Big Cat's Corner: Issue 6!

Read an interesting take on the Ironman, learn all about vitamin A supplementation and much more!
Note: The views and comments in this section do not necessarily reflect those of and its owners.

Editorial: Eyes Deceive & Ironman Musings

With the Ironman results in and the first pictures available for viewing, its seems the entire bodybuilding community is once again abuzz with the discussions of who should have placed where and why those stupid judges got it all wrong again. It's something that sometimes gets the better of me. Now I'm in this thing, I train international athletes and obviously I attend the shows with them, and if time permits I'll watch just about any other show I can.

So I'll be the first to admit that there are indeed judges or even entire judging panels that either have their eyes closed, shouldn't be judging or are giving out placings based on something other than what the eye can see. And God knows I've had many frustrating moments because of it.

But a simple fact remains, that you cannot judge a show from pictures. A lot depends on the photographer, the lighting, the background and so many other factors, how good a picture comes out. And when you look at comparison pictures, everybody just looks the same. Seriously. I was at the Belgian nationals last November, and remember when my star athlete, Philiep van Nuffel, walked out that I was thinking: 'this show is over, give him the trophy and lets go home'.

That's how painfully obvious the difference was. But a few weeks later when I saw the pictures, I could still tell he was better, but he didn't look remotely as head and shoulders above the pack as he did in real life. Which is a real pain in the ass for me as well, cause as a proud trainer you like to show off with your wins and how spectacular they were, how enormous the difference is between your athletes and the rest (or maybe that's just me ?).

But then you have these pictures and they don't accurately represent what happens. Photography is the great equalizer. Everybody looks good in the magazines, even the ones that aren't pro's yet. A picture shows you how good a photographer is, not an athlete.

Now I make a habit of teaching my athlete's and reminding them extensively, never to let their guard down, never to relax. But not everyone does that. And I imagine some pro's with years of experience tend to recognize the moments when it's safe to relax a little.

If someone snaps a picture at that moment, together with an athlete who finished close who is still holding his composure and captions it 'how soft competitor X finished ahead of rock-hard competitor Y is a mystery to everyone', then you are getting a very distorted image.

And no offence to the people who report on these shows for a living, but everyone is biased, and if you are just one person, its easy to let that bias seep in. Now you can hold an entire ethical debate about whether or not the fact that he did relax for two or three seconds doesn't mean he should be placed lower is entirely moot, because for all you know, the other guy was doing it more than he was.

But you don't see it. In the end, the judges score on what they see, and if they are good judges that will be primarily on what the athlete can present, and if you need a tiebreaker, then you can still sneak a peak at the athletes in the rear. That's not always the case, I'm aware of that, why else would I tell my athletes to always keep their guard up?

One judge scores different than the next as well, that's why we have 7 judges and the lowest and highest scores are ejected. What counts mainly is that the judging panel as a whole is consistent in how they score. Some competitions will place emphasis on freakish size (the NOC has a long history of that) while others will judge more on symmetry, cuts and what have you not.

If there is a consistency in that, we as the audience or the competitors, can't question their morality, the panel as a whole did judge in good conscience and presents an order that clearly represents their views, as a panel, on what a bodybuilder should be. Now personally, I find that in most pro shows the panel does an excellent job at doing that, with a few minor exceptions here and there.

Usually those grievances will be more accurately reflected by the attending audience calling the judges everything in the book, rather than by pseudo-experts who only saw a few pictures. Only one show on the pro circuit does an extremely poor job at being consistent, and that is the Mr. Olympia. Always has, and probably always will.

I guess we all sort of suspect something is fishy about that show anyway, but none can quite put their finger on it. On the one hand its very understandable that Ronnie wins his sixth, he was considerably heavier than the year before and was more deserving of this title than the three previous ones. But as usual he was soft as hell. No problem of course, if the judges are consistent in placing the bigger specimen higher.

But that was clearly not the case, because if that were so, then there is no way Dexter could have placed third. Gunther in fifth was insanely bigger than Dexter. I personally like Dexter in third, I would have had him win the show actually, its about time the more cut individuals get their rightful place.

