Background:
Im 19 years old, 5'11 and around 12% body fat.
Goal is 10%, then clean bulk.

-My diet consists of
Oatmeal
Apples
Chicken
Veggetables

Daily i consume 1400 calories, im not losing anymore, i have started doing cardio and burning off around 600-1000 calories a day, from just cardio the last few weeks, and eating whatever i burn off. Still no weight loss, my maintenance before was around 2800 calories, standing around 24% Body fat, 18 years old, yes thats how long i have been cutting for, i was in like a 100-300 calories defiect a day, no crash dieting.

I was doing weight lifting since i started, and even though i have only just started recording my results the last few weeks, i am still gaining strength, not mass though. I do squats, deadlifts...ect.

Im literally freezing my ass off, i can no longer wear t shirts anymore, even in my room. Has anyone got any advice they can give me?

Im thinking of consuming 200 calories more per week, untill im back at 2800, hopefully it will be all muscle mass im gaining...

Please give me some help, i have been to other BBing forums and they dont have a clue, they say "just eat 2800 calories and the metabolism will reset itself" i doubt it....

Any help?

Yeah, start adding the calories back in like you said, You are so low that I would actually go with 300 cal jumps for the first 3 weeks, to get you to 2300, then start with the 200 jumps.

as you already know, the body will try to fight extreme weight loss. I think you need to get back to maintenance for some time, then you could lower calories, much less drastically.

I have seen a docter for a blood test, as im freezing!

Thyroid TSH is normal 1.9 (range is 0.35-4.5)

I read a LOT of studies about T3 (thyroid hormone), do you think its a good idea to supplement on T3 and slowly taper off, as all studies show that the thyroid resets itself, even after 4 years on it.

Do you think this would speed recovery, im hoping you guys could help on this as i have the supp already (armour thyroid).

P R Health Sci J. 2006 Mar;25(1):23-9.

Supraphysiological cyclic dosing of sustained release T3 in order to reset low basal body temperature.

Friedman M, Miranda-Massari JR, Gonzalez MJ.

Friedman Clinic, Montpelier, VT, USA.

The use of sustained release tri-iodothyronine (SR-T3) in clinical practice, has gained popularity in the complementary and alternative medical community in the treatment of chronic fatigue with a protocol (WT3) pioneered by Dr. Denis Wilson. The WT3 protocol involves the use of SR-T3 taken orally by the patient every 12 hours according to a cyclic dose schedule determined by patient response. The patient is then weaned once a body temperature of 98.6 degrees F has been maintained for 3 consecutive weeks. The symptoms associated with this protocol have been given the name Wilson's Temperature Syndrome (WTS). There have been clinical studies using T3 in patients who are euthyroid based on normal TSH values. However, this treatment has created a controversy in the conventional medical community, especially with the American Thyroid Association, because it is not based on a measured deficiency of thyroid hormone. However, just as estrogen and progesterone are prescribed to regulate menstrual cycles in patients who have normal serum hormone levels, the WT3 therapy can be used to regulate metabolism despite normal serum thyroid hormone levels. SR-T3 prescription is based exclusively on low body temperature and presentation of symptoms. Decreased T3 function exerts widespread effects throughout the body. It can decrease serotonin and growth hormone levels and increase the number of adrenal hormone receptor sites. These effects may explain some of the symptoms observed in WTS. The dysregulation of neuroendocrine function may begin to explain such symptoms as alpha intrusion into slow wave sleep, decrease in blood flow to the brain, alterations in carbohydrate metabolism, fatigue, myalgia and arthralgia, depression and cognitive dysfunction. Despite all thermoregulatory control mechanisms of the body and the complex metabolic processes involved, WT3 therapy seems a valuable tool to re-establish normal body functions. We report the results of 11 patients who underwent the WT3 protocol for the treatment of CFS. All the patients improved in the five symptoms measured. All patients increased their basal temperature. The recovery time varied from 3 weeks to 12 months.

PMID: 16883675

Hold the phone --

So these people are using T3 to reset their thyroid basically? Once 98.6 is maintained for 3 weeks, they are weaned off -- and the higher temperature remains?

Interested, as my morning basal temperature is normally around 96.5. Was 96.2 this morning, and I've been eating heartily for the last week or so.

either way - unless you have thyroid problems raising your cals back up to a respectable level is going to level out your T3 naturally anyways. Suplementing something in lue of good nutrition seems silly and unwarrented to me. Raise your kcals back up and diet responsibly. Take some sea kelp or synthetic iodine and I bet your temp raises. No need to use your smith and wesson to swat mesquitos young padma

lol well said.

