemented with 200 microM of a crude mixture of CLA isomers or LA were harvested on days 1, 3, 6, or 9. Differences in TG content of cultures supplemented with 200 microM CLA compared to control and LA-supplemented cultures became apparent after 3 d of culture. Experiments 3a and 3b examined whether the fatty acid vehicle (BSA vs. ethanol) or the vitamin E status (+/-0.2 mM alpha-tocopherol) of the cultures altered CLA's impact on preadipocyte TG content. In Experiment 3a, ethanol-treated cultures had more TG than non-ethanol-treated cultures regardless of the fatty acid treatment. In Experiment 3b, cultures treated with 100 microM of either a crude mixture of CLA or the trans-10,cis-12 CLA isomer without supplemental vitamin E for 6 d had less TG than CLA-treated cultures containing vitamin E. In Experiment 4, postconfluent cultures were grown in media containing 100 microM LA or either a crude mixture of CLA isomers or the trans-10,cis-12 CLA isomer for 24-96 h to assess CLA's influence on the cell cycle and indices of apoptosis. Cultures treated with 100 microM CLA for 24-96 h had more apoptotic cells than BSA- or LA-treated cultures. Furthermore, cultures treated for 48 h with CLA had fewer cells in the S-phase than control cultures. The effects of the trans-10,cis-12 CLA isomer were more pronounced than those of the crude mixture of CLA isomers. These data suggest that CLA may exert its antiobesity effects by inhibiting proliferation, attenuating TG content, and/or inducing apoptosis in (pre)adipocytes.

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(3) Conjugated linoleic acid supplementation reduces adipose tissue by apoptosis and develops lipodystrophy in mice.

Tsuboyama-Kasaoka N, Takahashi M, Tanemura K, Kim HJ, Tange T, Okuyama H, Kasai M, Ikemoto S, Ezaki O.

Division of Clinical Nutrition, National Institute of Health and Nutrition, Tokyo, Japan.

Conjugated linoleic acid (CLA) is a naturally occurring group of dienoic derivatives of linoleic acid found in beef and dairy products. CLA has been reported to reduce body fat. To examine the mechanism(s) of CLA reduction of fat mass, female C57BL/6J mice were fed standard semipurified diets (10% fat of total energy) with or without CLA (1% wt/wt). Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick endlabeling (TUNEL) and DNA fragmentation analysis revealed that fat-mass decrease by CLA was mainly due to apoptosis. Tumor necrosis factor (TNF)-alpha and uncoupling protein (UCP)-2 mRNA levels increased 12- and 6-fold, respectively, in isolated adipocytes from CLA-fed mice compared with control mice. Because it is known that TNF-alpha induces apoptosis of adipocytes and upregulates UCP2 mRNA, a marked increase of TNF-alpha mRNA with an increase of UCP2 in adipocytes caused CLA-induced apoptosis. However, with a decrease of fat mass, CLA supplementation resulted in a state resembling lipoatrophic diabetes: ablation of brown adipose tissue, a marked reduction of white adipose tissue, marked hepatomegaly, and marked insulin resistance. CLA supplementation decreased blood leptin levels, but continuous leptin infusion reversed hyperinsulinemia, indicating that leptin depletion contributes to the development of insulin resistance. These results demonstrate that intake of CLA reduces adipose tissue by apoptosis and results in lipodystrophy, but hyperinsulinemia by CLA can be normalized by leptin administration.

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(4) Conjugated linoleic acid inhibits proliferation and induces apoptosis of normal rat mammary epithelial cells in primary culture.

Ip MM, Masso-Welch PA, Shoemaker SF, Shea-Eaton WK, Ip C.

Department of Pharmacology and Therapeutics, Roswell Park Cancer Institute, Buffalo, New York, 14263, USA. mip@sc3101.med.buffalo.edu

