“First they ignore you, then they laugh at you, then they fight you, then you win.” — Mahatma Gandhi
HCG Diet Analysis, Part III
Wherein we prod, poke, examine, analyze, diagnose and then finally lay to rest the theory that HCG is the active factor in Dr. Simeons’ HCG Diet. This will not be pleasant reading for some, so to them and to everyone else who reads this part, I ask only that they try to remember this eternal truth: A thing may not be both true and false simultaneously.
After Dr. Simeons outlines the various symptoms of obesity, he finally arrives at his own theory and outlines its foundation in “The Treatment of Obesity,” in which he states:
“I remembered a rather curious observation made many years ago in India. At that time we knew very little about the function of the diencephalon, and my interest centered round the pituitary gland. Fröhlich had described cases of extreme obesity and sexual underdevelopment in youths suffering from a new growth of the anterior pituitary lobe, producing what then became known as Fröhlich’s disease.”
Here’s what science has taught us since then. First, Fröhlich’s is not a disease, but a syndrome. Second, this Syndrome comes in two varieties: a tumor on the pituitary gland, or a tumor on the hypothalamus. Symptoms for each are slightly different; the tumor on the hypothalamus produces hyperphagia, or raging hunger. Given what we now know about leptin, this is not surprising. The genetic equivalent of Fröhlich’s is Prader-Willi Syndrome (PWS), which “typically causes low muscle tone, short stature if not treated with growth hormone, incomplete sexual development, and a chronic feeling of hunger that, coupled with a metabolism that utilizes drastically fewer calories than normal, can lead to excessive eating and life-threatening obesity.”
In other words, despite taking in fewer calories than one ‘burns,’ through exercise for example, or by eating less and creating a ‘deficit,’ fat is still created despite this deficit of nutrients and is stored rather than burned. So much for Calories In, Calories Out (CICO).
The official PWS website states: “The hyperphagia (extreme drive to consume food) lasts throughout the lifetime.” This is unsurprising, since suggested treatment for PWS includes a deadly low-calorie, low-fat, high carbohydrate diet, guaranteed to keep PWS sufferers obese, yet literally starving throughout their lifetime.
Back to Simeons, who goes on to state:
“It was very soon discovered that the identical syndrome, though running a less
fulminating course, was quite common in patients whose pituitary gland was perfectly normal. These are the so-called “fat boys” with long, slender hands, breasts any flat-chested maiden would be proud to posses, large hips, buttocks and thighs with striation, knock-knees and underdeveloped genitals, often with undescended
testicles. It also became known that in these cases the sex organs could he developed by giving the patients injections of a substance extracted from the urine of pregnant women, it having been shown that when this substance was injected into sexually immature rats it made them precociously mature. The amount of substance which produced this effect in one rat was called one International Unit, and the purified extract was accordingly called “Human Chorionic Gonadotrophin” whereby chorionic signifies that it is produced in the placenta and gonadotropin that its action is sex gland directed.”
So, boys with Fröhlich’s Syndrome of the hypothalamus are first and primarily suffering from sex gland and sex hormone signal disorders. These disorders produce feminine-like appearances, such as rounded hips. Patients are given HCG, whose primary action is sex gland/s directed. Et voila — some improvement results. Moving on, Simeons describes the treatment with HCG injections that produces this improvement, then notes:
“Thirdly … when such patients were given small daily doses they seemed to lose their ravenous appetite though they neither gained nor lost weight. Strangely enough however, their shape did change. Though they were not restricted in diet, there was a distinct decrease in the circumference of their hips.”
Nomad. Nomad. No-mad. Err-or, Err-or, Errr-or. The Changeling, Star Trek, TOS
Let’s parse. Simeons treated “fat boys” in India diagnosed with Fröhlich’s Syndrome (a sexual gland/hormone disorder), with a sex hormone. Despite appetite decrease (to be expected since the HCG restored some signaling to the hypothalamus), despite eating fewer calories, no fat was “liberated,” no weight was lost. No inches were lost either. Instead, the fat abnormally deposited around the male hips that was sex hormone directed, was simply moved to a more gender appropriate part of the body elsewhere. How do we know this? Because if the HCG had ‘liberated’ fat instead of merely transferring it elsewhere, that fat would instead have burned and weight would have been lost.
Thus it must be clear that this outcome (moving fat from a gender inappropriate to a gender appropriate area) is in fact sex hormone specific, and is not related to the abnormal accumulation or loss of adipose fat in any way. Nor does Simeons ever state this directly. But here he does make a great illogical leap and commits his second and third logical fallacy. He says:
“Remembering this, it occurred to me that the change in shape could only be explained by a movement of fat away from abnormal deposits on the hips, and if that were so there was just a chance that while such fat was in transition it might be available to the body as fuel.”
If. Chance. Might. Those are a lot of qualifiers in a single sentence. If you’re going to base an entire treatment for not only reducing obesity, but eliminating it (and the cause of it) on “if, chance and might,” you need to be able to conclusively show that your theory has eliminated all possibility of ‘chance’. As we’re about to see, Simeons never does.
