HCG Diet Analysis, Part IV

“Those who cannot remember their diet history are condemned to repeatedly diet.”   — a SugarFree paraphrase by way of George Santayana

The 800-Pound Gorilla can no longer remain silent. He’s eaten all the bananas, is on a sugar high, and is demanding to speak. Or to at least eat something beside bananas.

You: Are fat. Have been fat. Worry about getting fat again, or even fatter. You’ve tried every diet out there. Grapefruit. Atkins. South Beach. Weight Watchers. Jenny Craig. High Fiber. High Protein. Low Fat. High or Low Everything Under The Sun. Everything worked for a while; nothing worked for long. Absolutely nothing worked forever. Then came HCG. You tried it. It worked great. It didn’t work as good as you’d hoped. You had no hunger. You struggled with hunger. But regardless of what diet you tried, and what success you had or didn’t have, one thing was crystal clear in every diet book, plan or forum where you might have sought help: If it wasn’t working for you, it was your fault, not the fault of the book, plan, or theory. You didn’t understand it. You didn’t do it right. You didn’t do it long enough. Or you did it too long and ruined it. You. Forever You. Never them.

Me: Diet books, Plans and Theories are only good to the extent that they match the reality of YOUR body. This is the one ingredient missing from every diet book, plan or theory — including those that analyze your “blood type,” hair color, age, gender or body shape. That’s because all those things are extraneous to your metabolism, which some theories discuss in the abstract (slow, fast or missing in action), but which never tell you how to figure out what yours is. Exactly. Or, more importantly, how to heal it.

THE FAT FACTS

As Part I in this series illustrates, if you are fat (that is, have excess adipose fat, regardless of weight) you are insulin resistant. Human biology does not allow adipose fat to be stored without insulin, and it only allows adipose fat to be stored in excess if your cells become resistant to insulin’s effects. This is why a Type 1 diabetic (whose pancreas no longer  makes sufficient insulin, or none at all) has to inject it with every meal. Type 1’s do so because only insulin can remove the toxic glucose from their blood — but they must also use insulin because without it they would eventually die of starvation even if they ate thousands of calories a day. Without insulin, food will not be delivered as fuel to cells, which will deplete all adipose fat, and the body will eventually devour even its own muscle tissue and organs. Kidneys, but no fava beans. (Which is a good spot to bid adieu to CICO once more. I’ve decided to call CICO a Zombie Myth. No matter how many times you kill it, it keeps lumbering back to eat your brains).

You may also be leptin resistant, thyroid hormone resistant, or have any number of variations of insulin resistance, like adrenal fatigue or PCOS — or all the above. Every single one of these provides input to your brain to help it decide whether to Burn or Store what you eat. Burn or Store. The only two outcomes the brain can choose, made almost entirely on the basis of the metabolic variables listed above. Given that, doesn’t it make sense that you discover exactly what your variables are, in what stages, and how they affect you? And yet that is the one thing that no book on obesity — not even Good Calories, Bad Calories — suggests you do before deciding how and what, and in what ratios or quantities, you should eat. This not only isn’t very sensible, it’s irrational. Why should I believe that “all I have to do is X,” and that a million other people who don’t have my precise metabolic disorders should also “only have to do X” in order to either get slim, or remain slim? On what planet could that possibly be true?

–800-Pound Gorilla: Planet of the Apes?        –Me: Go eat a banana, I’m talking here.     –800-Pound Gorilla (channeling Eddie Izzard): A ba-na-na? You have an entire fridge filled with food and the best you can do is another bloody ba-na-na?

Fair enough. It’s nearly time to let the Gorilla — representative of all the people who have taken HCG and eaten Simeons’ protocol as is only to lose lots of weight without hunger — have his say. But in order to understand not just why HCG isn’t the active factor, but what is, and to understand why some people (at least 30% according to Simeons) fail to lose either weight or hunger, we should review some basic biology.