Agreed 100%.

Any thoughts on the results of the above study and ... setpoint?

I've been hypercaloric -- high PRO, moderate fat, moderate CHO -- supplementing with kelp caps TID (550 mcg iodine apiece, which is 367%DV) for over a month and my temp hasn't budged. T4 and TSH are normal (blood work), but this doesn't necessarily discount T4 -> T3 conversion issues, or perhaps TRH issues (which would be involved with my possible Prl issues).

What's to say that these are just mosquitoes?

EDIT: Full text for those interested... wait a minute, where'd the "attachment" button go? .... PM for full text then.

good chance the OP is iron deficient as well, how is the color of your hands?

no need for thyroid manipulation, gradually work your calories back up.

aren't you a skinny fat ecto!? I doubt your T3 is low, althought I've been wrong before. I'd definately seek out a way to test this before supplementing.

all this is fixing is an abnormal body temperature. It even admits it's not measure actual thyroid functionality. I suppose if you consider a temperature deficiency a problem then you'd definately have case. It states that in all cases patient's temperature went up. By those standards this also doesn't mean that they are doing shit to the thyroid.

Personally - supplementing thyroid hormones is taboo as hell. I'm not basing this off of anything other than personal stigmatism towards it having seen what happens when a thyroid malfunctions - I'll GLADLY leave mine alone unless absolutely necessary.

My calories have never really been that low to start with -- Was doing IF for a while (~10-14 weeks?) with sufficient calories to maintain weight. Got sick, and have had caloric surplus for a few weeks to try to regain lost weight (have regained ~4 lbs over 2 weeks). The entire time (besides when I had the fever for a few days), my morning temp is about 96.2-96.5, and my peak temp is ~97.2 during the day (96.9 right now, at 7:45 PM).

My hands are frequently (usually?) red/purple, have been this color as long as I can remember. My iron intake is pretty high (above the RDA), and I have always passed the tests required to donate blood. Might you tell me about iron intake and hand color? That's new to me.



Skinny fat ecto? I've never described myself as such, though I suppose others might think differently. BTW -- Lyle McD wrote that low T3 might be the reason that keto diets make bulking difficult, as T3 in involved in PRO synthesis rates...

I was addressing the original poster there. He said he was often cold, and I thought I remembered it being an indication of being deficient in iron (a lot of college students are). I was thinking anemic, and then the color or the pigment of the hands could be very pale.

I think in such a caloric restriction though, many things would start to happen. The original poster should bump calories back up, as we have all outlined. No need for thyroid manipulation at this point.

my mistake then. I'm not sure where I picked that impression up at. Apologies.

Not sure what lyle's comment has to do with your body temp...

lol -- no apologies needed. You could be right, you might have gotten the idea from the pics I've posted. I've just never really worried about categorizing myself into a distinct "phenotype"... I just know that I want to be bigger, stronger, leaner, more intelligent, etc...

My comment was partly in reference to the "skinny fat" comment -- figuring that you had inferred my phenotype from my pics, I suggested that if my T3 levels were indeed low (independent of T4/TSH levels, mind you), that could possibly be one of the influences in the "skinny" half of the equation. IOW, compromised T3 means lowered PRO synthesis means not as big as I could be (although I assume raising T3 simultaneously raises PRO oxidation with the synthesis)...

My hands are a normal colour, when im "moving", but if i stay in one place for a long period of time i will get cold, and my hands will soon turn very pale and get cold, until i start burning energy again. Im sure i dont have low levels of iron, as i have a whole chicken every day and a bowl of oatmeal. The rest is veggies and fruit 600 calories of them which i burn off through cardio.

The study is very intresting as it surely raises T3, considering they maintain a higher temperture, obviously i would need to bump my calories up to match the T3 intake, which increases other processes in the body not just body temp.

A intake of 120mg 'Armour Thyroid' and to start off with 2000 calories daily and adjust calorie intake untill i no longer lose weight or gain any at 2800 calories. Then slowly taper off the thyroid med.

Hmm I forgot which Avant heavyweight wrote an article about it, but from what I read messing with your thyroid isn't that risky.

Yeah theres a study out there on subjects who took T3 for a year on continously, and there T3 levels returned within 3 weeks - 3 months. Also at the bottom there was a person who was wrongly misdiagnosed, and was givin T3 for treatment for 4 years and his T3 returned to baseline after 4 weeks.