Simeons correctly observes that when a sex hormone disorder is treated with a sex hormone, fat abnormally deposited on the wrong part of the body moves to the gender appropriate part of the body. The fat doesn’t go away, it only moves. We know this because Simeons tells us that the boys, despite eating less, do not lose weight. And that the fat moves because the sex hormone restores (to some extent) sex gland signaling, the breakdown of which deposited it in the wrong place to begin with. His errors here are two.
First is Simeons’ unwarranted and incorrect assumption that abnormal adipose fat accumulation, like gender inappropriate accumulation, is also the result of a sex hormonal disorder that breaks sex gland signaling, and can thus be treated by a sex hormone. The second, most crucial error of assumption is that adipose fat, by such treatment, will then be in transition to another part of the body and therefore available to the body as fuel.
Translation: Since abnormal adipose fat accumulation is not the result of a sex gland or sex hormone disorder, and since it does not move from one gender inappropriate part of the body to a gender appropriate part of the body, adipose fat can neither be treated by a sex hormone nor can a non-existent transition ever make the fat available as fuel. Therefore we must conclude that application of HCG to treat non-gender inappropriate obesity can not meet the conditions that science calls both “necessary and sufficient” to declare one thing the cause of something else.
For example, to prevent AIDS, you would need to know precisely how the virus replicates itself (the ‘necessary’), as well as the knowledge of precisely how to stop that replication (the ‘sufficient,’ since no other knowledge or application would then be necessary). In the case of AIDS, science now has the necessary knowledge, but not the sufficient, to say they have discovered the cause of what will prevent it. Therefore many different treatment methods must be used against the virus after it has infected the body.
But for the prevention of Polio, science eventually satisfied both sides of the equation after much trial and error. We now have a vaccine (the necessary) that when administered, is the sole thing (the sufficient; no other variables are required) to prevent the disease. Nothing else for prevention is required, and thus we can state as a scientific fact that the Polio vaccine is the one and only cause of Polio prevention.
We also now know the cause of Yellow Fever: A human must be bitten by a mosquito that carries the virus (the necessary). The bite transmits the virus to the human (the sufficient). Since the equation is now satisfied, science may state that only one thing (a bite from a yellow fever-carrying mosquito) causes the other thing: Yellow Fever. Mosquitoes that carry the Yellow Fever virus cause Yellow Fever in humans by biting them.
So in order to successfully claim that HCG causes the “liberation” of fat from adipose fat cells, Simeons would have had to prove the necessary: first, that adipose fat is able to and does ‘transition’ from one part of the body to another part of the body; second, that it is the HCG itself (and nothing else) that causes this transition. In the intervening six decades since Simeons’ made those assumptions, science has in fact shown the opposite. Adipose fat is not a sex hormone disorder, but rather a metabolic disorder, which even Simeons himself states clearly in the opening of his book. Therefore adipose fat does not transition from one gender inappropriate area to a gender appropriate area upon being successfully treated. Instead, when abnormally accumulated adipose fat is correctly treated, the fat does not move, but is instead liberated and burned as fuel. Thus we can say with certainty that not only did Simeons fail to prove the necessary, proving it is in fact impossible.
And so Simeons’ leap does not compute. HCG certainly restored some sex hormone signaling in boys with Fröhlich’s syndrome of the hypothalamus, but it did nothing whatsoever to affect their fat loss. But Simeons jumps from Fröhlich’s to metabolic disorder obesity despite the Indian boys’ zero weight or fat loss, and despite the fact that his underlying assumption: that HCG transitions adipose fat and then “liberates” that fat as it moves — is false. But after declaring the false to be true, he goes on to say:
“This was easy to find out, as in that case, fat on the move would be able to replace food. It should then he possible to keep a “fat boy” on a severely restricted diet without a feeling of hunger, in spite of a rapid loss of weight. When I tried this in typical cases of Fröhlich’s syndrome, I found that as long as such patients were given small daily doses of HCG they could comfortably go about their usual occupations on a diet of only 500 Calories daily and lose an average of about one pound per day.”
With no clinical trials that, say, eliminated HCG, but which was low-calorie with varying nutrients (such as high fat, low-fat, high protein, low protein, high carbohydrate, low carbohydrate), Simeons still piles onto his false assumption the loss of weight that comes with every low-calorie diet. He confuses cause with effect. In this case, the true cause of the weight loss — which did not come earlier, with HCG but without an extremely low-calorie diet — is something else entirely, but the effect matched Simeons’ observation: that fat is lost quickly, without hunger, because fat IS liberated and it DOES feed the body.
But even if we imagine that Simeons could have somehow proved the necessaries above, he would still have to have proved the sufficient — that as adipose fat ‘transitions’ from one part of the body to another as a result of being supplied with the sex hormone HCG, only HCG then causes those fat cells to open, release their fat and thereby make it “available to the body as fuel.” Since the first condition of necessary is not, and can can never be met, the second condition of sufficiency can also never be met, and thus causation can never be proved. Simeons’ underlying assumptions were false, and thus any conclusions he drew from those assumptions must also be false. So says Aristotle and Mathematics.