The trace fatty acid conjugated linoleic acid (CLA) inhibits rat mammary carcinogenesis when fed prior to carcinogen during pubertal mammary gland development or during the promotion phase of carcinogenesis. The following studies were done to investigate possible mechanisms of these effects. Using a physiological model for growth and differentiation of normal rat mammary epithelial cell organoids (MEO) in primary culture, we found that CLA, but not linoleic acid (LA), inhibited growth of MEO and that this growth inhibition was mediated both by a reduction in DNA synthesis and a stimulation of apoptosis. The effects of CLA did not appear to be mediated by changes in epithelial protein kinase C (PKC) since neither total activity nor expression nor localization of PKC isoenzymes alpha, betaII, delta, varepsilon, eta, or zeta were altered in the epithelium of CLA-fed rats. In contrast, PKCs delta, varepsilon, and eta were specifically upregulated and associated with a lipid-like, but acetone-insoluble, fibrillar material found exclusively in adipocytes from CLA-fed rats. Taken together, these observations demonstrate that CLA can act directly to inhibit growth and induce apoptosis of normal MEO and may thus prevent breast cancer by its ability to reduce mammary epithelial density and to inhibit the outgrowth of initiated MEO. Moreover, the changes in mammary adipocyte PKC expression and lipid composition suggest that the adipose stroma may play an important in vivo role in mediating the ability of CLA to inhibit mammary carcinogenesis.

when u drink that much soda how many calories do you count it as? i have heard that there is 4 calories in each serving of soda but the companys are alowed to round down. i can drink like 3 1/2 liters of soda a day myself im going to get cancer...

I don't count the calories, as they don't exist, or come as minimal. Where did you get that information? ----I'm not chiding you, I'm quite serious. Perhaps that's true (just as like the concealed Trans-fat information---a package states "2.5 grams of saturated fat", but they don't reveal that there's also 2.5 grams of additional Trans-fat).

Even if true, I doubt the impact of presence to be overwhelming, so that one would need count.

O/T I am not up to date on the issue if the carbonation of soda interferes with protein. Is it true that it degrades protein or not? or does it just not to an extent that matters? I may have to pick up this diet cola habit.

I am in the same boat as all of you food junkies. I am a former fat boy myself. My body loves to float around 180-185(being that i have never done an extensive bulking cycle because of a fear of getting fat, so it is actually a bf% my body wants to be, i just don't know it). but i have kept myself at 165-170 for about 8 months. i have just bloated up to 178 in the past month, bf around 20%. i was burned out, i couldn't take being so incredibly strict anymore and lost control. I have an unsatiable appetite also. If i start to cheat, or even bend the rules of eating clean, it turns into a night at the buffet as if hadn't eaten for months, eating to the point of nausea and vomiting. Uncontrollable. For a while EC helps, then ECY helped. now even after many weeks off, it doesn't work. Has anyone noticed if adding pounds of lean muscle has helped change the bf% In other words, if you add 10 pounds lean muscle, will your set point be a number less because the same amount of fat accumulated, but is more spread out over muscle? Or regardless, the body wants to be at the same exact number?

Hmmmmm Dante, and which of us pray tell is the expensive necessary appliance and which is the playland for toddlers? LOL!

Point well taken, but it is nice to know that I am not alone in the coke problem or the appetite problems. There is now a named mental illness that deals with irregular eating, but didn't we cover that on another thread? Maybe we could all get some diability! 'just joking.

Anyway, if anyone cares, I spent all summer trying desperately to survive on a perfect diet and kick the coke habit, and could not do it. Finally, my workout partner (a seasoned old gym rat) told me to give it up and eat a balanced diet, just make sure that I had several servings of meat a day. Guess what, I have lost fat and not been voraciously hungry. I still eat 5-6 times a day, I just quit counting everything. I have noticed no muscle or strength loss and mentally I am much better--no real cravings or binges, depression, etc..

I'm a recovering fatboy too, though I don't have the uncontrollable appetite issue (thankfully). I do have the diet soda problem though.

If I lose control, it's usually triggered by certain "problem" foods that usually contain fat and carbs in combination. Pizza leaps to mind. I really have no discipline around pizza. If I eat one piece, I'm going to eat as many more pieces as I can get my hands on. If I avoid the first bite, I'm usually OK.

As for CLA/EFA, I have an anecdote.

So I've been taking CLA (~ 8-9g) and fish oil for about 3 months now continuously. I was sort of unimpressed by the results.

I just got back from a week long cruise (my first), which is a very sedentary way of vacationing. There is not much to do at times but eat, and every meal is a buffet. When they aren't serving meals, snacks (pizza, hamburgers, hot dogs, frozen yogurt) are all-you-can-eat, too. It's ridiculous.

After making a glutton of myself for a week on that floating buffet -- with very little exercise -- I didn't gain any weight. In fact, I'm in the low end of my normal range.

I don't really know whether CLA and EFA had any role in this, but I was shocked. When I got on the scale after the cruise I was sure I'd be 5-10 pounds heavier.

