If this is the case with estrogen-receptor immunoreactive cells, what are the implications for a fasting-refeeding type of nutritional approach and adipose tissue metabolism, accrual, feeding behavior etc.

The implications seem rather large, although vastly unexplored (at least in man).

I'm not sure if this is the kinda "neuroanatomy alterations" that you mentioned. Are you asking about how menarche or puberty can be induced earlier with the changes in sex-steroid status that typically accompany it? I know leptin seems to play a key role in the induction of puberty.

Short-term -- 2-4 day TRIPLE baseline overfeeding in young adults seems to cause large increases in energy expenditure do to increased activity. Regularing tripling my maintenance caloric intake for 2-3 days -(followed by maintenance caloric intake for 7-12 days and then repleated) -- helped me gain over 60lbs in 15 months in my early twenties. This weight-gain was over ~75% lean muscle mass with very little water-retention during each of the 2-3 day periods of massive over-feeding that I planned out during that 15 month period of time.

My T-3 blood levels were very high come to think of it when I had a thyroid panel performed on day 3 of one of my overfeeding experiments...Lemme know if this is what you are discussing, or whether I'm off base or not...thanx...


Int J Obes Relat Metab Disord. 2001 May; 25(5): 593-600.

Changes in energy metabolism in response to 48 h of overfeeding and fasting in Caucasians and Pima Indians.

Weyer C, Vozarova B, Ravussin E, Tataranni PA.

Clinical Diabetes and Nutrition Section, NIDDK, National Institutes of Health, Phoenix, Arizona 85016, USA. cweyer@phx.niddk.nih.gov

OBJECTIVE: Differences in the metabolic response to overfeeding and starvation may confer susceptibility or resistance to obesity in humans. To further examine this hypothesis, we assessed the changes in 24 h energy metabolism in response to short-term overfeeding and fasting in Caucasians © and Pima Indians (I), a population with a very high propensity for obesity. METHODS: We measured the changes in 24 h energy expenditure (24 -EE) and 24 h respiratory quotient (24-RQ) in response to 48 h of mixed diet overfeeding (100% above energy requirements) and fasting in a whole body respiratory chamber in 14 male subjects (7 C/7 I, age 30+/-6 y, mean+/-s.d.). Results were compared to a 24 h measurement under eucaloric conditions. RESULTS: Mean 24-EE increased in response to overfeeding and decreased in response to fasting (all changes P<0.01), with no differences between C (+9.1% and -9.1%) and I (+8.6% and -9.6%). Similarly, mean 24-RQ increased/decreased in response to overfeeding/fasting, respectively (all changes P<0.01), again with no differences between C (+0.06 and -0.05) and I (+0.05 and -0.05). The changes in 24-EE in response to overfeeding and fasting were positively correlated (r=0.70, P<0.01), whereas those in 24-RQ were not (r=0.40, NS). CONCLUSIONS: Pima Indians do not appear to have an impaired metabolic response to short-term overfeeding and fasting that could explain their propensity for obesity. Individuals with a large increase in energy expenditure in response to overfeeding appear to have a small decrease in energy expenditure in response to starvation (spendthrift phenotype) and vice versa (thrifty phenotype).

PMID: 11360139 [PubMed - indexed for MEDLINE]

Large perhaps if you're a prepubertal rat.

Maybe even a prepubertal human.

Irrelevant for adults IMO.

Lyle

Ergo
yes, this is what I was getting at.
Obviously I was using this example of neuroanatomical alteration (whether transient or not) to point out that something of this nature may happen to those that consistently take a fasting-overfeeding type of approach to their lean gain/maintain or even cut. Obviously, with repeated overfeedings and then semi-starvations, there will be some sort of adaptation. For example, is it possible that the body adapts to a scenario whereby by starvation signals (lets say low leptin, increased proteolysis and excretion of protein among others) tell the body to partition the overfeed more towards muscle tissue growth and repair upon refeeding? The studies with army Rangers comes to mind when after a period of starvation (and subsequent refeeding ad libitum) all of their key anabolic hormones jumped above baseline (pre starvation) incl. T, IGF-1, GH etc. Perhaps something might happen at the level of the PVN or VMH as well? For the record, and as discussed in the fasting thread, I experienced similar lean gains as yourself using a fasting-refeeding type approach consistently. By adjusting the intervals between refeedings, I was able to titrate between cut, maintain, and gain.