So: I’m walking down the street when a stranger turns to me and asks: “Hey, what was your fasting glucose number this morning? Your one and two-hour glucose after breakfast? Your seven-day average? Thirty-day? Your fasting insulin? A1c? Your leptin level, Free T3, Reverse T3, Free T4? Your Total Cholesterol, LDL, HDL and Triglycerides? Pattern A or Pattern B VLDL? APo B from your VAP? Iron and Ferritin levels? And how do they all compare to six months ago?

So I tell her. Could you? If not, you’ve just failed the:

First Law of Losing: To the extent you are insulin resistant is the extent to which any given diet plan will work or not work for you, regardless of its rules.

WHAT FLAVOR IS YOUR INSULIN RESISTANCE?

In order to figure this out, you’ll need the blood tests listed above, and in most cases someone other than your PCP to help interpret them. You’ll also need to buy a cheap blood glucose meter from your local pharmacy, or accept one of the free offers online. Do a bit of research on meter features first, because unless you only have five or so pounds to lose you’ll be using one for a long time. The meters are cheap or free (even the really good ones) because the companies want to sell you their test strips, which are expensive unless you get a prescription for them from your doctor, or buy them online. And you’re going to need a lot of strips.

But I’m not a diabetic, I hear you say. So why use a meter? Well, I’m not diabetic either. But I was fat, and presumably so are you. Which means we are, by definition, insulin resistant. If we are to get permanently slim, we need to see just how insulin resistant we are, and in what way. But the meter will serve another purpose: it will tell us on any given day or hour how well our insulin is working, and how what we just ate is affecting us, including our ability to go into lipolysis and lose fat. Later on we’ll take a look at how to “eat to the meter” in order to help promote weight and fat loss.

But knowing your blood glucose level isn’t sufficient to let us do that. So many times people tell me that despite being thirty pounds overweight, their “doctor says” they’re “fine” because their fasting glucose — usually the only number their doctor measures — is low. However, without looking at the context of that number, without knowing why it’s low, they actually know nothing at all. And the context can only be provided by two additional tests: an A1c and a Fasting Insulin.

The A1c tells you where, in general, your glucose levels have been for the last 90 days. Is your insulin response just enough to keep tight control over them, but not overly high? If not, you can not enter lipolysis, the fat burning stage. Or you can enter it for only brief periods of time. And the longer lipolysis continues (that is, the longer insulin is not present in your bloodstream), the more excess adipose fat you’ll lose.

The Fasting Insulin test tells you whether or not you have large levels of insulin floating in your system most of the time.  If you do, if your FI is over 4 (despite being within a ‘normal lab range’), your high insulin levels are artificially depressing your fasting glucose numbers. Which means that your ‘low’ number not only isn’t good, it’s actually bad. High levels of fasting insulin means you are in some stage of Hyperinsulinemia.

Digression #1: Hyperinsulinemia. IMO, the worst flavor of IR is over-production of insulin, which remains high 24/7. Insulin like that, and at high enough levels, can cause kidney, liver and other organ damage if left untreated. And it often goes untreated because it often goes undiagnosed.

Doctors aren’t taught more than a few minutes worth of knowledge about this in med school, so they usually only order a Fasting Glucose or a an A1c test. When those results come back ‘low or normal’ they tell the patient they’re “fine” and often refuse to order the matching Fasting Insulin test because you “don’t need it.”

The truth is, Fasting Insulin is the yin to Fasting Glucose’s yang. Both are needed on the same blood draw to show the true picture about how well (or not) your body is handling blood sugars. Without one, the other is useless.

Your FG results tell one half of the story: it looks good. Your FI tells the other half: you’ve got way too much insulin in your body at all times, which is often still insufficient to handle even the sugars from a single yogurt parfait or a few pieces of fruit. Left untreated, your skeletal muscle cells will grow ever more resistant to insulin, whose levels will continue to rise until you do something about it.