After all, it takes a much bigger heart and more dedicated man to sacrifice a few pounds and suffer a few weeks longer to present a symmetrical, cut and dry physique than it does to show up 5 pounds heavier and totally flat. To me that's not bodybuilding, that's not building at all. Buildings with an unequal distribution of material usually collapse.

But I wasn't at the O, so I won't judge on what the outcome should have been, I have no right of speaking. Merely commenting on the obvious discrepancies in the judging and pointing out that aside from the O, most pro competitions are judged quite well.

So people need to remember when they view the pictures that they are presented with a distorted image. They don't see what the judges see and they don't see what was really there (or not there, like Ronnie's calves, sorry, see what I mean about that bias ?). Commenting on who should have won based on that, is like discussing what your favourite flavour ice-cream is.

Some people are just more photogenic than others. And if it was up to me, and I had to judge by pictures, I'd let Chris Cormier win every year. No matter what shape he is in, he always looks good in pictures.

So on to the talk of the day, the Ironman of course. After this whole dissertation I obviously won't lower my standards and comment on who should or shouldn't have won. But I do have my thoughts. A top 3 of Dexter, Lee and Gustavo is definitely a plus for the more hardworking athletes as opposed to the mass monsters. Dexter seems to show up in perfect shape for every competition.

I'm a little afraid he may be wanting to trademark that a little too much and that in the long run, it will interfere with how much mass he can gain. That's the other side of the coin obviously. You have to keep bringing the package, but you have to give yourself some off-time to grow as well, or else you will just be the same every single competition.

Lee Priest seems to have recuperated nicely from his Mr.O disaster and turned a bad situation good. Realizing he wasn't ready for the O, that gave him plenty of leeway (no pun intended) to perfect and tune his physique for the future competitions, which, judging by his placing, he did quite beautifully. I'm glad to see Lee on the stage and doing well, considering last year he spoke of quitting.

With the disappointing lack of character among the younger pro's, losing any of our older pro's would be a severe blow to the sport. So I hope Lee gets his Top 6 placing again next year at the O. Gustavo, wow, what a surprise. I had thought the Puerto Rican had all but fallen off the world. This is definitely another face I am glad to see again, definitely now that he qualified for the O.

Gustavo, like Cormier, is one of those people who invariably looks good in pictures. One of those truly aesthetic poster-boys of the sport, regardless of what shape he is in. I'm very pleased to hear he is getting his career on track again, and I hope we see more of him.

In fifth, Craig Titus, another one of my favourites. Character-wise that is. A colourful person who likes to speak his mind, and isn't afraid to accidentally put his foot in his mouth either. These are rare characters in top-sports. Usually words are weighed so carefully among athletes. Craig has a top notch physique as well, but he can't seem to get rid of the belly distension and bring a complete package.

I think Craig needs to get himself a new trainer and some new motivation and finally make happen what everyone has always seen in him. Lastly, in tenth place, Ronny Rockel. An athlete I'm watching with hawk's eyes. Ronny won the BPF world championship in 2001. A competition where my star athlete, Philiep van Nuffel, finished sixth.

Two years later, Ronny finishes fifth in the Maximus pro, then disappoints a bit at the NOC, but confirms with good placings at the Dorian Yates Grand Prix and now at the Iron Man. He is sort of the man to watch for me, since being the perfectionist I am, I always believe I should be able to do just a little better than the next guy.

In that regard Ronny is a perfect role model. A hard worker who has come a long way in a short time. And eyeing the IFBB world championships for Philiep at the end of this year (step up from the BPF world champs) he is the marker I'm setting for us. Keep an eye on this one, he has the talent to go a very long way. Good poser, complete physique. Just needs a little more finishing and I think he can start finishing in slots that qualify for the O.

On to the Arnold!

Vitamin A: Cutting Wonder-Drug?

For once I'm not just reporting something theoretical here, or rehashing old information and lacing it with new. I just recently discovered the benefit of using Vitamin A for dieting, as an addition to the current line of dieting aids, both in enhancing actual fatty acid oxidation, and in reducing adipogenic markers.