Ergo,
this is debatable somewhat. As noted in Roemmich and Rogol (98) "We propose that there is not yet sufficient evidence to conclude that the initiation of puberty is due to the attainment of a threshold leptin concentration due to the accrual of a critical amount of adipose tissue."

However, I would happen to agree with your thoughts and that leptin acts as a gate on puberty by acting as metabolic signal to the hypothalamus that energy stores are adequate (Ahima et al., 1997; Cheung et al., 1997)

In looking at various systems (for example protein synthesis, fat cell metabolism) with various things, the pattern that seems to turn up is this: with chronic fasting/depletino of a given system (i.e. protein deprivation or even a decrease from a habitual intake, fat loss) you get an increase in storage capacity (i.e. the decrease in protein breakdown that occurs should allow faster replenishment when nutrients become available, changes in fat cell storage dynamics are similar).

And when you look at refeeding, by the time you get the person back to where they started, the effect is more or less lost. This is especially true over the long-term.

So, for example, if you look at protein breakdown (or use nitrogen balance as a proxy), you find that with protein deprivation, there is a gradual decrease/adaptation in protein breakdown and you eventually achieve nitrogen balance at thhe lower intake (takes 3-9 days in humans or so). When you increase protein, you see a concommitant increase in nitrogen balance (meaning you are storing more nitrogen initially) but you pretty much are right back to normal once you've rebuilt everything you lost. The net result tends to be a break even situation (which makes sense when you think about it).

Studies on metabolism generally support that view. The adaptive decrease in metabolism allows you to replenish depleted fat stores at a far more rapid rate when you refeed. And by the time you get about back where you started, you're pretty much back to normal. End result: break even more or less. This is especially true if you look at it in the long-term. With short-term machinations (like what you guys are describing) it may be possible to get some net positive effects. Over a day or three, you may be able to get things to work better (is this where I'm supposed to pimp my book again, since that's what it's goal is?).

Now, is some of this mediated through neurophysiological cahnges (as opposed to peripheral changes). I'd say yes. Changes in stuff like NPY/CRH affects metabolism centrally (you get partititioning twoards fat cells so that when you refeed, you gain back what you lost when you diet for example) but there are also peripheral effects.

Lyle

This sounds like the protein cycling diet that was proposed a few years ago.

I think lyle is talking about somtething that sounds similar, but it's totally different.
the protein-cycling-diet supposed that the higher nitrogen balance could lead to muscle-gain.
lyle wrote some time ago that higher nitrogen balance doesn't mean muscle-gain.

Yes, Akerfeldt wrote about it first and then some dumbshit on T-mag wrote about it. Dharkham wrote an anabolic/catabolic diet for Dirty Dieting.

Basically you drop protein to extremely low levels (losing LBM at a rapid rate) and get adjustements to protein turnover (and breakdown) which decrease as part of the adaptation.

Great, so you jack protein back in and get this huge positive nitrogen balance.

But before you can gain NEW tissue, you have to REgain everything you lost during the low protein phase.

And you find tha, at the end of it, by the time you've rebuilt what you lost, all of the adaptations are gone and you're right back where you started.

The dumbshit on T-mag claimed that the decrease in protein breakdown (or was it oxidation) was maintained long-term which was total bullshit. The body doesn't work that way.

Akerfeldt suggested that you'd somehow lose mainly liver protein during the starvation phase and gain muscle protein when you overfed which is not only bullshit but nonsensical. The body would NEVER do something so maladaptive; his idea suggested that you could somehow destroy everyy bit of liver protein during the starvation phase and your body would put incoming protein back into muscle.