What is particularly disturbing  is that several people on HCG have now also sent me their recent blood tests for review, and I am starting to see an alarming pattern of
Hyperinsulinemia, often a harbinger of PCOS in women and a precursor of diabetes. For more information see: http://www.healingmatters.com/hyperin.htm

If the 2007 study of HCG is correct, and I believe it is, this pattern makes perfect sense. First, the HCG creates extra new adipose fat cells from proto-fat cells, so there’s lots of new storage tanks to hold adipose fat. Then, eating the Simeons’ protocol as written — with two fruits a day — can make things worse. More and more insulin is raised to continue to handle that fruit (fructose tends to raise insulin rather than blood glucose), but because your skeletal muscle cells are already rejecting insulin’s effects (the essence of IR, and why you got ‘fat’ in the first place), all that glucose will have to be sent down to the liver to be converted into adipose fat, then locked away.

To the extent that you are insulin resistant then, is the extent to which you will struggle with the diet as written, in terms of lower weight/fat loss, and hunger.

But it gets worse. If the condition continues untreated, the liver will also become insulin resistant, and the condition known as Non-Alcoholic Fatty Liver Disease (NAFLD) may begin. This is essentially cirrhosis of the liver without the booze. And there’s an epidemic of it now raging among children in this country, as more and more pediatricians now report of their obese young patients.

Also, your triglyceride levels will begin to soar as the inflammation from all that fat begins to affect your arteries, setting up conditions for higher risk of heart attack or stroke. All in all, not a good destination. So get your Fasting Insulin checked now. End Digression.

However, not every flavor of IR is the same, and Hyperinsulinemia is rare relative to high levels of blood glucose. Example: my fasting glucose and A1c, while slowly creeping up over a few years (101 and 5.2 respectively), was still in the so-called normal range. And my fasting insulin was low: 4. But given how hard it was for me to lose any weight at all (especially adipose fat tissue), it was clear to me — though not my doctor — that I had IR.  And despite my age, my flavor of IR was PCOS. In PCOS, you don’t usually have high levels of  insulin, though you can, but the small amount you do have isn’t doing much of anything. It’s inefficient at handling even the small amount of glucose I produced while eating a high fat, low carb diet. And PCOS is insidious. It raises (and keeps high) Cortisol levels, which also helps raise insulin, which stores fat. And it promotes gluconeogenesis, which converts protein to glucose. Which my inefficient insulin was unable to handle. A vicious circle.

DIET ALONE MAY NOT FIX INSULIN RESISTANCE

A change to a high fat/modest protein/low-ish carb diet may help improve insulin sensitivity, but depending on how broken your metabolism is, and on the number of months or years it’s been broken, pharmacological help is often required to supplement the food.

Research indicated that metformin would be ideal to help break my broken metabolic circle. First, metformin helps to manage and lower Cortisol levels. Second, it stops the enzyme that’s needed for gluconeogenesis. If my self-diagnosis was correct, metformin would fix the PCOS and allow me to lose fat, particularly adipose fat, once more. And it did. It takes a few months for metformin to work, but once it did it lowered my blood glucose and A1c by 6% and I began to slowly lose weight and adipose fat — while eating precisely the same food in the same amounts as before when I couldn’t lose an ounce. That’s because metformin made my insulin work more efficiently. It did its job, then got out of the way. After a year on metformin, my FG is now between 82 and 92, which means my A1c in June will likely be 4.5 – 4.7; truly healthy. And I’ve lost over 30 pounds.

That’s because with metformin’s help (while eating properly) I was able to enter lipolysis more easily and once there, stay all night. And metformin did this without raising my Fasting Insulin or Free Testosterone levels, which I had checked a few months later. Because if your FI or FT rises while A1c lowers, that means your insulin is not working harder at all; your pancreas is simply producing more of it to handle the glucose. Which means you are not only still insulin resistant, your resistance is getting worse. Which is not what you want. At all.

But not all IR medications are equal. A good case in point is Avandia. Which is really a ‘three-fer’ since it, 1: Illustrates the type of medicine many doctors practice today, and 2: Demonstrates a few of the drug’s unfortunate similarities to HCG.

Once upon a time doctors treated patients, not numbers. Patients would describe their symptoms, doctors would research the symptoms to find out what disease might cause them, and then they would prescribe a medication that they hoped would eliminate the disease. Today’s doctors simply order a variety of blood tests that return numbers in or out of a range. If a number is out of range, they prescribe medication that will only cause those numbers to go up or down into range even if the medication does nothing whatever to eliminate the underlying disease, let alone alleviate the symptoms.