This time around I'm happy to report however I have plenty of practical information to share, and to let you know that the first trial runs have been absolutely astounding! I have been using it myself, and have implemented in the diets of two of my athletes, and so far its really paying off.

Vitamin A is a cheap and easy to get supplement for nearly everyone and makes a lovely addition to most available cutting supplements available today.

How Does It Work?

Ok, we will refer to Vitamin A, as well as all its metabolites, simply as VitA, to make things easier to understand and cover all this ground quickly and efficiently.

Reduction Of PPARgamma
The first benefit of VitA is the reduction it causes in adipogenic (fat-gaining) markers. We have discussed PPAR's, or peroxisome proliferator activated receptors, a few times in this column before, mainly after the emergence of the use of PPARalpha antagonists, which increase fatty acid oxidation in the liver.

I then commented that a better approach to initiating fat loss may be using PPARbeta agonists, that increase fatty acid oxidation in the muscle, and more importantly the use of PPARgamma antagonists. PPARgamma plays a key role in the development of adipose tissue. Blocking PPARgamma would reduce the effects of transient insulin on fat growth, and somewhat reduce the chance of fat gain on cheat days as well. (For more information read the second part of my 'Physiology of Fat loss' series).

The key was to find a safe, effective, legal and affordable drug that could block the PPARgamma. Vitamin A appears to be that drug. VitA binds other nuclear receptors, namely the retinoic acid receptor (RAR) and the retinoid X receptor (RXR). These receptors, when bound, heterodimerize with other receptor/ligand complexes. That means they hook up with receptors of another sort, such as for instance PPARgamma.

One study (1) looked at the effects of vitamin A deficiency and supplementation on adiposity and activity of PPARgamma2. Rats fed a vitamin A deficient diet showed increased adiposity. In White adipose tissue this led to increase PPARgamma2 activation, which meant an increase in the size of the adipose tissue. In Brown adipose tissue this led to a decrease in PPARgamma2 activation.

This too is not exactly positive, since brown fat cells are metabolically active and BURN fat. More importantly they result in increased calorie expenditure by rendering energy production less efficient via the modulation of UCP1 (thermogenin). When the rats were fed a VitA rich diet, they noticed a decrease in PPARgamma2 activity in all tissues, leading to reduced adiposity and lowered body-weight that correlated with the downregulation of PPARgamma2.

Reduction Of C/EBPalpha SREBP1
This study, as well as another (2) not only confirmed the reduction of PPARgamma2, but also the reduction of other renowned adipogenic markers such as CAAT element Binding protein alpha (C/EBPalpha), an initiator of transcription known to be involved in adipogenesis. The first study also demonstrated a reduction in Adipocyte determination and differentiation dependent factor 1 (ADD1, also called SREBP1 or sterol regulatory element binding protein 1), a factor known to increase adipocyte differentiation (duh!) and gene expression.

Since VitA repressed all these factors it may play a key role in keeping the fat off and promoting an environment more suited to fat loss. It may actually be through a reduction in ADD1 that VitA is able to repress PPARgamma2 (3). In either case the conclusions are definitely in favour of VitA inhibiting adipocyte differentiation and promoting a more suitable fat loss atmosphere (4).

The Role Of VitA In Uncoupling And Thermogenesis
VitA has been implicated as being able to activate Uncoupling protein 1 (5) (UCP1 also called thermogenin) and may increase it by as much as 31% (6)! UCP1 is a protein solely expressed in brown adipose tissue and is solely linked to non-shivering thermogenesis. UCP1 is likewise induced via norepinephrine (predominantly via the beta3 receptor, since brown adipose cells lack beta2 receptors).

What it does is render energy production less efficient. When calories are burned, they normally produce energy (ATP) and some heat. UCP1 uncouples the energy production so that less ATP is manufactured and more heat (thermogenesis). This results in more calories being burned for the same amount of energy being produced. Thus you are burning more fat without having to do more for it.