They all had a very superficial understanding of the whole issue of protein oxidation in the first place. It's true that protein oxidation increases with increasing protein intake and they were suggesting that this somehow limited muscle gain. What they missed was that the body only oxidizes EXCESS protein intake (i.e. it burns off the extra above and beyond what it needs). But it still gets enough to support basic function,growth, etc.

Lyle

What I described, is not related to protein cycling and the other theories that you mentioned were written about in magazines and books in the past. I simply tripled my maintenance caloric intake for 3 day periods of time - followed by returning to my baseline caloric intake for a little over a week, and then repeated the process as I saw fit.

7-8 years ago - (when I gained the 60lbs in ~15 months), all I knew was that some research had shown increased anabolic hormone levels in response to short-term over-feeding in men. I figured it made sense, applied the concept to my diet/training at the time, and enjoyed a ~60 pound weight-gain over a short-period of time.

The 2 week high-protein/calorie phase followed by a 2 week period of dieting 'concept' for gaining mass via hormonal manipulation etc. --sounded silly to me when I read about Bill Phillips interviewing some Finnish or Swedish guy who was describing his research to him in Muscle Media if I remember correctly...

Anyhow, I'm just glad I was able to gain mostly muscle during the 15 month period of time in my early twenties...

It wasn't until MUCH later that I began to study and learn the art of NINJITSU !!! j/k...

Lyle, I guess what I was getting back to in a roundabout way was the set point deal. Obviously, I know where you stand on this issue as we discussed in a prior thread. However, I guess what I was thinking is that if the overfeed is clean (i.e., all carb, no fat--DNL being a costly process) are their possible alterations that could occur from a neuroantomical standpoint which would facilitate a negating effect on the fat rebound (i.e., to baseline). I draw a metaphor from psychology in some ways. Often we see kids with a certain attachment based on early socioemotional experience. This style is associated with various brain structures and neuroanatomy. However, given the 'corrective experience' there seems to be some plasticity to the system so that they can learn to better self-regulate; this may involve alteration of neuroanatomy. I am wondering if a fasting-refeeding mentality can circumevent set-point vis a vis extrme variation in metabolic homeostasis.

I can't parse the sentence starting with However.

As far as changes in setpoint, I suspect that it is a matter of degrees, mainly degrees of extent and duration of overfeeding/getting fat. If you go back and think about our evolutionary food pattern (let's simplify say it was more or less 6 months with pretty good food availibility, 6 months without), it'd be surprising if setpoint were changing (going up) on short-term cycles (say less than a 6 month of even a year's time). It wouldn't be adaptive because the body is just dealing with 'normal' yearly fluctuations (I'm aware of one study lookinh at metabolic rate in an ethnic group that yo-yo diets throughout the year and there are no permanent changes observed).

Now get and stay fat for a couple of YEARS and maybe you're talking and setpoint might move up. I'd be really surprised if it happened in significantly shorter terms than that.

As always, not a lot of good data in humans, a bitch to study because of the time frames and study control issues involved. But using growing animals (prepubertal rats) is a losing proposition to try and figure this out because they're still in a developmental phase. It's fairly well established that getting/being obese at certain critical time points (think right after birth/as a baby and puberty) drastically increases the risk of adult obesity. There is a metabolic flexibility (and potential to fuck it up) there that just isn't seen in adult animals.

Once you're an adult, the system is more concerned with homeostasis than anything else (i.e. you're done with the major part of your development tho some parts of the brain continue to grow even into the 20's).

But I wouldn't expect short-term perturbations (yes, I know, define shor-term; as above, much less than a year) to really do much in non-growing humans. I certainly don't expect weekly fluctuations or anything like that to have *permanent* effects on neurophysiology.



The key word in that paragraph and the one that you have to remember in this discussion is:

"kids"

Ask yourself how much the above happens in humans in terms of psychology or anything else

Don't get me wrong: it is possible to alter an adult's psychology but it takes extensive, extensive work (tho Tim Leary claimed he could break and reset imprints with LSD and many esoteric systems are concerned with doing the same but they still take a lot of time and effort) and, even then, you frequently see them reverting to old patterns.