This is why 99% of all the controlled, random double-blind studies (where even the doctors don’t know which patients are receiving the drug, and which are receiving a saline placebo) demonstrated the same thing: HCG is not the active factor in either the weight loss or the lack of hunger. Now we know why HCG could never be the factor: it is neither necessary nor sufficient. If Simeons’ observation that obese people treated with HCG lose fat rapidly and without hunger is true (and it is), then the cause for the fat loss and lack of hunger must be brought about by a different means that is both necessary and sufficient. Another way of looking at this is through a logic trail, in which you must get a ‘yes’ every step along the way to go on, and must have a final yes to logically prove the hypothesis.
Hypothesis: HCG liberates fat first by setting it in transition, then by making it available to be burned for fuel as it moves. The Indian boys were fat? Yes. The Indian boys had a sex gland and hormone signaling disorder that deposited fat inappropriately on their hips? Yes. The Indian boys were given the sex hormone HCG? Yes. The Indian boys had their hip fat move — transition — to a gender appropriate place as the sex hormone HCG re-established hypothalamus signaling? Yes. The boys therefore lost fat or weight as the fat, in transition, became liberated from the cells and was used for fuel? No.
Let’s try it another way. Hypothesis: If you consume fewer calories than you did when you were getting fat (CICO) you will lose weight. The boys were fat? Yes. They had raging appetites and ate a lot? Yes. The boys were given HCG, which “liberates fat” in transition, making it available to be burned for fuel? Yes. The boys consumed fewer calories than they did when they were gaining weight? Yes. The boys therefore lost weight or fat? No.
Let us gently lay HCG to rest once and for all by using Simeons’ own words and observation. In the section Vegetarians, Simeons says:
“To supply them with sufficient protein of animal origin they must drink 500 cc.
of skimmed milk per day, though part of this ration can be taken as curds. As far as fruit, vegetables and starch are concerned, their diet is the same as that of non-vegetarians; they cannot be allowed their usual intake of vegetable proteins from leguminous plants such as beans or from wheat or nuts, nor can they have their customary rice. In spite of these severe restrictions, their average loss is about half that of non-vegetarians, presumably owing to the sugar content of the milk.“
How is this possible? After all, HCG ‘transitions’ fat, then liberates the fat as it moves, yes? Yes. HCG and not a caloric deficit causes this transition? Yes. Thus HCG and not the calorie deficit liberates the fat? Yes. The vegetarians were given HCG? Yes. They were also restricted to 500 calories a day as non-vegetarians? Yes. They lost as much fat and weight, and as rapidly, as non-vegetarians? No.
Simeons even gives the reason for this supposed anomaly. A bad batch of HCG? No. Too many calories (relative to non-vegetarian caloric consumption)? No. It was the sugar content of the milk. In other words, the only difference between the vegetarian and non-vegetarian fat/weight loss was the carbohydrate level in their diets. And what process does a higher carbohydrate level interrupt by raising more insulin? Lipolysis.
As Parts I and II have clearly demonstrated, when fat is indeed liberated via lipolysis — which occurs in the absence of insulin — you must lose (burn) stored excess adipose fat. You must lose weight. If lipolysis goes on longer, you lose more excess weight/fat. If lipolysis is short, you lose less weight/fat, but you still lose. Only if there is no lipolysis at all do you not lose any excess weight or fat and you may in fact add more of both. Clearly, for the “fat boys” of India, no lipolysis took place despite the HCG.
Before moving on to discuss what is the active factor that causes rapid fat loss without hunger even on a severely calorie reduced diet that would otherwise cause hunger and “starvation mode” from kicking in, let me quote Simeons once more: “HCG is never found in the human body except during pregnancy.”
This is true, and yet without HCG, either due to pregnancy or injected, rapid fat loss in men and non-pregnant women — without hunger — is common in many who understand lipolysis and which foods promote it, and which foods prevent it. Could that be the secret of low-calorie fat loss with no hunger? The very particular composition of foods eaten? Foods that either prevent lipolysis (fat storage) or promote lipolysis (fat burn), thus opening the fat cells, liberating the fat and “feeding the body” so that despite caloric deprivation you feel full? Yes, indeed. That is precisely what happens. Lipolysis is the active factor, not HCG. But important questions remain. Can we prove lipolysis is necessary? Can we prove lipolysis is sufficient? And if so, what will guarantee that lipolysis takes place?
On to Part IV, in which the 800-pound gorilla says Hello.
This sounds rather disheartening. esp given that what you propose is that nothing will remove the fat cells and so once fat always fat.
Jonathan, fear not. While it is true that losing a cherished belief (like going from believing the sun revolves around the earth — making humans the pinnacle of the universe — to knowing that it’s the piddly little earth that revolves around the sun, just like all the other planets) is difficult at first, it is the beginning of true knowledge. Because once you know what doesn’t work, you can stop doing/using it and move on to what does work. And I intend to talk about just that in Parts IV and V.
Also, please don’t confuse adding or eliminating fat cells with filling fat cells. Yes, our fat cells are always with us, and always in the same number, but when they are kept skinny and lean — so are we! And in Parts IV and V you will learn precisely how to control what they do, forever. What could be more heartening than that? Thanks for reading!
Very enlightening. Keep writing. 🙂
I’m looking forward to the rest. 🙂
I’m fascinated by your analysis and looking forward to the next installment.