ATP Molecule

VitA And Norepinephrine Induced Fat Loss
This is a mixed effect. While increased VitA shows no apparent effect on NE or NE-induced fat loss, a depletion of VitA shows both an increase in NE release, but a decrease in NE beta receptors (7) and in the affinity to these receptors. In this regard one could plead that depleting VitA is positive since more NE is released, but since NE excretion was increased significantly as well, there is no reason to assume that this led to more available NE.

On the other hand, an increase in beta adrenoreceptor number is a positive thing, from a fat loss point of view. So sufficient VitA must be present to maintain NE induced fat loss long term. As we will see later, dieting invariably depletes VitA, so there is a definite need for supplementation to maintain beta adrenoreceptor density.

VitA And The Effect On The Somatotrophic Axis
VitA definitely increases growth hormone output. That much we can be sure of, which will eventually lead to somewhat increased fat loss as well. Whether this increase leads to a concomitant increase in IGF-1 and IGF-1 activity, and whether or not this would be beneficial or not remains to be seen.

Especially in combination with glucocorticoids, which would be present in high levels in the latter stage of a diet, VitA has been shown to increase the expression of Growth Hormone releasing Hormone (8) in the hypothalamus. This hormone directly affects the secretion of growth hormone from the pituitary, so an increase here definitely opens a door to possible increases in growth hormone levels.

But this is a genomic effect and would take a long time. VitA seems to increase growth hormone very rapidly. Apparently it does so via a cAMP mediated pathway, directly in the pituitary, resulting in a very fast increase in growth hormone levels (9). In this particular study the pituitary was infused with VitA, and secreted growth hormone within 4 to 8 minutes.

Logically, in vivo it would take a while for the VitA to metabolize and reach the pituitary, but would still result in a fast increase in Growth hormone levels in the serum. No immediate effect is seen on serum levels of IGF-1, but this doesn't mean much. Serum levels are determined largely by hepatic output, so there is no way of telling if there are local increases in IGF-1 in various cell lines.

We do know that there are changes occurring in levels of IGF binding proteins. Mainly slight increases in IGFBP3 (10) systemically, and increases in IGFBP6 as well as decreases in IGFBP5 in osteoblasts (11) . Again the meaning of this is not well known, apart from IGFBP4, which is an entirely negative regulator of IGF-1, the other 5 BP's are both positive and negative regulators of IGF-1, so the effect cannot be determined.

It could be that we are seeing an increase in IGF-1 activity in some tissues, or a reduction. And again, both could be detrimental or beneficial. IGF-1 builds tissues, including adipose tissue, via the same pathways as insulin. Since reducing insulin is generally beneficial to fat loss, so may be reducing IGF-1 activity.

VitA And Insulin Sensitivity
Since VitA also reduces IL6 (12) (interleukin-6) it may have an effect on reducing insulin sensitivity. Since insulin is the primary adipogenic hormone, this too would help create a status more prone to fat loss.

VitA increases fatty acid oxidation in muscle
Do you remember way at the beginning of this paragraph, when I reintroduced you to PPAR's? And I said that instead of targeting PPARalpha agonism, we should be focusing on PPARgamma antagonism and PPARbeta agonism instead as better means of promoting fat loss? Well, it so happens that VitA is not only a safe, cheap and effective blocker of the PPARgamma receptor, it is also an agonist of the PPARbeta receptor (13).

The PPARbeta is the receptor predominantly responsible for turning the mitochondria in the muscle cells to burning fat instead of glucose. Since muscle is largely devoid of PPARalpha, the agonists of that receptor do little if anything, and our liver is already burning fat on a diet. But by using a PPARbeta agonist we increase fat burning capacity in over 50% of our metabolically active tissue.

That's a significant increase in fat burning capacity. Together with its enormous reduction in adipogenic markers, increase in beta receptor concentration, increase in growth hormone release and reduction in insulin sensitivity, that makes VitA a powerful tool in aiding fat loss. A powerful and often overlooked tool.

Why You Need Vitamin A When Dieting

Vitamin A is a fat-soluble vitamin. It is primarily stored in fat cells (14). On top of that comes the fact that its storage is promoted by insulin, and that low insulin means lower storage of vitamin A (15). Low insulin combined with low calories means more norepinephrine, which increases cAMP in the cell. On top of that you may or may not be supplementing with a variety of lipolytic supplements that achieve that increase in cAMP one way or another.