So CLA/EFA certainly didn't get me down to 6% body fat or anything, but I'm wondering if it prevented me from fattening up during a period of increased caloric intake and reduced activity.

Well im still looking for a link on an article about food companys rounding down calories to zero but i did find one for a list of calories in diet soda

http://www.calorieking.com/foods/category.php?cat=41

they range from 0-4 calories

Hardly worth counting. Even if one is drinking 10 cans a day.

Jon:

Thanks for that post. Your anecdote is encouraging.

Your body's apparrent weight stability in the face of your temporary gluttony is exactly what should be expected of CLA supplementation. Remember Bryan's post ... his idea was that CLA makes your body act as if it is genetically lean. (Rephrased, it lowers the bf setpoint.)

When I was taking my CLA (10 pills of tonalin), I did not notice anything in terms of accelerated weight loss. I did not notice increased energy either. I discontinued its use after a while, because it was not helping me lose weight any faster.

I should have realized that my fat loss rate is simply the function of the rate of calorie deficit, and that CLA would help me stay lean.

It is probably time for me to try CLA again.

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P.S.

BTW, when I eat like the way you described, I notice weight increase immediately. Probably in the form of water that is taken up along with increased glycogen store. Unfortunately, real fat increase generally follows the weight increase (for me).

Again, I have to hasten to add my experience is purely anecdotal and not too much should be made of it.

But I was stunned by the fact I didn't gain any weight (and remained as lean as I was at the end of my last training cycle). Honestly, we often ordered multiple desserts after our second dinner. It was sick. I know my body pretty well, and I fully expected to have put on some weight.

Psychologically, it makes deconditioning (or detraining or whatever you want to call it) much easier to accept. If you know you are not going to shrink or get fat, you can just relax and enjoy it.

Low blood sugar levels are the biggest stimulators of appetite. Even when the stomach is stuffed with food a drop in blood sugar will still send a strong signal to EAT! For you guys who just can't control your appetites I used to be like this big time no matter what bf% I was at but the last couple of years I've lowered the carbs and increased the fats and protein. I now have to practically force myself to eat enough or at least eat frequently enough as I no longer have the blood sugars swinging up and down every 2 hours.
For the individual who mentioned the appetite suppressant and stimulating effects of the girlfriend breakup I too have noticed this. I guess it's just a natural epinephrine and cortisol high. (great for cutting but will eat the hell out of your muscles!!)

That's a point most excellent, and one that I did not consider (although it's not applicable in my instance [even with stable blood sugar, I'm hungry], and for those far so the lean, all things Leptin likely is the greatest agitator).

But that's most definitely something for the ravenous among us to consider.

I have considered that before as well, being that i thought i was hypoglycemic at one point. i was tested and i am not. if that were the case, i wouldnt quite be able to sit down and eat a jar of natural peanut butter, while eating a ton of chicken or anything high protein. it doesn't matter what the combination of protein, carbs, and fat, i eat till i'm painfully stuffed. i dont understand it though, i know it will be uncomfortable, yet i continue to eat. Diet soda has helped though.

bump to this question:
Do any of you worry about the carbonation interfering with protein synthesis? if so, how do you handle that?

Read the following, and then I will put forth some ideas:

This is a section of an atricle I found over at LE

The dopamine effect

Human beings take pleasure in eating in part because it releases a brain chemical called dopamine, which produces a sensation of satisfaction and even euphoria. Ingesting cocaine also releases a lot of dopamine.

Over time, the brains of drug addicts become less sensitive to dopamine, forcing them to take a greater quantity to produce the same high. The same is true for those with overeating disorders.

According to Dr. Gene-Jack Wang, the brains of severely obese people are less sensitive to dopamine than the brains of other people. That forces obese people to eat a lot more food to get the same amount of satisfaction.

That finding raises a chicken-and-egg question. Do people become obese because their brains were less sensitive to dopamine? Or are their brains less sensitive to dopamine because they eat so much? Wang and his colleagues are now trying to find the answer.