Getting my blood test done this afternoon and going to ask for the following;
TSH
Free T4 + T3
Anti-TPO + TgAB
Ferritin
Cortisol
Estrogen
Progesterone
Free Testosterone
DHEA
Reverse T3

I get my results back on thursday, im keeping to 1500 calories a day untill the blood test, which is late afternoon today.

which study is this? The one I read measured temp not T3

The higher the body temperture, the higher the metabolism which is controlled by the thyroid. Just my take on it...

Is there anyone knowledgable to help out here?

EDIT: Which is proberly why you run a temperture when having a fever, the metabolism increases.

"Fever increases heart rate and metabolism" http://en.wikipedia.org/wiki/Fever

please refer to post #12 where i highlight why I have doubt on your causation = n here. I don't even have to look at other studies when the one posted clearly states that thyroid experts don't agree with it.

Medical experts probably don't agree on 99% of the shit we talk about on this forum.

Went for a my blood test to check for Free T3...They REFUSED to do so, and then said to me "Just between these 4 walls, are you taking anything, thyroid tablets or steroids of any kind" i replied No and just gave me a look as if im lying. I explained that i had done some research and that checking my TSH means jack sh*t, if my thyroid is low, and that T3 needs to be checked, they gave me firm "no, that is incorrect the people on the internet are trying to make money out of you". "How?" i asked there reply was "They are very clever people" i looked at them with a blank face, and walked out.

So i need someone who is knowledge to help me out here, as not even the NHS (national health service) are going to help me now.

For dash I finally broke down a wiki'ed body temperature:



raise due to temperature - your hypothylmus responding to pathogens - NOT metabolic activity.



You lucky bastard, you.



and my favorite:



how about the thermic effect of food?




I suppose supplementing with T3 would be under the same classification as supplementing AAS. You don't need it but it could do pretty incredible things if your not worried about the shut down it causes.

EDIT: Honest to god the reason i thought you thought you were a skinny ecto was because you asked my thoughts on how they should train vs rest. I wasn't judging your pics. Who am I to judge?

No, i rather live life 20 years less and be happy and energetic, compared to a long life of depression, which if i keep going, it will be, due to my hormone levels dropping. i need a cig just to smile. When logically thinking i should be the most happiest person i have been in my life, but emotionally im not with it at all.

Which is why im going to stop cutting and slowly build up calories or taper of T3 meds.

Also your sentance about taking T3 did not make any sense, typo? I would like to know what your opinion is.

jesus christ dude.

I'm at 97.8 right now, which is pretty damn good, although it is 5:15 PM (when my temp should be at its max). Further evidence (IMO) that there might be an issue: yesterday immediately after the gym (while I'm sweating my ass off, possibly due to high TRH?) my temp was barely at 98.0 -- I would have expected at least a few degrees higher. Again, the sweating w/o high body temp makes me curious if the TRH -> TSH -> T4 part is going fine, with problems in T4 -> T3 conversion. Just wondering, though, no evidence.



You're right -- at least according to the wiki entry, doesn't look like thyroid is involved. Interesting.




I'm not sure -- I'd rather life a fuller but (potentially) slightly shorter life.




Hmmm... who defines "normal" in this case? May be considered normal... for a person with underlying undiagnosed thyroid issues? May be normal temperature... for an extremely lean individual with low leptin? Not sure about that one.



Shutdown seems quite reversible, and I don't know how much hard could be done with doses up to 90 mcg BID (as per this Dr. Wilson's highest dose). In fact, according to Dr. Wilson, one tapers off the T3 at a slow enough rate that the body temp (98.6) is maintained, never dropping below as it would with real thyroid shutdown.



I agree, although 20 years is quite a bit. You haven't even posted body temps as far as I can see (might have missed them). Get yourself a thermometer and post up some temps -- morning basal (immediately after waking, before you even roll out of bed), then ever 3-5 hours throughout the day. Be interesting to see.

Maybe I should look into selenium...

Type I iodothyronine deiodinase is a selenocysteine-containing enzyme.
Berry MJ, Banu L, Larsen PR.

Howard Hughes Medical Institute Laboratory, Brigham and Women's Hospital Boston, Massachusetts.