But increased cAMP leads to increased release of Vitamin A (16). Initially this is a good thing, more free Vitamin A to exert an action. But long term this, and especially a combination of these factors will lead to a depletion in Vitamin A stores.

So when you are dieting, you will notice a reduction of Vitamin A as your diet progresses. Insulin is low, cAMP is high, so fat cells store less Vitamin A, and on top of that you may experience a slight reduction in fat cells when dieting as well.

Now reviewing all this data, you will want a higher level of Vitamin A, but your diet seems to be doing the opposite. This makes an extremely good case for additional high dose Vitamin A supplementation. Now I could be giving you the runaround, like some guru's and just provide you with the 'might's' and the 'if's' and all the theoretical background.

But this is something I stand behind squarely. I have not only used additional vitamin A in the diets of some of my athletes, but am currently using it in my diet myself.

How To Supplement Vitamin A

Most people have normal Vitamin A. So I talked this over with some medical professionals on how Vitamin A is normally supplemented and how best to avoid hypervitaminosis. The recommended daily dose for Vitamin A in a normal diet is 5000 Units. Now using 10,000 Units for periods longer than 15 months can already lead to hypervitaminosis.

But apparently doses as high as 45,000 Units are frequently used for shorter periods (2-3 months) without complaint or difficulty. In fact, all the doctor's I consulted seemed to agree that it was invariably safer to use a very high dose for a short period, than a moderately high dose for longer periods of time. On top of that we must remember that, as our diet progresses our storage of Vitamin A is heavily reduced.

So the safe zone for normal patients should definitely be a safe zone for us. That doesn't mean you should immediately hop on 45,000 Units a day of course. A lot depends on how fat you are to begin with and how versed you are at dieting. I have been successfully supplementing with 15,000 to 25,000 Units per day, both in myself and 3 of my athletes. As the diet progresses I may try 30 or even 35,000 per day.

A built-in safety protocol is to supplement with beta-carotene as your preferred form of Vitamin A. Beta-carotene usually gives you an orange discoloration of the skin prior to inducing hypervitaminosis, which could serve as a warning sign that its time to stop, just in case anybody does get the bright idea to go extremely high.

Please keep in mind that all doctors agreed that long term supplementation of Vitamin A, even in moderate doses, can lead to hypervitaminosis. If you are the type of person who diets very long (longer than 3-4 months) or the type that uses products to stay lean year round, vitamin A may not be your thing. In these cases simply making sure you get your RDA should be sufficient.

The Results

At first I was a bit disappointed. My diet didn't seem to start off very well, but the fat has been bugging me and I may have been a bit over eager. A good week into supplementing with Vitamin A (15,000 Units at the time) I suddenly started noticing a change. My mood seemed to improve. I had been going too low in my calories for too fast (a little impatient I guess) and that usually makes me very grouchy, but above all lustless.

You know that feeling when you just don't want to do anything, and whatever you do end up doing gets old real fast? Since the Vitamin A kicked in, bout 8-9 days after starting the protocol, that improved drastically, despite making no changes to diet or supplementation otherwise. I also felt a reduced sense of hunger throughout the day.

I take the Vitamin A in the morning, since your body usually burns more fat than glucose when sleeping anyway, so I figure that's the best time to take a PPARbeta agonist. Soon after my hunger starts going away and this lasts pretty much until the early evening.

Visible results only came recently. But for myself and one of the athletes that's hard to judge unbiasedly because I'm also experimenting with a something else (will fill you in on that in the next paragraph), so I can only speak for the other two people. They seem to be ahead of schedule for now, not that much that I would raise my hands in wonder, but considering it appeared they were having a slow start, the fact that they are ahead at all seems to be quite astonishing.

Will have to watch if the trend continues to make a correct assessment. Especially since Vitamin A doesn't really get depleted till late in the diet. In myself I noticed something strange (though this may be related to something different entirely and should not be taken as anything more than a side note), earlier this week I was down 3 kilo's from my initial weight.