This shift came about in the last few decades as new lab tests were created by Big Pharma, who spent billions developing the A1c, lipids and TSH tests to name a few. It is they, not doctors, who choose the ‘normal ranges’ below or above which requires medication.

Digression #2: When hypothyroidism was formerly diagnosed by a select range of symptoms, like low daytime temperatures, always feeling cold and tired, an inability to lose weight, hair loss, etc. — treatment usually consisted of natural, desiccated thyroid hormones. That type of diagnosis and treatment changed dramatically in the last two decades. That’s because Abbott Labs, maker of Synthroid, developed the TSH test.

The TSH test doesn’t measure the health of the thyroid gland (except by inference, since it actually only measures pituitary function), and it certainly does not measure thyroid hormones in any way shape or form. Why use this test then, handicapped as it is, instead of continuing to treat symptoms?

First, it provides a “number on a range” that can be measured and compared. Second, when the “number” is wrong, you don’t have to think about what to prescribe, you just have one medication: Synthroid. And Third, but not least: Abbott Labs funds most Medical Schools all over the country. Especially those schools that award Endo degrees. That’s right. You can look it up. Abbott Labs pays for most medical school funding. They also fund most of the research grants whose studies deal with the thyroid. And amazingly, those studies all seem to show the same thing: TSH tests are good; Synthroid is good, and no dissenting opinions or study grants need apply.

This is why various types of Hypothyroidism are practically a raging epidemic today. But if you don’t have a goiter or another problem with your gland (which is rare), Synthroid treatment will make thyroid hormone problems worse. After all, since thyroid hormone resistance means that T4 is converting to metabolically inert Reverse T3 and not metabolically active T3, the last thing you want to take is more T4! Which is precisely what Synthroid is. Pure T4. End Digression.

But back to Avandia. When Avandia works the way it was designed to work, what it does is remove glucose from the bloodstream very quickly, more quickly than your inefficient insulin. Does this mean Avandia eliminates that glucose by making your muscle cells more insulin sensitive, thus reversing insulin resistance and healing your metabolism the way eating a healthy diet and proper exercise (like weight-lifting, which increases insulin sensitivity) does? It does not. Instead, it removes the glucose from the bloodstream by shuffling it down to the liver, which converts it into triglycerides, then stuffs all that lipid into adipose fat cells. The patient gains weight and fat/inches around the middle, but the doctor is happy because blood sugar numbers are often dramatically lower on the meter.

Followed by a pat on the patient’s shoulder and a “well done; keep it up,” from the Doc. Meanwhile, something more insidious is happening to the patient. Once adipose fat cells are full to bursting, Avandia signals the proto fat cells to become full-fledged fat cells (just like HCG) and begins to stuff them, too. Massive inflammation that affects arterial walls commences. The patient’s diabetes is actually getting worse, but huzzah — those blood glucose numbers are looking good!

Eventually, the insulin resistance in the skeletal muscles moves to the liver (which can often start the process of NAFLD), and then to the fat cells themselves. They are no longer willing to accept insulin’s messages and actions. Blood sugar numbers no longer look so good, and as the diabetes worsens, so too does diabetic neuropathy. Risk for CVD and Stroke grows exponentially. Then people start to die. This is what finally caused the FDA to review Avandia and issue a Black Warning Label for the drug. Of course, what they should have done was yank Avandia from the market, but let’s not allow the practice of good medicine to interfere with political lobbyists and profit. Still, sales plummeted, and now a new ‘act-like’ drugs are in the wings. Which doctors will prescribe in droves, still without doing the proper research on how these drugs actually work. And so medical “progress” marches on.