Although thyroxine (3,5,3',5'-tetraiodothyronine, T4) is the principal secretory product of the vertebrate thyroid, its essential metabolic and developmental effects are all mediated by 3,5,3'-triiodothyronine (T3), which is produced from the prohormone by 5'-deiodination. The type-I iodothyronine deiodinase, a thiol-requiring propylthiouracil-sensitive oxidoreductase, is found mainly in liver and kidney and provides most of the circulating T3(1) but so far this enzyme has not been purified. Using expression cloning in the Xenopus oocyte, we have isolated a 2.1-kilobase complementary DNA for this deiodinase from a rat liver cDNA library. The kinetic properties of the protein expressed in transient assay systems, the tissue distribution of the messenger RNA, and its changes with thyroid status, all confirm its identity. We find that the mRNA for this enzyme contains a UGA codon for selenocysteine which is necessary for maximal enzyme activity. This explains why conversion of T4 to T3 is impaired in experimental selenium deficiency and identifies an essential role for this trace element in thyroid hormone action.

PMID: 1825132 [PubMed - indexed for MEDLINE]

In fairness, Matt was the OP of this thread....

OP = original person??

And yes, I apologize for the hijacking -- I'll probably open a thread of my own on this so as to facilitate discussion of the different subjects presented here.

I would advise less cowbell.

and i believe he was addressed first and fore most by all participants. I posted one post for dash with research. You do have a point, but I do feel like we gave him sound advice before moving the discussion down the twisty narrow.

Obviously my leptin is VERY low which is whats causing my low testosterone and T3 levels. As leptin cannot be increased if you stay the same body fat (set point), i have read that leptin pretty much controls all hormones so would there be any point in even increasing my calorie rate if my T3 and Testosterone are not going to budge anyway, as they are controlled by leptin.

I really would love a answer to this!?

Why wouldn't your leptin increase? Refeed will bump leptin and a higher daily caloric intake with at least 45grams of fats will set your test. Your making this way too complicated.

the funny part is in your OP you state that NOT crash dieting worked for you very well with a 12%bf loss. Now that you want to drop 2 your crash dieting and finding out it's not a smart decision. Your fighting your previous knowledge about what you know works. Your being irrational.

Leptin would not increase as its regulated by fat cells, obviously if i have very little fat mass in the cells then theres not much to regulate leptin.

I read laynes article on leptin and many others and im trying to get to grips with it, so if im wrong please point me in the right direction, thanks

ok well your wrong on both points about leptin. It's NOT regulated by fat cells (not sure where you got this from) and you DON'T have very little fat mass if your at 12%. Maybe you should read the article again then try Par's version.

not to mention that crash dieting kills leptin levels so if you've read the article why are you so hell bent on doing something that is negative towards your focus?

I never said i was crash dieting, i want to get increase my calories, im only eating this low because my metabolism has slowed down so much, which is why i want to increase T3 hormone which in turn will increase Testosterone but if they can only be increased by leptin then theres no hope. Layne wrote a article saying that refeeds do not have much effect on leptin, if any.

I will search for Pars version now.

Look, Matt.

Your misinterpreting everything obviously if you think fat cells regulate leptin. You also have no clue what your doing if you've been dieting that long without refeeds. Refeeds DO spike leptin and are the whole fucking purpose for it. Lowering calories due to not losing weight any more is ok IF your scheduling modest refeeds. I get the feeling you haven't been. I've had numerous email conversations with Layne, and he was at my first BB contest. He supports refeeds.

You need to refeed immediately and stick your cals at 2000. Refeed every 10days with your carbs for the day correlating around workout times like Lyane suggests and you'll lose weight I guaren fucking tee it. I'm a Layne Norton poster boy myself, but you obviously aren't comprehending the material.

EDIT: Layne's refeeds are very very controlled as well. It's not just a cheat session gone wild. It's twice your daily carb intake with fats almost completely eliminated that whole day.

EDIT EDIT: Layne also says there isn't much room in a cut diet for fructose but I see you're including apples in your regimen as well.

your also going to have to link me to where Layne has a leptin article because I've never seen it.

anyhow - you want to do a Layne/Dr. Joe diet - then read this 15-20x's rewrite in your own words with a dictionary, a thesaurus and wikipedia to decifer it all.

http://www.bodybuilding.com/fun/layne36.htm

Leptin responds to caloric intake -- specifically carbs are the way to go. Read the 6 part leptin series by spook and par -- you probably won't get a whole lot out of it the first time... but I recommend you print it and reread it every few months as your understanding of physiology improved.