Even then I have to wonder how much you're truly altering the imprints/patterns that are there, I suspect you're simply overlaying new imprints (and hopefully strengthening them to the point that they become automatic/'natural') on top of the old. Which is why, under conditions of stress or what have you, adults tend to revert to the earlier (stronger) imprint.

For example, you can take someone who's shy and eventually teach them to become more social (I know, I did this to myself last year). Initially it takes sheer force of will (I'd sit there and have internal dialogues with myself to get myself to approach a stranger and strike up a conversation), over time it becomes easier and easier, eventually it should become second nature. Even then, I found that once I got out of the habit (my drinking buddy moved and my best friend who I was going out with all the time didn't have time), I fell right back into old patterns. I hadn't removed the old pattern at all, I simply overlaid a new one on top of it. And when I quit 'practicing' the new one, the old one re-emerged.

Kids have more flexibility compared to adults.

Lyle

Lyle,
Interesting example with your shyness de-training.
Indeed, comparitive research in psychobiology suggests that while behaviors can be transiently altered, cytoarchitectural changes in brain biogenic amine systems tend to remain the same after critical time periods (this most often seen in monkeys who are socially isolated after birth and then taught to engage in social behaviors).

However, and let me just throw out some heavy ass bullshit here, in the context of dyadic relationships and appropros time in therapy we have seen (in contemporary psychoneuroendocrinological literature) some possibility of changing this cytoarchitecture, suggesting some plasticity of the brain (the adolescents are all past the 'critical period' point).

Furthering this to our current conceptualization. A set point is biologically set, but like the dyadic relationhship and its importance in hardening emotional regulatory predispositions, it is vulnerable to social stimuli (in this case food eating behavior). Somewhere in the arcuate nucleus changes could occur in the number of leptin responsive cell beds due to chronic firing (POMC-CART [less leptin needed to fire] NP-Y/AgRp [less leptin needed to inhibit]) due to severe underfeeding and then overfeeding (e.g., a 'learning' or 'molding' process. Perhaps drastic drops in leptin (underfeeding) coupled with a transient spike in leptin, suggesting acute 'okay periods' may cause functional changes in the cell groups which then affect the PVN and other central and peripheral tissues downstream. Such changes would decrease what was originally considered a heretofore 'normal' leptin mediated arcuate-pvn response, thus affecting feeding behavior and hence adipose tissue (the thermostat is changed). This process would occur over a period of sustained time and require similar behavior to 'buttress' the response; with chronic 'regulated' eating patterns, this cell group change would then re-modify back to a different structure. As you said and I agree (duh), the body seeks homeostasis. Wouldn't this be one way to achieve it (at the primary level rather than the secondary--central structure [brain] versus periperhal tissue [adipose]?


---->Thus could a sustained eating style (dysregulated by 'human' standards) allow for a modification of set-point partitioning as long as that style is maintained. Drawing from my initial example, if a monkey is taken from a socialized environment, and subjected to severe social deprivation or even change, plasticity of brain structure is revealed, contigent upon the nature-nurture interaction.

A key principle of brain function is self-organization (and re-organization). Later aspects of neural self-organization can be distinguished as experience expectant and dependent processes. Experience dependent processes incorporate experience that is peculiar to the individual (fasting-refeeding). Further, experience dependent information storage appears to be the generation of new synaptic connections in response to the occurrence of a to-be-remembered event (refeeding). Both process (expectant and dependent) lead to the formation or reorganization of neural patterns that will not exist unless the organism has certain experiences (i.e., keeping the pattern in-tact) and makes certain repsonses to them.




On a completely unrelated note (at least now). If the overfeeding portion of this plan is EXTREMELY fat-free (i.e., >30g/fat), would not this make it extremely hard to 'rebound' from an adipostat perspective due to the extremely energy-inefficient process of DNL, both hepatically and in adipose tissue?

this sound similar to some diet suggesting to increase catabolism of everything(fat, prot, glycogen), starving and working out on ampty stomach, to get more muscles during refeeding after the w/o.(an example:mauro de pasquale suggested to train on morning on ampty stomach on morning on this purpose).
maybe anabolism is higer after starving, but u have to rebuild the lost muscles. my body has really changed when I understood this.