THE 800-POUND GORILLA WARMS UP IN THE WINGS

Regardless of your IR flavor, two things are imperative: to keep track of what insulin is doing (or not doing) in your body at any given time, and to keep track of what any given food is doing to your insulin, at any given time. That’s where the meter comes in, and it helps to explain why HCG or Simeons’ Protocol (as written) never worked for me. Back in 2009, on one of my long, long stalls (when the variant of the low carb diet that had ‘worked’ for a while suddenly stopped working), I tried it.

At this time I was eating a high fat, low carb diet that ignored calorie intake and had been for years. This meant my body was already ketone adapted (more about which later). Given my research I realized the “load days” were smoke and mirrors designed to let new patients see “high losses” quickly, but those losses were only water. Water added, and caused directly by the carbohydrate loading. Eliminate most of the carbohydrates on Day 3 and afterward, and you eliminate all that excess water in the next few days or week. So I injected without “loading” and followed the protocol.

It was a disaster. The fruit alone added more carbs in a day than I usually ate in a week. Which spiked my insulin. And spikes — when insulin levels rise very high very quickly to deal with a very high and very quick glucose load (made worse because the protocol contains no animal fat to slow the sugars conversion down) — mean two things.

One: blood sugar drops faster than usual as all that extra insulin deals with it faster than usual. So you get hungry. Very hungry. Which is exactly how it’s supposed to work, but on a sped up time-table. If you eat well, ingested sugars will convert to glucose in the bloodstream slowly over many hours. Insulin is raised slowly and steadily to deal with the glucose to deliver the energy to the cells. After many hours have passed, insulin has done its work, you’re out of fuel, your blood sugar drops and your brain sends out hunger signals to get you to eat more food. When your insulin spikes instead, your blood sugar can drop in as little as an hour and your brain sends hunger signals again.

Two: because my insulin levels were now high (higher even than eating plain table sugar would have made it due to the high fructose content of fruit, which raises glucose, yes, but which raises insulin even more), I not only could not get into lipolysis and therefore lose weight, and over the course of several weeks I actually gained fat. Taking more HCG would have made things even worse. It would have created more fat cells into which to stuff all that glucose/lipid (because HCG works like Avandia), which is only a good thing for non-IR pregnant women, as evolution intended. But due to a little thing called biology, it would have done nothing whatever for non-pregnant me in terms of the hunger or the fat gain.

There are many HCG supporters who say that hunger only means “you’re not taking enough HCG!”  Hmm. Let’s see if the efficacy of HCG is in fact “dose-dependent” as many have repeatedly stated when users have complained that HCG “isn’t working for me.” Here’s what Simeons himself has to say about it:

1: “If the daily dose of HCG is raised to 200 or more units daily its action often appears to be reversed, possibly because larger doses evoke diencephalic counter-regulations.”

2: “Of such a solution 0.25 cc. contain the 125 I.U. which is the standard dose for all cases and which should never be exceeded.”

While searching through P&I for this information, I came across yet another instance in which Simeons claims that HCG puts adipose fat into transition (here he uses the word “circulation”), which is a first and separate action from what comes next: liberating the fat after it’s been put into circulation:

“This is because HCG only puts abnormal fat into circulation and cannot, in the doses used, liberate normal fat deposits; indeed, it seems to prevent their consumption.“[Ed. note: as opposed to adipose fat, which Simeons shows is consumed]

In other words, first the one (circulation), and then the other (liberation/consumption). This is Simeons’ description and belief in how HCG works, and as I demonstrated in Part III, neither the description nor the belief was correct. Adipose fat, unlike abnormal gender fat placement when treated with a sex hormone like HCG, never ‘transitions’ or ‘circulates’. Only when the fat cells open via lipolysis does the excess adipose fat convert to ATP (the form in which the body can use it as fuel), after which it’s burned. Thus HCG is not, and can never be the active factor in fat liberation or lack of hunger during a VLCD. I’m just saying.

INSERT 800-POUND GORILLA SCREAMING TARZAN YELL HERE

Wow, that’s loud. I guess being pent-up and forced to listen to me talk for a month will do that. So what about all the folks who take HCG who lose weight on a VLCD without hunger? If it’s not the HCG, which doesn’t meet the “necessary and sufficient” criteria of science, what could it be? I’ve said quite a lot about lipolysis in these pages. Does that meet the criteria? But even if it does, what causes or prevents that process from taking place?