First study I came across, I'm sure hundreds of better ones are out there if you just look:

Relationships between leptin levels and carbohydrate intake during rowing training.
Desgorces FD, Chennaoui M, Drogou C, Guezennec CY, Gomez-Merino D.

Department of Physiology, IMASSA - BP 73, Brétigny/Orge Cedex, France f.desgorces@free.fr.

AIM: This study was designed to determine the relationship between diet and leptin levels during rowing training. METHODS: Dietary intakes using 3-day food records, training volume and leptin responses to a 90-min exercise (measurement before, at the end and after 2 and 24 h of recovery) were assessed at the beginning and at the end of an 8-month training season for heavyweight rowers. RESULTS: During the training, we observed increases in energy intake and in training volume (12.1+/-1.8 and 14+/-1.4 MJ/day, and 3.8+/-1.1 and 6.5+/-1.8 sessions/week, respectively at the beginning and at the end of the season). Carbohydrate (CHO) and protein intakes were increased (P<0.001 and P<0.05, respectively), whereas those of lipid were unchanged (P=0.08). Leptin levels at rest were unchanged, while delayed decreases occurred (at 2 h postexercise) in response to the 90-min exercise (P<0.01). At the end of the season, postexercise and 24 h postexercise leptin levels were positively correlated to CHO intake (r=0.62 and r=0.69, respectively; P<0.05). CONCLUSION: There is an increase in CHO intake over a training season for rowers. Our results suggested that repeated hypoleptinemia in response to acute exercise triggered the particular choice of CHO in order to insure the energy homeostasis.

PMID: 18212714 [PubMed - in process]




Jake is right in that you do actually have a perfectly fine amount of bf. 12% is not especially lean, to be honest.



Refeeds are not going to make long term differences in leptin, but there is a short term effect (~ 5 hrs later?) that will make a difference if refeeds are used frequently.




Many fruits have pretty low fructose content, actually. I mean, look at Colin, he's low carb (jk buddy ).

No, but seriously nutritiondata.com says ~13g fructose for a large apple, only ~8.8g for a small.

I understand leptin WRT applying it to dieting. I'll by no means claim to up to par with you as far as MOST of the microbiology goes; however, receptor sensitivity has a shit ton to do with effects of leptin. So do refeeds. If your completely shutdown and vacant of leptin then maybe on a short term scale you wont see a raise in leptin but if your running at a healthy level to begin with and notice the signs of a steady decline I feel that from personal anecdotel evidence suggests it's a good tool to help you maintain healthy levels of it. The less bf you have the less leptin your body will produce, but it's not modulated by it. Nor is receptor sensitivity. If you cycle carbs in a refeed type fashion your going to reap the benefits of having potent receptors.

In the case of Matt in which he's likely been void of a leptin response to his feeding habits for an abnormal amount of time then I would agree that a refeed isn't going to be the answer to ALL his problems - which is why my refeed suggestion was accompanied by the raise in cals.

As far as fructose goes Layne does pretty much say that fructose shouldn't be involved in a cut cycle and it is pretty damn useless. Having practiced what his opinion on the subject suggests I'd have to agree. Bulking is something completely different.

I'll read the link provided and will be ready to remove my foot from my mouth, but I think the suggestion that leptin is controlled BY fat cells is way off base. Not to mention you always have the same NUMBER of fat cells they just shrink or expland unless you purposefully use exogenous mothods of cause apoptosis of such. It normally doesn't occur. So with this in mind the only thing you could say would be that the insulin response in the fat cells would be a governing factor of leptin in which case I MIGHT be able to buy that. But not as it stands.

EDIT: I loved the slam on colin, hilarious!

Dash you relize I was a contributor to this thread, right? Check out posts 7 and 14. The rest seems to be a pissing match between VC and Startingserious.

I disagree with some of what each is saying but most notibly is VC's lack of providing a study to connect the correlation that leptin is effected BY fat cells or is produced therein. Leptin is a huge contributing factor is fatloss but it's not the only thing involved in it.

I can't stand trying to sift throught two men's brickering. Can you point me towards relevant post numbers?

I guess I just don't understand your terminology here. This sentences seems contradictory within itself "The less bf you have the less leptin your body will produce, but it's not modulated by it."