I think the great mis-concept is that people apply something related to glycogen metabolism to the protein metabolism.
muscles do not experiment anything that is "protein supercompensation".

supercompesation is a theory developed to explain sugar metabolism, and nothing can be appolied to protein.

'98 is kind of ancient, when it comes to leptin.

You know it gets me hot when you talk like this.



The key word there is possibility and some. I'm not denying that it is *possible*. I'm saying it takes extensive work and effort. I don't think you'll disagree with me on either. Also, plasticity of the brain probably depends heaviliy on what part of it your'e talkign about. Different structures may retain relaively more or less plasticity depending on the relative benefits of such. In what I've seen looking at bodyweight and the hypothalamus, the plasticity isn't really there (unless you're talking about adjusting setpoint upwards). Might other areas of the brain (cf. if someone loses a given senese in an accident and others improve to take over for it) show more plasticity? Sure. But it's not generalizable (IMO) across the entire brain.



And in everything I've seen to date (usually looking at some en point like metabolism), it just doen'st happen. I know of at least one study that monitored post-obese dieters for something like 2 years (and they kept the weight off). Metabolism did not recover. Now, is it possible taht it occurs over longer periods? I suppose. 5 eyars, 10 years perhaps setpoint comes back down. For 99% of dieters (who will regain the weighht within a year or two), that's effectively saying it never happens. Of course, bodybuidlers and psycho athletes aren't 99% of dieters.

Empirically, folks who get and stay lean do seem for extended periods do seem to have a relatively easier time of doing it. But you have to ask if that's an actual change in setpoint dynamics or if it's simply a permananceafying (making permanent, if you can make up words like dyadic, I can make up words too) of BEHAVIOR PATTERNS. I suspect the latter. The behaviors that keep them lean, training intensely, monitoring diet become habit. But I doubt that true biological setpoint has come down. Data from the Natinoal Weight Control Registry would seem to bear this out. Those folks have lost weight and kept it off for extended periods but they show many consistent BEAHVIOR PATTERNS. One of them is continuing to restrict calories, maintaining activity, monitoring changes in weight (to see if they are falling off the wagon). I would expect studies (to my knowledge they haven't been done) to show that they are still showing signs of a depresed metabolism and the rest (i.e. metabolic rate below what would be predicted for bodyweight, as is common in post-obese individuals).




But you have to ask yourself if it's adaptive or not. Within the context of bodyweight, it's generally not going to be adaptive for the body to 'learn' to maintain a lower bodyweight because that prediposes you towards death when/if the next famine comes. Biologiclaly, it's adaptive to be fat (up to a point) and maladaptive to be lean. Which is why the system evolved in the assymetric way it did (generally easy to get fat, hard to get lean). Millions of years of evolution shouldn't be able to be undone by 2 years of staying lean.



I suspect that how will this works depends a lot on the age of the animal. As above, genralizing brain plasticity from something like behavior to bodyweight is a dangerous proposition. All parts of the system don't necessarily show the same adaptability or plasticity.




Do note that one of the conditions where DNL capacity upregulates is in the context of extremely low fat (>10% fat) diets. There's still probabyl some energetic efficiency but Acheson's massive carb-overfeeding studies shoed that with several days of super high carbs (700-900 g/day over 5 days or so), you can make plenty of TG.

Lyle

Is there sufficient evidence now?

Sufficient evidence for what?

Lyle

I screwed up, I meant this post to be in relation to Par's comments above in regard to the 98 study I mentioned in relation to 'not yet sufficient evidence....'

Ah, that makes more sense.