NEXT we have a snippet that indicates D1/D2 stimulation can be used to lower body fat (it appears to act through appatite reduction)

In one study, "Dopaminergic D1/D2 Synergism Reverses Obesity and Lipid Disorders in the Leptin-Deficient ob/ob Mouse," by E. Tozzo, et. al., Ergo Science researchers established that stimulation of two dopaminergic receptors produced a significant (between 50 and 60%) reduction in food intake, dramatic weight loss and a decrease in fat stores of 22-32% with no significant decrease in lean body (muscle) mass. This approach also improved glycemic control, reducing glucose 57% and insulin 50%, respectively. These effects were accomplished without the administration of exogenous leptin. In a second study, Ergo researchers found that timed administration of a dopamine agonist and a serotonin agonist reduced body fat 30-75% and body weight gain 40-60%. In this study, lean body mass was increased 5-17% confirming that the two drug regimen was able to reduce weight by selectively reducing body fat. Again, these reductions were accomplished without the administration of leptin. The selective reduction in body fat and preservation of lean body mass has significant implications for the treatment of human obesity as improvement in the lean-to-fat ratio is thought to be closely associated with a reduction in the cardiovascular risk factors resulting from chronic obesity.


Now drawing the conclusion that a substance which increases dopamine could help those overwieght runs into an immediate roadblock.... dopamine antagonists from my understanding cause a reduction in sensitivity just as the food does, therefor while they might work for a while you would be worse off if you stopped taking them and if you continued to take them you would need something stronger eventually.

So what we need here is something to reset the system, to improve dopamine sensitivity. SAMe is the obvious first choice and for those whose problem is a lack of dopamine then DL-phenylalanine and St. John's wort would be possible remdies... now knowing which one you need, that I can't say.

Now I asume that if sensitivitly has gone down, dopamine levels would be increased, and its likely that 'reseting' the system would be the only way to get everything back in working order beyond the lenth of a supplement cycle.

Let me introduce one final atricle about an herb I know very little about... its use has been for cocain addiction but the concepts are very similar.


ibogaine

does anyone know how much aspartame is in diet soda? enough so taht there is enough l-phenylalanine to help this dopamine problem? if so, is that why so many of us former fat boys or drug addicts drink diet soda like an addiction(i have picked this up over the week, it has worked quite well)?

It seems to me increasing the baseline dopamine production permanently would have the same effect as decreasing dopamine sensitivity permanently.

So, your choice of drugs might work ... They are not addicting, I hope.

I don't know if that would work, I think if you increase baseline dopamine the recptors will eventually downregulate so that the effect of the dopamine would be close the what it was before, therefore defeating the purpose.

Now thats just my asumption, and even if I'm right you might still be able to get around it by cycling the drugs so that they didn't get used long enough to cause a permanet modulation of the whole dopamine system.

I would asume likewise of you increase sensitivity that dopamine production will drop off asuming sensitivitly is naturally low to begin with. If sensitivity is low from chronicly high dopamine due to overeating or something else then I would think it would be somewhat easier to shift this back to what it was before hand but maybe not.

now the ibogaine is actually illegal in the US. although you can buy the seeds but its illegal to grow, its active compound seams to be a cholinase inhibitor (I think thats right) as well as a strong CNS stimulant... I asume that means it acutally stimulates dopamine release along with other CNS hormones, but at the same time its effecting choline levels which has some interesting possible implications.

Of the three supplements you have mentioned, DL-phenylalanine does not seem that promosing. It seems to temporarily increase dopamine level -- I didn't see any articles that indicates otherwise. I have heard from friends that they were "addicted" to diet coke for a while, so, I suspect that l-phenylalanine is not a good way to go.

St. John's wort is interesting. I looked at some research abstracts and they said that there is inhibition of "reuptake" at presynaptic junction. This basically means more seratonin and dopamine will be available as neurotransmitters at post-synaptic junction.

What I'd like to know is if the effect permanent. Unlikely ... but the idea here is that available dopamine and seratonin level increases (similar to the concept of raised baseline dopamine level).

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Of the three supps, ibogaine seems the most interesting and promising. I really would like to know more about its effects, its active ingredient, etc.

Oh yeah, there is also 18-Methoxycoronaridine, synthetic ibogaine.

Does anyone know avaiability of this thing?

Just another fact about dopamine receptors.

There are research experiments that show it is the _increased_ dopamine sensitivity (in other words, there are more receptor cites) that cause "addiction," not _decreased_ dopamine sensitivity. Come to think of it, there is some indication that ibogaine is neurotoxic -- perhaps it kills off dopamine receptors, and thus decrease overall dopamine sensitivity ...

if thats the case then i would think a cycle of SAMe of sufficent lenth would decrease receptor expresion.

I suspect theres a little more to it then that... I can see that increased sensitivity would help make something as common as food have a greater impact on one but unless these receptors at some point loose sensitivity why would anyone need to eat more then baseline to get the same stimulation?