I don't know a whole lot about leptin receptor sensitivity -- but I do remember reading about leptin BBB permeability issues being a big deal. I always thought transport was a huge issue, and that (for example) obese individuals exhibited elevated plasma leptin but that it didn't necessarily translate to proportionately higher leptin in the CSF. Then again, obesity is a different animal entirely.

Other than M&M's leptin articles, where else can you point me to learn more about the receptor sensitivity?



I believe PPARgamma agonists, as well as extreme obesity can induce adipocyte hyperplasia outside of childhood (when it is common). This is how thiazolidinediones improve insulin sensitivity. You're right that generally the fat cell numbers will stay the same. I don't see what you're arguing against WRT fat cells "controlling" leptin. There are many factors, one of which is the fat cell size (positive correlation), another would be fat cell number (which, as you said, is relatively constant in a given individual but will vary across a population).

Relationship between adipocyte size and adipokine expression and secretion.
Skurk T, Alberti-Huber C, Herder C, Hauner H.

Else Kröner-Fresenius-Centre for Nutritional Medicine, Technical University Munich, Am Forum 5, D-85350 Freising-Weihenstephan, Germany. nutritional.medicine@wzw.tum.de

CONTEXT: Adipocytes are known to release a variety of factors that may contribute to the proinflammatory state characteristic for obesity. This secretory function is considered to provide the basis for obesity-related complications such as type 2 diabetes and atherosclerosis. OBJECTIVE: To get a better insight into possible underlying mechanisms, we investigated the effect of adipocyte size on adipokine production and secretion. DESIGN, PATIENTS, AND MAIN OUTCOME MEASURES: Protein secretion and mRNA expression in cultured adipocytes separated according to cell size from 30 individuals undergoing elective plastic surgery were investigated. RESULTS: The mean adipocyte volume of the four fractions ranged from 205 +/- 146 to 1.077 +/- 471 pl. There were strong linear correlations for the secretion of adipokines over time. Secretion of leptin, IL-6, IL-8, TNF-alpha, monocyte chemoattractant protein-1, interferon-gamma-inducible protein 10, macrophage inflammatory protein-1beta, granulocyte colony stimulating factor, IL-1ra, and adiponectin was positively correlated with cell size. After correction for cell surface, there was still a significant difference between fraction IV (very large) and fraction I (small cells), for leptin, IL-6, IL-8, monocyte chemoattractant protein-1, and granulocyte colony-stimulating factor. In contrast, antiinflammatory factors such as IL-1ra and adiponectin lost their association after correction for cell surface area comparing fraction I and IV. In addition, there was a decrease of IL-10 secretion with increasing cell size. CONCLUSIONS: The results clearly suggest that adipocyte size is an important determinant of adipokine secretion. There seems to be a differential expression of pro- and antiinflammatory factors with increasing adipocyte size resulting in a shift toward dominance of proinflammatory adipokines largely as a result of a dysregulation of hypertrophic, very large cells.

PMID: 17164304 [PubMed - indexed for MEDLINE]

I found the overall thread interesting, notably the dearth of "good" evidence that metabolism drops significantly independent of fat mass during caloric restriction. The majority of the metabolism drop seems to be due to fat loss. See post 36, even startingserious admits this although it is contrary to his position.

VC didn't cite info on leptin production in adipocytes or correlation with size because that's pretty well known material...

Here's a quick one (first that came up), showing leptin production is from adipocytes, and that production is based on many factors, including "adiposity."

Leptin signaling, adiposity, and energy balance.
Jéquier E.

Institute of Physiology, University of Lausanne, Switzerland. Eric.Jequier@iphysiol.unil.ch