I lost 40 lbs last year using HCG, but I am a bit skeptical about keeping the weight off long term. I doubt that I’ll be able to convince my regular doctor to order the tests you’re advocating, but it’s worth a try, once you’ve completed the series!
Corbow, what I intend to do in Parts IV and V is hand you the Key to the City: the ability to look inside your body at any given moment and to control what it does next. With that key (the tests and tools), you will be able to stay slim forever if you want to. Sure, you’ll first have to diagnose what particular flavor of metabolic disorder you have, and what stage it’s in. And then you may have to correct that if diet alone doesn’t do that, but once you’ve restored full, healthy, metabolic signaling, simply eating great food in the right ratios — for you — is all it will take to keep from gaining any more fat. Because if you do gain a few pounds, it will signal an insulin resistance problem. If it’s just eating badly for a few days, and correcting that corrects the weight gain, no problem. But if you correct the eating and the weight continues the climb, it’s back for more tests and then revision. Hope this makes sense.
I have been following your blog and very interested in what you are writing! I am due for a checkup tomorrow (Tues) and wondering if you recommend having that full leptin panel done now? I have been off hcg for almost 3 weeks (lost 40lbs) and after reading up on Wilson’s syndrome, wondering if I have that too (always had a lower temp as do my 3 kids) along with just a couple of the symptoms. Now in my 50’s with a parent that is diabetic (type 2) but she is just off all meds through diet (not overweight – lost 10lbs though by changing diet) Irish descent (both parents from Dublin). Guess just want your opinion as where to start with dr.
Thanks!!
If you’ve been off hcg for that long, by all means have the leptin panel done … and post the results here if you’re comfortable doing that. I’ll be happy to help interpret them, since doctors tend to rely on ‘ranges’ that are woefully inadequate.
As for Wilson’s Temperature Syndrome (completely different than Wilson’s Syndrome!) there’s an easy way to test:
1: Take your temp with a digital thermometer three hours AFTER getting up for the day. Write the number down.
2: Take your temp three hours after THAT (as long the three hours comes before eating a meal, or 30 minutes after; going a bit more than 3 hours because of a meal is okay). Write that number down.
3: Take your temp three hours after THAT (same rules apply). Write the number down.
4: Average the three numbers. Write that down. A single low or high number means nothing.
5: Repeat for three days. Average the averages. If the average is between 98.4 and 98.6, you don’t have WTS. If it’s lower, you may well have it, but final diagnosis will depend on all the results of the panel.
Hope that helps!
I hope you continue this series and do not become disheartened by the aggressive posturing of some on the hcg forum. I cannot fathom why those packing the six-shooter ad hominems are firing before you’ve concluded the presentation. There indeed may be cause for such an hysterical response then…but it seems premature at this stage.
Having “done” hCG, I am in the camp that believes hCG does *something* based on experiencing a significant decrease in appetite when I tweaked my dose. That said, I am open to considering the merits of what you are offering and I thank you for your time and efforts. I just wish we could get to the meat of it — like someone else posted, I am impatient! 🙂
If I could plug my brain into my laptop and have it all pour out into my blog, I would. 😀 But being merely human I can only write as fast as my klutzy fingers and the number of hours in a day allows. So thank you in advance for your patience.
As for the forum, well, they say hell hath no fury like a well-beloved theory scorned. I don’t mind the attacks (some are quite funny and reveal far more about the attacker than they do about me), but I admit to being a bit disappointed that no one — not a single person — has tackled the logic in my argument itself. I mean, if someone can show me how hcg causes immobile adipose fat to ‘transition’ to another part of the body, please, show me! I’d love to know where my fat is visiting at night. 🙂
As to hcg doing ‘something’ well, you’re going to have a chance to put that to the ultimate test yourself if you have the courage to do the experiment I will lay out in Part IV. If you do, I don’t believe you will ever say “it does *something*” again. Or, I could be proven completely wrong. If I am, I am. We’ll see.
After herding enough nerve to inject myself with hormones (need the smiley that makes the cuckoo sign), I’m certain I would muster the courage to try your experiment. I should note, however, I no longer am on hCG so perhaps that would exclude me from your “study.” I still have significant weight to lose — 40lbs — thus I’m eager to see where your interpretation of relevant data leads and lands.
And, ok, I will be patient. 🙂
Yes, unfortunately in order to do the “hcg experiment” you need to be on hcg. But not to worry, you will be able to try my modified Simeons’ diet, which should also be able to prove that you can lose fat quickly on a reduced calorie diet with the right type of calories, without hunger, and without the need for any hcg whatsoever. I will start that protocol once the entire series is done, and will report the results here, as I hope others who join me will do. I will give the nutrients, the calorie count, etc. as well as explain why these particular calories will work better than the ones Simeons chose — though I do intend to explain why he was sort of boxed into the ones he chose.
I look forward to your joining me then.
Then consider me part of the “modified Simeons diet” team and eagerly awaiting the next installment. (thanks — 🙂 )
I’ll be patient too, well… I will try! I am glad that you aren’t letting the pack at the hcg forum deter you. I’ve gotten good results on the hcg diet so far, but the truth is I am sometimes very hungry. I have never bought into the “fat on the move” concept that fat will magically move from one body part to another, but I do believe that fat cells can become unlocked to burn better. As Covert Bailey used to say, be a better butter burner!