I did a quick Medline skim after I saw your post. The most recent reviews (abstracts only) still mention leptin as being permissive for the start of puberty. That is, it has to reach a certain level before other things can kick in to get the system started. Which doesn't really decrease it's overall relevance to the start of puberty (in the one or two cases of human leptin deficiency, puberty had not occurred) but it appears at this point that it's not exactly causal in starting the process. Simply required for everything else to get moving.

Lyle

BTW: dyadic is a real word

Most words in psychology are made up.
And then defined in a fashion that is internally consistent with whatever schema the definer wants.

Lyle

Anyhow, I think you meant dRyadic.

As in having characteristics of a dryad.

http://elfwood.lysator.liu.se/loth/j/e/jer.../dryad.jpg.html

Lyle

I love digression.

Muhaha

ergo,
really interesting.
I'm doing something similar in this priod.
I starve for 4days, then I eat like a carzy for 3.
I'm gaining so may muscles, the guys in my gym think I'm on roids!
what I notice is I'm not losing fat.
becuase my priority is a "shredded look", I've some questions.

1)can the diet I follow during the starving days be of any importance for DNL occuring during high-carbs diet. what I mean is this: following a low-fat diet can increase DNL occuring during refeedings?
lyle's assertion made me think about this and I figure the answer is yes.[from lyle:Do note that one of the conditions where DNL capacity upregulates is in the context of extremely low fat (>10% fat) diets. There's still probabyl some energetic efficiency but Acheson's massive carb-overfeeding studies shoed that with several days of super high carbs (700-900 g/day over 5 days or so), you can make plenty of TG.]

2)big cat wrote in his article on leptin that leptin decreases TSH. if during the 3days overating I eat a lot af carbs, can this be harmfull on fat loss, loweing leptin?
I thought leptin should rise t3, so this confuse me.

I know. it does't look appropriate for avanced theory, so if u want answrer me pointing on DNL and THS/leptin and their relationship with undereating/overating.
thanks

Duchaine
on your 'starve' days, are you eating a low-fat diet? For me, when I go severely hypo, I consume ~100+g of Fat per day. Thus, one has to wonder if DNL is really contigent upon type of diet but rather time spent overconsumming carbs and other related factors (depletion etc.). Since I precede my hyperfeeds by a high-fat, low carb, low-cal diet, I am hoping other possible metabolic alterations can take place.

Vain

There are tons and tons of studies on high fat lowering expression of various lipogenic enzymes and high-carb increasing them.

I know high carbs increase lipogenic enzymes.
I know high fat lower them.
what I ask is:if I eat a vary low fat diet during starving day, can this increase DNL during refeedings?

vain:I'm a light guy, so, whan I want starve, I can't go over 40gr of fats and 50 of carbs.

par deus: what about leptin and tsh?

high fat-low cals??

Typically 1800-2000kcal with intense training (ice hockey); ~ 30cho, 1110F, 200ish PRO

I think it would, though I would not venture a guess as to the significance.

Leptin lowers TSH but increases t3

I'm curious as to the timeframe for these enzymes/adaptations.
If one is using some sort of cyclical diet, during the diet phases one eats ~60/30/10 %cals from p/f/c, and during the carb-load phase keeps fat very low, will one see a signifigant amount of DNL

2.5 days dieting/6hr refeed?
3-4 days dieting/24hr refeed (ala UD2, tho keeping the fat lower on the refeed than the ~50g given in the book)?

Basically, are these long term diet adaptations or short term? If for the majority of the time, one's diet contains a fair amount of fat, will short term high carb/low fat lead to increased DNL, or does the increase in DNL with low fat only occur during longer periods of time?

"ergo,
really interesting.
I'm doing something similar in this priod.
I starve for 4days, then I eat like a carzy for 3."

Duchaine, what I described actually is quite different from what you mentioned above. Eating below maintenace cals for 4 days is something I NEVER strategically have attempted or implemented. I don't think my protocol is similar because I always returned to my maintenance caloric intake/day (which of course continued to increase) after each 2-4 day overfeeding period of time. Also, at the age I was eating in this manner, I was not yet done growing which likely allowed my results to be much greater than if I were to try to eat in this manner after age ~25 or so.