Yesterday I weighed in almost 1.5 kilo's heavier (only 1.5 k reduction from initial weight) but my body-fat measurements had continued to decrease (both by electrical impedance and body calliper). This is literally the first time I have seen an increase in weight of this magnitude during a hypocaloric diet (especially an excessive hypocaloric one like my impatient person is on right now) for a natural person.

But like I said, it could be related to another factor, such as the other experimental change I'm testing right now.


    (1) Ribot J, Felipe F, Bonet ML, Palou A. Changes of Adiposity in Response to Vitamin A Status Correlate with Changes of PPAR 2 Expression Obesity Research 9:500-509 (2001)

    (2) Schwarz EJ, Reginato MJ, Shao D, Krakow SL, Lazar MA. Retinoic acid blocks adipogenesis by inhibiting C/EBPbeta-mediated transcription. Mol Cell Biol. 1997 Mar;17(3):1552-61.

    (3) Kim JB, Wright HM, Wright M, Spiegelman BM. ADD1/SREBP1 activates PPARgamma through the production of endogenous ligand. Proc Natl Acad Sci U S A. 1998 Apr 14;95(8):4333-7.

    (4) Bonet ML, Ribot J, Felipe E, Palou A. Vitamin A and the regulation of fat reserves. Cell Mol Life Sci. 2003 Jul;60(7):1311-21.

    (5) Teruel T, Hernandez R, Benito M, Lorenzo M. Rosiglitazone and retinoic acid induce uncoupling protein-1 (UCP-1) in a p38 mitogen-activated protein kinase-dependent manner in fetal primary brown adipocytes. J Biol Chem. 2003 Jan 3;278(1):263-9. Epub 2002 Oct 31.

    (6) Kumar MV, Sunvold GD, Scarpace PJ. Dietary vitamin A supplementation in rats: suppression of leptin and induction of UCP1 mRNA. J Lipid Res. 1999 May;40(5):824-9.

    (7) Nakano K, Mizutani R. Increased sympathetic nervous system activity in rat spleen and heart following vitamin A depletion. J Nutr Sci Vitaminol (Tokyo). 1984 Apr;30(2):163-70.

    (8) Nogami H, Matsubara M, Harigaya T, Katayama M, Kawamura K. Retinoic acids and thyroid hormone act synergistically with dexamethasone to increase growth hormone-releasing hormone receptor messenger ribonucleic acid expression. Endocrinology. 2000 Dec;141(12):4396-401.

    (9) Djakoure C, Guibourdenche J, Porquet D, Pagesy P, Peillon F, Li JY, Evain-Brion D. Vitamin A and retinoic acid stimulate within minutes cAMP release and growth hormone secretion in human pituitary cells. J Clin Endocrinol Metab. 1996 Aug;81(8):3123-6.

    (10) Raifen R, Altman Y, Zadik Z. Vitamin A levels and growth hormone axis. Horm Res. 1996;46(6):279-81.

    (11) Zhou Y, Mohan S, Linkhart TA, Baylink DJ, Strong DD. Retinoic acid regulates insulin-like growth factor-binding protein expression in human osteoblast cells. Endocrinology. 1996 Mar;137(3):975-83.

    (12) Kozawa O, Tokuda H, Kaida T, Matsuno H, Uematsu T. Retinoic acid suppresses interleukin-6 synthesis induced by prostaglandins in osteoblasts. Prostaglandins Leukot Essent Fatty Acids. 1998 Mar;58(3):215-9.

    (13) Shaw N, Elholm M, Noy N. Retinoic acid is a high affinity selective ligand for the peroxisome proliferator-activated receptor beta/delta. J Biol Chem. 2003 Oct 24;278(43):41589-92. Epub 2003 Sep 08.

    (14) Villarroya F, Giralt M, Iglesias R. Retinoids and adipose tissues: metabolism, cell differentiation and gene expression. Int J Obes Relat Metab Disord. 1999 Jan;23(1):1-6.