I’ve got about 35 to 40 lbs to lose, and am currently on the hcg so I may be in the perfect position to test with and without hcg. I know how hard it was for me to lose weight prior to hcg, so I will have something to compare it to.
And someday I will be able to eat cheesecake.
Lisa, the only thing on the forum that would upset me is if had been banned, as some of the moderators want/ed to do. Because I hope the information I bring will help at least one person … like someone who despite the ‘hype’ is actually hungry at times while on this diet. I know why you’re hungry (when others are not) and that’s precisely what I’ll write about in Part IV. There is no need at all for anyone to be hungry while losing weight — a lot of weight. I’m glad to hear that you’ll be one of the hcg testers, because if you experience what I believe you will when you try the hcg experiment, you’ll be in a position to say: she’s been right all along and I proved it to myself. Actually, it was Dr. S who gave me the clue on how to design the experiment. Are you on injections or homeopathic drops?
LOL – yes, you will.
I’m doing injections, 150 iu of Ovidac Rx brand.
I’ve been pointing out to the naysayers on the forum that a) you’re posting in a section of the forum where controversy should be expected–it’s called The Boxing Ring for a reason–and b) they’re being as judgmental about your theories as other people have been about HCG.
I’m close to my original goal weight, although I could still stand to lose another 10 lbs. I’d love to be part of your experiment. I’ve been off HCG since the end of October.
I will certainly join in your experiment. I statred the HCG diet using homeopathic pellets. and I was hungry – very very hungry and very very weak, I gave up after 15 days as I could barely walk to the end of my street which, for someone who is a regular exerciser is quite disheartening. I was probably eating about 600 calories, didn’t eat the melba toast, rarely ate the fruit, instead ate more protein and after a week added in coconut oil. I’m now giving it another go with injections because I’m intrigued – I want to see if there really is a difference. On the pellets I felt like I was starving – and I probably was. Eagerly awaiting your next instalment!
Playing devils advocate here (though I’m personally rooting for hcg to be unnecessary to the fat liberation process): so we know that hcg does interact with adipose cells – we know that from the 2007 paper at least – either by causing new cell formation and/or causing the cells to secrete leptin. Once in the body of a non-pregnant human who has multiple systems operating and hormonal signaling and cascades of reactions, I’m not sure what we know about the specific activity of hcg in relation to fat cells.
While the boys with the fat hips might not have been the ideal group to use as an example (since they were not merely suffering from being overweight, but had other issues that impacted fat deposition), they weren’t his target group anyway. It doesn’t seem to rule out hcg interacting with adipose cells in the body of a non-pregnant person and effecting some change – even if the change is a bad one from our perspective, such as increasing the number of fat cells, etc. Do his observations prove hcg was the active factor in liberating the hip fat from the boys – no. Does his absence of proof rule out hcg as a necessary part of some fat liberation process – no. I’m assuming your next section will describe a process in which fat is liberated and hunger is controlled in the absence of hcg, which would indeed show it to be unnecessary for some types of fat burning. Looking forward to it.
Ann, play away. I love playing devils advocate myself … sometimes to myself. 🙂
Correct. To which I will add: secreting leptin, in the face of leptin resistance, will only serve to make you fatter. Probably the point in pregnant women.
Assuming the pregnant women in question are human, they would have the precise same multiple systems operating, hormonal signaling and cascades of reactions – perhaps slightly modified for a bit. The difference is that non-pregnant women should not have hcg (in any quantity) in their bodies to begin with! There is absolutely nothing in human biology to suggest that the adipogenic properties of hcg with regard to creating additional fat cells, are changed in any way because a woman isn’t pregnant.
It doesn’t seem to rule out hcg interacting with adipose cells in the body of a non-pregnant person and effecting some change
IT doesn’t rule that out … but the controlled, random, double-blind hcg diet tests DO rule that out. If hcg was effecting some change — any change at all — that would have shown up on the tests even if the researchers had no idea how hcg was doing what it was doing. There was NO CHANGE whatsoever. None. Zero. Zip.
Agreed. Simeons observations are based on logical fallacies and prove nothing. But that’s okay, that’s what tests are for.
HIS absence of proof does not rule out hcg — but I’m afraid the tests do. That’s what tests are for. However, Simeons himself also ruled out hcg when he described how, even when eating 500 calories and even when getting the injections, Vegetarians did not have the same ‘liberation’. He didn’t say, but by following his own logic — more liberated fat means more hunger control — they must have been more hungry as well] Vegetarians did not therefore burn as much fat. Vegetarians therefore did not lose the same weight, and not by a pound or two, but by HALF. This violates Simeons’ own theory, because either hcg liberates the fat in the face of VLCD — or it doesn’t. And he knew this, because he stated the cause of the difference: more carbs for Vegetarians. The CAUSE. It’s the nutrient make-up of those 500 calories, and NOT the hcg in any way, otherwise the Vegetarians would have lost as much fat as the meat eaters. Any other construct violates logic and reason.