At 30 years of age now, my program has been modified in that I consume Double my maintenance caloric (30/40/30 -- p/c/f ratio) intake/day followed by ~6-7 days of maintenance caloric intake/day. My training is adjusted around my overfeeding days strategically also which I didn't strategically consider or care about 7 years ago...

Regarding DNL, IMO, I really don't know/understand enough about the physiology behind this process for me to answer you with any info that would be accurate/worthwhile.

"big cat wrote in his article on leptin that leptin decreases TSH. if during the 3days overating I eat a lot af carbs, can this be harmfull on fat loss, loweing leptin?
I thought leptin should rise t3, so this confuse me."


What was written in the article you mention was not accurate in multiple areas which is probably why your understanding of leptin/TSH/t-3 inter-relationships was confounded...


"...what I notice is I'm not losing fat.
becuase my priority is a "shredded look",


My priority/goal during my 15 month experiment was simply to gain bodyweight w/o much concern as to how much of the gains would be fat vs. muscle vs. fluid etc.

IMO, 4 days of underfeeding/fasting/extreme sub-maintenance caloric intake is not going to continue to benefit you if you want to NOT lose muscle while losing bodyfat also. With exogenous androgen/GH/thyroid manipulation, perhaps you could minimize LBM losses while continuing to lose bodyfat - as your priority is a "shredded look".

I'm curious about a similar thing:
researches about the DNL show that this increases after some days of overeating.
can frequent refeedings increases body's ability to convert fats into muscles?



ergoman:
in your protocol u rised cals for 3days after about 2weeks on mant.cals.
this is supposesd to rise anabolic hormones in the body.
so agree with this diet to gain muscles.

I think: we know that the body won't lower anabolic hormonce at once when we diet.
this means that the first days of dieting we have a great partitioning of cals.
if we try to rise and to lower cals in short period of time(and, special bonus, and we strategically train in this periods) should this create a great anabolic/antacatabolic combo?
I consider researches about supercompesation. the researchers found that 3 days of carbs deprivation follwed by a depletion w/o increase body's ability to store glycogen.
this means a good partioning for sugars we eat.
this means we can eat a great amount of carbs without gaining fat.
this also means overeating, that is supposed to rise anabolic hormones.
so, if we starve and have 3/4low carbs days, this is good for 2 reasons:
1)we can overeat for 3 days to achive supercompensation
2)we stay into an anticatabolic state during the 3 starving days, because we enanched partitiong during the 3 days overfeeding.


this is "the rationale"behind my cycle.
I need to take measurement to say if the diet is working.


I remember mr.question on this board wrote he nedds 1week to lose water retention gained during a carb-up.
maybe I'm gaing a lot of water with this diet, so it seems it doesn't work for cytting.
I'll let u know
(mine is a "general question post" )

"This suggests that one effect of orbital frontal lesions in rats is to lower the set point. Therefore fatted rats are aphagic longer than others because it takes longer for these animals to reduce their body weight to the new set point...The possibility that a neocortical lesion reduces body set point is novel but quite consistent with an hypothesis that there is an important descending projection system from the orbital cortex to areas in the hypothalamus and brainstem...Whatever the explanation, the important point is that there appears to be some sort of modulation of catecholaminergic neurons by the frontal cortex and the aphagia and reduced set point observed following orbital frontal lesions could result from a disruption of this modulation." (Kolb, Whishaw, and Schallert, 1977).

Comparative literature and old, but worthy of note.

Lyle supporting some comments I recently made (to HL was it?). Not hard science, but he's a smart guy.

And a cool thread anyway.

As noted earlier in the thread, someone said leptin was permissive for puberty. I grew fast and had deepening of my voice around 12, but never really grew pubic hair until I was 15 or so (I had some but not much) and didnt grow armpit hair until I was almost 19, even at that I barely have any now. Is there any ways in which a leptin imbalance could have precipitated this? How would that imbalance present in eating habits and body comp?

Any other general ideas of what this might be caused from?