A chronic minor imbalance between energy intake and energy expenditure may lead to obesity. Both lean and obese subjects eventually reach energy balance and their body weight regulation implies that the adipose tissue mass is "sensed", leading to appropriate responses of energy intake and energy expenditure. The cloning of the ob gene and the identification of its encoded protein, leptin, have provided a system signaling the amount of adipose energy stores to the brain. Leptin, a hormone secreted by fat cells, acts in rodents via hypothalamic receptors to inhibit feeding and increase thermogenesis. A feedback regulatory loop with three distinct steps has been identified: (1) a sensor (leptin production by adipose cells) monitors the size of the adipose tissue mass; (2) hypothalamic centers receive and integrate the intensity of the leptin signal through leptin receptors (LRb); (3) effector systems, including the sympathetic nervous system, control the two main determinants of energy balance-energy intake and energy expenditure. While this feedback regulatory loop is well established in rodents, there are many unsolved questions about its applicability to body weight regulation in humans. The rate of leptin production is related to adiposity, but a large portion of the interindividual variability in plasma leptin concentration is independent of body fatness. Gender is an important factor determining plasma leptin, with women having markedly higher leptin concentrations than men for any given degree of fat mass. The ob mRNA expression is also upregulated by glucocorticoids, whereas stimulation of the sympathetic nervous system results in its inhibition. Furthermore, leptin is not a satiety factor in humans because changes in food intake do not induce short-term increases in plasma leptin levels. After its binding to LRb in the hypothalamus, leptin stimulates a specific signaling cascade that results in the inhibition of several orexigenic neuropeptides, while stimulating several anorexigenic peptides. The orexigenic neuropeptides that are downregulated by leptin are NPY (neuropeptide Y), MCH (melanin-concentrating hormone), orexins, and AGRP (agouti-related peptide). The anorexigenic neuropeptides that are upregulated by leptin are alpha-MSH (alpha-melanocyte-stimulating hormone), which acts on MC4R (melanocortin-4 receptor); CART (cocaine and amphetamine-regulated transcript); and CRH (corticotropin-releasing-hormone). Obese humans have high plasma leptin concentrations related to the size of adipose tissue, but this elevated leptin signal does not induce the expected responses (i.e., a reduction in food intake and an increase in energy expenditure). This suggests that obese humans are resistant to the effects of endogenous leptin. This resistance is also shown by the lack of effect of exogenous leptin administration to induce weight loss in obese patients. The mechanisms that may account for leptin resistance in human obesity include a limitation of the blood-brain-barrier transport system for leptin and an inhibition of the leptin signaling pathways in leptin-responsive hypothalamic neurons. During periods of energy deficit, the fall in leptin plasma levels exceeds the rate at which fat stores are decreased. Reduction of the leptin signal induces several neuroendocrine responses that tend to limit weight loss, such as hunger, food-seeking behavior, and suppression of plasma thyroid hormone levels. Conversely, it is unlikely that leptin has evolved to prevent obesity when plenty of palatable foods are available because the elevated plasma leptin levels resulting from the increased adipose tissue mass do not prevent the development of obesity. In conclusion, in humans, the leptin signaling system appears to be mainly involved in maintenance of adequate energy stores for survival during periods of energy deficit. Its role in the etiology of human obesity is only demonstrated in the very rare situations of absence of the leptin signal (mutations of the leptin gene or of the leptin receptor gene), which produces an internal perception of starvation and results in a chronic stimulation of excessive food intake.

PMID: 12079865 [PubMed - indexed for MEDLINE]

correlation doesn't equal cassation. I think you know that. While I agree cell size reduces and leptin quantities reduce simulatiously but my argument is with the sentiment that fat cells are the limiting factor here. That's all I'm saying. But remember that you also need less leptin. As far as homeostasis goes it would be silly for your body to keep on pumping out a huge amount of fat reducing hormone without the large quantities of fat. Doesn't mean that what's there isn't used, just that there is less of it.

I could say I have more test levels than my mom but she's got enough of it for what she needs. Same as leptin. I think it's silly to assume levels would stay the same, but i don't think your fat cells are behind maintaining leptin homeostasis when fat is reduced. Just as your gonads aren't responsible for testosterone release frequency or amount. They just do what they're told. Assuming receptors are in working order and free.

Receptor sensitivity is why obese people have high levels of leptin... I think. Different animal but i think it's been speculated that either transport or receptors are the culprit in this regard. I shouldn't be so bold as to state either way if I'm not 100%.


in order for your study to be relevant I'd need to know the connection between adipokine and leptin which I don't (sorry). Assuming adipokine is a limiting factor of leptin (is it?) it would be fat cells -> adipokine -> leptin???? As I said I don't know the connection but that doesn't seem right.

ahhh now this sheds on light on things... I'm not gonna be a complete dick and say this is in mice... but it does cross my mind.

I acknowledge that leptin is released by fat cells... but that doesn't necessarily explain why you have less leptin with small cells does it? I think I'm getting a little confused.

Uh..... you guys should probably go read the Leptin series.

I
II
III
IV
V

huge edit:

I will intake 2000 calories daily, 800 calories from protein, 400 calories from fats, and 800 calories from carbs. Wont this massive increase in calories almost 2 fold to what i would normally consume, cause massive fat gain?

When i cut sgsin i will incorporate refeeds around my workouts.