Yes. Part III showed why hcg is unnecessary for fat burning, because it doesn’t, in fact, burn anything. Part IV will show what does ‘liberate’ fat and stave off hunger, and the test I’ve devised for those still on hcg will prove that to them without any further doubt.
Devil refuted? 😀
>>Assuming the pregnant women in question are human, they would have the precise same multiple systems operating, hormonal signaling and cascades of reactions – perhaps slightly modified for a bit>>
Well, but they don’t really have the same signaling and hormone activity, nor should they. I’m just curious if pregnant women have hcg receptors in greater number than non-pregnant folks, have regulatory pathways that work in concert with other pregnancy related hormones that non-pregnant folks wouldn’t have, feedback loops we don’t have, etc. I don’t expect hcg to work in the same way in people across all metabolic circumstances. Or even in the presence of all nutrition input, such as the vegetarians eating more cheese/sugar. Since I don’t know the specific activity of hcg in the presence of certain other hormones/receptors and feedback loops, nutrients, sugars, fats, etc., then I have no way of knowing if the diet of vegetarians interfered with the activity of hcg (either directly or indirectly) or if hcg had nothing to do with weight loss as you’ve indicated.
Ann, you’ve just successfully proved that indeed, hcg does nothing whatsoever for fat loss, thank you.
1: Simeons’ says that regardless of diet, hcg ‘transitions’ fat, and while fat is in transition, hcg opens the fat cells and liberates the fat.
2: He says this in context of the “fat boys” — whose treatment with hcg (despite NO special diet and especially not while on a VLCD) — when he treats them with hcg and their hip fat ‘transitions’ magically away from their hips, which are “reduced in circumference.” In fact is is his “observation” of this effect that leads him to believe hcg would work with the obese. It is the very rationale he gives for why hcg works, and how it works. Remove this, and you remove his theory completely. This is why he worked so hard with the boys to, through trial and error, find the “lowest possible dose” that would provide this same “effect” on anyone from a small person to someone weighing “three hundred pounds.”
3: Therefore he says, apply hcg, transition adipose (rather than hip) fat, open the fat cells, flood the body with fuel, and thus be able to lower caloric intake dramatically — hence causing weight loss — without hunger. He is quite clear that it is NOT the caloric intake that causes the ‘transition’ and ‘liberation’ of fat, only that hcg does both these things and thus allows lower calories with no hunger. It is the lower calories that “causes the weight loss” and not the hcg.
3: Therefore, if hcg works this way, it works. If, on the other hand, the ‘liberation’ of fat is not dependent on hcg — but rather on the calories themselves (as Simeons’ stated was not true) — then hcg does nothing. It is neither necessary nor sufficient (stands on its own to transition/liberate fat regardless of calorie intake, since high calorie intake would only mean that less fat needed to be liberated that day) to explain the ‘liberation’ process.
4: The vegetarians took hcg. Therefore, according to Simeons’ their fat would ‘transition’ and while in transition would be ‘liberated’. The vegetarians ate only 500 calories a day. Therefore, according to Simeons’, a lot of fat would need to be ‘liberated’ to make up the calorie deficit. Therefore also, a lot of fat would be burned for fuel, and a lot of weight would be lost.
5: But, as Simeons’ himself tells us, this never happened. Despite his theory, and caloric deficit, only half the weight and fat was lost. That is a statistically significant difference — and then some.
6: Since two out of the three variables (hcg, VLCD, composition of calories) remained identical to non-vegetarians (whose metabolic processes and pathways for insulin, glycogen, ghrelin, leptin, thyroid hormone, etc. etc. etc. are also identical to non-vegetarians — which is why vegetarians have the highest rate of diabetes in the world, and why India, which has the highest rate of vegetarians, has the highest rate of diabetes in the world), the only conclusion we must draw is that the one change between the two groups is the composition of the calories. One is low carb, one is higher carb.
— Does carbohydrate intake directly affect all the metabolic processes? It does.
— Did it do so in this case? It did.
— Did it do so in a measurable, replicable way? It did.
— Do the scientific facts about precisely how metabolic processes work allow us to have predicted the precise outcome vegetarians experienced? They do.
Therefore, case closed: it is the composition of calories on a VLCD (and how they effect the metabolic processes that either burn or store fat) that are the driving force behind fat liberation, slow or fast liberation, or no liberation — and NOT hcg in any way. Because once you say that hcg works, but only works depending on what you eat and not how much you eat, you have just invalidated Simeons’ own theory about what hcg does, and how it does it.
Lisa, Just returned from Doc. She is a new dr for me (changed to hmo) and had no problem ordering the list of tests EXCEPT Leptin! Arrgghhh. She needed to check with an endocrinologist to find out what the purpose of this test/result was for (I’m guessing so the hmo will cover the cost). I couldn’t help much as I have been following you but not having a medical research background, I could only explain it in very simple terms – not to her satisfaction. I offered to email some info to her which she readily accepted. Problem? I don’t know what to send to her! I have come across a number of studies but not sure if they plead my case as to why I want this test. Any help/direction much appreciated. I do see a naturopath too, and guess I could try to convince her to run the full panel if this doesn’t work out, but it would be sure nice to have it all done (they took 5 vials of blood today – so I’m hoping she ordered it and will deal with the “reasoning” later but who knows).