    (15) Krempf M, Ranganathan S, Ritz P, Morin M, Charbonnel B. Plasma vitamin A and E in type 1 (insulin-dependent) and type 2 (non-insulin-dependent) adult diabetic patients. Int J Vitam Nutr Res. 1991;61(1):38-42.

    (16) Wolf G. Release of stored retinol from adipocytes. Nutr Rev. 1998 Jan;56(1 Pt 1):29-30.

Leptin: Maybe The Next Big Thing After All?

How Reducing Leptin Fast May Aid Your Diet

After my recent exposé on leptin I was pretty much convinced that leptin would be a non-factor in terms of dieting. I may have been wrong.

Consistent reports of weight reductions being considerably greater when leptin is reduced faster, and data more or less indicating that reducing leptin is more beneficial to weight loss did lead to one experimental hypotheses, namely that we should try implementing a rapid drop in leptin early in the diet, and maintain it, to see if we can attain a faster and more successful weight loss with more muscle mass retained.

The Problem With Leptin

For those who want the detailed low-down, I refer you to my third column, where I did my leptin exposé. It's more detailed, but also more contested. Here I'm largely focusing on what I know for a fact. We know that leptin is secreted by adipose tissue (predominantly) as a signal of triglyceride stores. That means, the bigger your fat cells are, the more leptin they secrete.

This leptin then promotes a number of positive (reduction in appetite, increase NE release) and negative (increased PPARgamma activity, increased glucose uptake) effects as far as fat loss is concerned. The latter leading to the previous hype that leptin was the next big thing in fat loss. When all was said and done, leptin exerted as many negative as positive effects on fat loss, leading me to believe it was again a non-factor.

Just like with the previous hypes over GH boosters and insulin sensitizers. Just another hype. Recently it appears more and more that increased leptin and leptin activity is a predominantly negative factor in fat loss.

It has been established that a low serum leptin level at the beginning of diet was a solid predictor for losing weight faster, and keeping the weight off (1). The study itself hypothesized that leptin is only of insignificant importance to neuroendocrine response on a hypocaloric diet, but it was stangely enough this study that first led me to my hypothesis of reducing leptin for increased weight loss.

On top of that came my concern that leptin, in conditions of low serum glucose, was establishing itself as the prime regulator of most endocrine responses. It was regulating thyroid output directly, but lowering TSH. It was regulating testosterone output directly, but was reducing HPTA functioning and it was effectively increasing cortisol and promoting its release further.

Cortisol Molecule

That meant during the time leptin was sufficiently high and operational, there was no problem. But remember that leptin is a signal of triglyceride content in the fat cell. As you diet, your triglyceride content lowers and leptin release lowers as well. At this point leptin is no longer regulating testosterone and thyroid, and keeping cortisol in check.

And because it totally obliterated TSH and LH release, nothing else is either. Now you have low test and low thyroid and high cortisol, resulting in lower metabolism, less calories burned and more muscle lost. Now the main problem with keeping leptin high is that unless you are directly injecting leptin, its not of much use. Leptin increases are expressed in percentages.

That means the increase is relative to the current level of leptin. The lower your body-fat percentage, the lower your tri-glyceride content, the lower your leptin secretion. That means when you diet, you INVARIABLY LOWER LEPTIN. By keeping leptin higher than normal you are effectively reducing the other hormonal regulators, so that when leptin does drop, and it does, you are experiencing a rapid deregulation of all hormonal markers.

The hypothesis therefore was that if we managed to reduce leptin a lot, right from the start, the other hormonal regulators would remain intact and metabolism could be kept higher, and less muscle would be lost. Of course as with all hypotheses it was just theoretical, until someone tested it.

Further implications that must be considered are that optimal means for fat loss always lower leptin. Since regardless of outcome of this trial, the aim is still to lose the most fast and maintain the most muscle in the shortest time period. Induction of uncoupling and thermogenesis in brown adipose tissue leads to lower leptin, lipolysis and triglyceride secretion in white adipose tissue leads to reduced leptin secretion , higher levels of T3 lower TSH which lowers leptin, higher levels of androgens lower leptin, the list is endless.