Supnut

I think we are using the term "dopamine insensitive" differently. When some researchers say a receptor is "dopamine insensitive," what they mean is that the receptor does not respond well to incremental changes in dopamine levels. Thus, decreased sensitivity is good for fat loss -- because changes in the level of dopamine due to decreased food intake is not "seen" by the brain.

I am guessing, but when you say "increased sensitivity," what you mean is that the receptors respond to less dopamine concentrations, which is the same thing as when some researchers say "decreased sensitivity," right?

I tend to use your first deffinition actually.

But I haven't been looking at decreased sesitivity as a good thing. The research I posted below said this:

According to Dr. Gene-Jack Wang, the brains of severely obese people are less sensitive to dopamine than the brains of other people. That forces obese people to eat a lot more food to get the same amount of satisfaction.

and then the other information was that D1/D2 stimulation reduces appatite, the conclusion I was drawing was that with something other then food stimulating dopamine there was not a craving for food to do so.

To apply the concept for wieghtloss I would gather that one could either stimulate dopamine recpetors with an increase in dopamine, a dopamine receptor agonist or a receptor sensitizer.

Now the body generally resists change with receptor resistence being perhaps the only change which doesn't have an effective safeguard.

from that I asume the following:

increasing dopamine above baseline for an extended period of time will reduce sensitivity to bring the body's response down to normal levels thus creatine a new baseline.

Using a drug to simulate dopamine and trigger recptors will have the same effect only dopamine production will also drop off leaving on impaired if they stop taking the drug/herb/ or whatever.

increasing sensitivitly will cause the body to reduce dopamine levels to return the bodies response to normal thus creating a new baseline.

I doubt any of these methods would be permanent but the last one seams to have the most promise from what I can see.

there would be no impairment, or need to up the doseage, if the body was insensitive to begin with it might be possible to return things to normal thus repairing the dopamine response. Also dopamine would be elevated along with food intake which seams like it would likely produce the best effect.

This would change your appatite's setpoint but not your bodies... I think this whole discussion would have to be applied to leptin if not leptin/npy/grelin at least before we could really have an effect on true setpoint.

Hi

> This would change your appatite's setpoint but not your bodies... I think
> this whole discussion would have to be applied to leptin if not
> leptin/npy/grelin at least before we could really have an effect on true
> setpoint.

This is interesting point ... But my hunch is that one probably would not need to worry about appetite set point v. leptin setpoint. There has been some evidence that working on the brain only is good enough. For instance, there are research experiments in which subjects were administered dopamine increasing agents; the result was fat loss (not just weight loss).

Also, I have known some regular drug users ... namely cocaine. These guys were cut as hell. Perhaps cocaine does work. I think it is likely cocaine exert its effect mainly on the brain and not directly on leptin.

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I was really happpy to read your post that mentioned 4 supplements that could "reset" the dopamine level. BTW, Lyle's bromocriptine therapy was based on that dopamine theory of leanness.

I am most curious about ibogaine & its synthetic counterpart. It is exceptionally interesting because its use is "one-shot." I wish they were legal here; but they aren't!! Oh, well.

The next interesting candidate is St. John's wort (SJW). This is anti-depressent drug, that increases the availability of neurotransmitters at the post synaptic junction. When the neuro-transmitters are released by the firing neuron, there is "reuptake" at various receptor sites at the same, firing neuron. More uptake there is, less will cross the junction and flow into the receptor. By inhibiting the reuptake, the receptor will have more dopamine to absorb.

In effect, you are raising the level of dopamine at the receptor. My problem with this approach is that the constant use of SJW may cause the receptors to expect the same high level of dopamine. The receptor will have become desensitized (according to your use of the term). Basically, I am worried that it might be addicting.

I checked on SAMe -- this increases dopamine level temporarily. I am wary of temporary dopamine increases that are induced by any drug -- there is potential for addiction.

There must be more anti-depressant drugs that are worth looking into, for dopamine receptor control ...

changing the dopamine setpoint would likely lead to fat loss yes, but if thats only by supression of appatite then its not exactly what I'm looking for.


What I would like to be able to do is make it so that one could be very lean without having a supressed leptin level or any other level and at which an increase in body fat to much above that leaness would illicit leptin increased metabolism.

Now unless this could be done so the effects are permanent then it really doesn't matter if your loosing wieght from dopamine, an uncoupler or something else, whatever works would be great. But if we could somehow make the effects permanent then leptin setpoint would be the way to go.