The best and easiest thing to say is that you believe you have leptin resistance, where leptin is pooling in your bloodstream instead of going up the hypothalamus as it should do. Then say if that’s true, it would very likely be affecting your metabolism, especially in regard to losing weight. I’m assuming that you are overweight because you’re doing hcg, and if so, tell her that a simple leptin level will diagnose that. Docs love numbers. 🙂
You can also google ‘serum leptin level test’ to gather info, as well as leptin resistance. But beware, the first sites that come up won’t be information (there’s still not all that much that you don’t have to pay for at PubMed for instance), but will be books and pills for ‘cures’. Then, if she still won’t listen have her do some research in PubMed, to which the HMO has a prescription.
Now at this point you’ve just told her 100% more than she knows, so either she will be doc who appreciate learning something, or she will balk. If she does, you’ll need to order the leptin test (just that one test, not the whole leptin panel) yourself. I think it’s under $70.
Hope this helps! And don’t forget to let us know the results so we can help with interpretation.
Ok Lisa, here is what I have so far from tests. Everything came back “normal” – help me figure out what is missing and any interpretations. Still don’t have the leptin test though. *Been off hcg for a little over 3 weeks – stabilized with no problems, no cravings, no hunger. Eating about 1500-1800 cal per day, just adding in potatoes, breads now but scale still showing 2lbs below LIW. Still need to drop at least 30 lbs to be under BMI of 25. Was planning R2 for the end of April. All results are better than they were 2 years ago (and 40lbs heavier). I did a modified Simeons – 500-600 cal per day but much more fruit/veg variety and dairy but still low fat. 66 days P2.
FREE THYROXINE 1.02 [0.9 – 1.8]
REVERSE T3 170 [90 – 350]
Missing Free T3
TSH 1.02 [0.3 – 5.5]
SODIUM 140 [135 – 145]
POTASSIUM 4.1 [3.5 – 5.2]
FERRITIN 110 [13 – 150]
INSULIN 11 [3 – 11]
GLUCOSE 102 [64 – *130*]
CHOLESTEROL 190
HDL CHOLESTEROL 59
TRIGLYCERIDES 70
LDL CHOLESTEROL 117 [*30* – 129]
LDL IRANIAN Formula TRUE LDL: **105
http://homepages.slingshot.co.nz/~geoff36/LDL_mg.htm
TRI/HDL RATIO 1.2 [less than .9]
CHOL/HDL RATIO 3.2 [1.5 – 5.0 RATIO]
CRP- CARDIAC (HIGH SENSITIVITY) 2.0 [1.0 – 3.0]
NewMe — I edited your note to keep the important numbers. The good news is your ferritin is fine. As for the rest, there are problems.
1: Thyroid. Even before your Reverse T3 number came in at a whopping 170, I suspected that would be the kind of number we’d see, since it appears that your Free T4 (thyroxine) and TSH are being suppressed. There’s no way to tell precisely how thyroid hormone resistant you are unless you had a Free T3 done in the same draw. If not, you’ll need to go back and do FT3/FT4/RT3 again, all on the same draw.
What this means is that you are starting to show signs of hypothyroidism, of the type classically seen on extended VLCD. Specifically what this means is that instead of your hypothalamus telling your liver to convert T4 into T3, which revs up the speed of the metabolism, it’s instructing the T4 to convert into RT3 instead. Reverse T3 is metabolically inactive, essentially a black hole. And even worse.
The ( ‘ ) molecule on FT3 is what tells the liver how much cholesterol is in your blood, so that the liver (which is responsible for all cholesterol production, arguably one of the most important substances in the human body) can make exactly the right amount to keep your cells surrounded with it and your brain functioning properly. The RT3 molecule is missing the ( ‘ ) (pronounced “prime”) and thus cannot signal the liver, which now has no idea how much cholesterol you have, or how much it should make. Even worse (yep, there’s worse), the RT3 now surrounds the proper cell receptors in the liver like a moat, so even the little FT3 you have, cannot reach them. In other words, this is slowing down your entire metabolism, and combined with what now looks like severe insulin resistance (more on that in a minute), it’s indicative that instead of burning mostly adipose fat, you are in fact now burning muscle and lean muscle mass as you “lose weight.” Finally, if you allow this condition to continue, expect to see your total cholesterol to rise as your liver makes more and more cholesterol to compensate for the lack of signals getting through. Which means that you are putting a lot of unnecessary stress on the liver.
2: Insulin Resistance. First, your fasting insulin, which should be 4 or less (the idiotic lab ranges will be covered in Part IV, believe me). You are nearly 300% higher than that. This means there’s a lot of insulin floating around your system at all times, which is not only inhibiting lipolysis (adipose fat burning), but is artificially depressing your fasting glucose, which is still high. The upper range for a truly healthy non-diabetic is 64 – 95. You’re also missing an A1c, but judging from your glucose, it would be about 5.2 or so. Truly healthy is less than 5.0 and every .1 above that is an order of magnitude higher. In other words, you’re on the way to diabetes. Time to get a glucose meter (I’ll be writing about that in the series too), and start taking your glucose every morning before eating, then 1 hour after the start of a meal, and 1 hour after that. For every meal, every single day. You will have to start “eating to the meter” and Part IV or V will have full instructions of what that means. Luckily, my modified Simeons plan will be precisely what you need to eat, expanded upon once you’re in maintenance.