Whether their involvement in reducing leptin and leptin activity (lowered insulin sensitivity increases fat loss, insulin and leptin use the same signalling cascade) is what makes them effective fat loss aids, or is simply a by-product of them being effective fat loss aids is largely secondary. As I intend to prove, reducing leptin fast is a major plus, but regardless of that we should recognize that effective fat loss is effective fat loss.


In short, I implemented it. Both on myself and another athlete currently preparing for the semi-finals of the nationals here in Belgium. The idea was to opt largely for those fat loss aids that lower leptin fast and effectively (Vitamin A is one of those, reduces leptin by as much as 65% (2)) and to reduce the intake of nutrients that may positively affect leptin, such as Vitamin E and zinc.

This would be the first diet I EVER did without zinc. So far, this athlete is WAY ahead of schedule. So much, that I've had to moderate his dietary intake so he would not lose fat too fast. He is nearly two weeks ahead of schedule. Some of that is due to the Vitamin A supplementation, no doubt. Since the other two athletes on Vitamin A are slightly ahead of schedule as well.

I reported these findings as an aside on Cutting Edge Muscle, and Lyle McDonald replied and dismissed them as merely being the result of the fat loss aids, that these were responsible for the increased fat loss, and that the decreased leptin was a result (All decent fat loss aids lower leptin (3)).

Before this experiment that was my very point as well, that lowered leptin is a total non-factor in the diet, and that increased of decreased leptin, fat loss remains dependent on the most effective fat loss aids and a good diet. But apart from adding vitamin A, I'm not using any new fat loss aids or a new diet in particular, the primary change was a short depletion of Vitamin E and zinc prior to the diet.

So Lyle's assumption was off. Unless there are certain adipogenic properties linked to vitamin E and/or zinc (zinc has been known to lower thyroid output in chickens (4)) that I'm not aware of, I can only attribute the increased rate of success to the lowered leptin status.

Now fat loss is not that difficult. I hear all kinds of exotic, borderline mad stories about things to do to increase fat loss. I still stick to milder, proven products, a good diet and mental support for all my athletes, and I invariably deliver the driest and most cut athletes to the stage with a diet lasting no longer than 12-15 weeks.

If you think fat loss is harder than that, you are either trying too hard or not hard enough. So the fact that this athlete is ahead of schedule is not of that much consequence to me. Unless I'm ever in a bind, with an athlete that is suddenly called for a guest posing or shoot and needs to prep in a hurry. What was of more significance to me, was rather the confirmation of my hypothesis that when we reduce leptin fast, early in the diet, more muscle can be retained.

This is a young athlete, I don't have much data to compare to, so I can only offer the findings I see in myself, and well, as I stated in my paragraph on Vitamin A, this is the first time I'm seeing an increased gain in mass that is significant, paired with an increased loss in body-fat (measured by callipers and impedance).

I'm not saying this is normal, this could even be happening for a variety of uncontrolled variables I may not be seeing, so you won't hear me propose that because of this I can suddenly gain muscle and lose fat (in fact I HIGHLY doubt it), but it does allow me to state that the combined alteration of adding vitamin A and lowering leptin has led to a better retention of muscle mass for me.

If findings remain this satisfactory at the end of the trial (semi-finals of the nationals are April 18th) then I will be applying these principles in the diets of higher profiled athletes as well.

It has come to my attention that there is a leptin product in the making for obese people that targets leptin sensitivity. Since I know of no way to increase sensitivity of the Ob receptor itself (other than lowering leptin) this means the product will target various downstream targets.

These are the same targets used by insulin. People who are not obese would experience an opposite effect from this. And if you ARE obese or suffer from type II diabetes, which is most likely the case if you are leptin insensitive, you would do wise to search medical assistance and get proper drugs for this condition instead of spending a lot of money on a supplement. Just my 2 cents, and that of the entire medical community of course.


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    (2) Kumar MV, Sunvold GD, Scarpace PJ. Dietary vitamin A supplementation in rats: suppression of leptin and induction of UCP1 mRNA. J Lipid Res. 1999 May;40(5):824-9.

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