3: Lipids. Some not so good news there either … though it fits with the profile developing with thyroid and insulin resistance. The only two numbers that matter for gauging cardiovascular health are your HDL (actually not a lipid at all, but a carrier of the lipids. that’s also true of LDL), and your triglycerides, especially in the ratio TRI/HDL. First, the real range for TRI is less than 100. Yours is 70, which is good. HDL for women should really be above 60, and you’re almost there. However, the ratio between them is the true determinant for low or high CHD risk, and low risk is .9 or less. My TRI is 42 and my HDL is 97, so my ratio is .4 — half of the lowest possible risk. Every .1 above .9 is, again, an order of magnitude more risk. And this is borne out by your high CRP of 2.0 — when 1.0 or less is low risk. What this means is that you have inflammation in your arterial system, and probably the beginning of arterial plaque. What raises HDL, lowers TRI and lowers that risk? Only one thing: saturated fat consumption, and lots of it, combined with little to no sugar (and small amounts of fruit, mostly berries) and modest carbohydrate intake. My modified Simeons will provide that as well.
Finally, your actual LDL is not 117 but 105. That’s because the Friedwald (sp?) formula that calculates LDL only works when TRI is 100-400. Anything below or above that requires the use of the new Iranian formula. I gave a link where everyone can plug in their numbers if their TRI is less than 100, and there are pages on the net that will explain how it is calculated. However, given the state of your lipids, your insulin and thyroid hormone resistance and arterial inflammation, I suggest that you get your doc to order a VAP (vertical auto panel) immediately. This is a very sophisticated lipid test that will break down your lipids into the parts that matter. LDL has 5 parts. 1 incredibly bad, 1 not as bad, 2 neutral and 1 very, very good. HDL has three components and one of them is very bad. What you’re looking to find out is whether your bad LDL is light and fluffy and heart protective (Pattern A) or whether it is tiny and dense and deadly (Pattern B). I suspect you are starting to lean toward Pattern B, though you might still be a mix now. This should not be put off; it’s that important.
Not what you wanted (or expected) to hear, I’m sure … but the good news is that you’re in the early stages of everything, there’s time for a complete turn-around — and my modified plan will provide it.
I’m back and I think finishing the post here is the best bet in case there are others that may be helped with this info… I received the free T3 (I think it is the free T3) today which is (cut and paste from my online account):
T3,TOTAL 87 [70 – 170]
Wow…a lot of info to try to figure out but I think I have the gist of it. I have been feeling like I have insulin or thyroid issues for over a year now. I can feel a distinct difference in heart-rate and other metabolic actions in my body when I eat simple carbs and generally have felt awful within about an hour of doing so. Guess that is one reason I have felt so great doing HCG. It does look like my doc ordered everything except the leptin test but maybe you can confirm that for me? Just noticed that you mentioned Ac1 test too – still missing? So a few questions:
1. All of these numbers are much better than I had 2 years ago. Is this due to the weight loss alone?
2. The VLCD was mentioned as problem causing – should I no longer do that as in R2?
3. My hmo requires a dr. reference to see the endocrinologists on staff – should I push for that or wait for your modified plan (would rather take care of this through diet if possible!)
4. Should I still push for the leptin test or can you tell from all these numbers what’s happening there?
5. I remember you discussing in one of the sections, the name of book for resistance training? The person had ordered it on Amazon – can you remember this?
Again, thanks for all the input. REALLY helpful! My last kidlet is off to college in a year and I am finally trying to tackle my own health so I can be around for a long time to come! Patiently awaiting the next installment of the blog 🙂
NewMe, I think the book you are looking for is “Body by Science” ? Lisa has mentioned it in another area.
Thanks Lisa! Yes, that’s it- just couldnt find the convo.
New Me,
Oh how frustrating for you! Total T3 is not the same as free T3. Maybe Sugar can weigh in on whether or not the Total T3 is useful. I have always read that it’s not. It’s more useful to have the Free’s tested (T3 & T4) because that is what is unbound and available to the body.
Thanks ego- darn! I know SF is working away for me so yes, we will see what she says – I may have to get these done on my own if I want them done right.
I congratulate, your idea is brilliant.
Thank you for all your research and helpful advice.
Wow, what great information! Thank you so much for all your hard work in pulling all this research together.
We are a group of folks trying to lose weight and become healthy again. Your site provided us with valuable information to work with. You have done an impressive job and our whole group will be thankful to you.
I’ve been following this blog with great interest, since until now losing weight has been just about impossible for me. I followed the SFP for the last few weeks and it’s a miracle! Not only have I lost weight on the scale, I’ve lost almost 2 inches from my waist. Thank you SugarFree for inventing this, and taking the time to share it with us all. Please write your book soon, I want to buy one for all my friends.
Great subject, very nicely done. Kudos on writing a really informative blog.