Before we look at why Simeons chose precisely 500 calories a day (and not 350 or 1000, say — which are both very low-calorie), and how he came to decide on precisely which calories could be eaten or not, we must first see what Simeons knew about blood sugars, insulin, and diabetes (the next stage of untreated insulin resistance). He says:

“The so-called stable type of diabetes (Type 2) heavily involves the diencephalic blood sugar regulating center. The diencephalon tries to meet this abnormal load by switching energy destined for the fat-bank over to the sugar-regulating center, with the result that the fat-banking capacity is reduced to the point at which it is forced to establish a fixed deposit and thus initiate the disorder we call obesity.”

In other words, when you’re diabetic (or IR) and eat excess carbohydrates (for you), especially sugar carbohydrates, instead of the resulting glucose being used for fuel it’s turned into adipose fat. He doesn’t mention insulin’s effects here, but later:

“Towards the end of a course or when a patient has nearly reached his normal weight it occasionally happens that the blood sugar drops below normal, and we have even seen this in patients who had an abnormally high blood sugar before treatment. Such an attack of hypoglycemia is almost identical with the one seen in diabetics who have taken too much insulin.”

I’ll bet. Given what we now know about HCG’s adipogenic nature, and the high fructose, insulin-raising propensities of Simeons’ protocol (a lot of fruit as a high proportion of calories eaten, along with a lack of fat in the diet to slow glucose conversion), this isn’t a surprising outcome. After all, it was the over-fat who came for his treatment, which means it was the already insulin resistant who were his patients. Simeons goes on:

“In the course of treatment the possibility of such an attack is explained to those patients who are in a phase in which a drop in blood sugar may occur. They are instructed to keep sugar or glucose sweets handy, particularly when driving a car.”

If this sounds familiar to readers who may have clicked on the link in Digression #1, it’s because this sudden deep drop in blood sugar is indicative of hyperinsulinemia (in which hypoglycemia often plays a part) , and a quick fix is indeed to ingest glucose.

So Simeons was aware of insulin’s effects, diabetes (and thus insulin resistance) and even of hyperinsulinemia. Did this knowledge play a role in his choosing the number of calories to eat, as well as their make-up? I believe it did. After all, according to Simeons it is the low calories that cause the weight loss, not the HCG. I agree. Further, the role of HCG, he states, is to “liberate the fat from the fat cells. When the fat is liberated and burned as fuel it’s as satiating for the patient as if she had consumed many more calories. And when the liberated fat is used for fuel in this way, the patient experiences no hunger. I agree with this too. The Gazillion Dollar Question is: what actually liberates that fat to begin with?

Simeons says early on in P&I that he spent a long time on “trial and error” in coming up with his protocol, and therefore it must be followed precisely in order to work. That is, in order to lose weight without hunger, the patient can eat no more than 500 calories a day, and those calories are laid out in detail.

But of course, that poses an immediate contradiction to Simeons’ theory just above. After all, if  HCG ‘liberates the fat’ regardless of caloric intake or makeup (and he tells us this is true at the beginning of P&I where he describes the “fat boys” who ate what they liked but whose hip fat ‘lessened’ upon HCG treatment), then even if patients eat 500 calories a day of candy bars HCG should open those fat cells, the fat should be liberated and converted to fuel, the fuel should lessen hunger, and with such low-calorie consumption, the patient should lose weight. But now Simeons switches horses mid-stream and claims — without stating so explicitly — that it is the composition of those calories that are crucial to fat loss and lack of hunger. And here again, I agree. In fact, Experiment #1 was designed to demonstrate this very point.

But that still leaves the question of how and why Simeons chose that particular composition to begin with. The answer to that riddle will also explain the “500 calories” number.

If you were a knowledgeable doctor who wanted to induce rapid weight loss in insulin resistant and diabetic patients, what would you have them eat? Fat, of course, and lots of it. Sure, you’d cut out table sugar and candy … but you’d understand that even starch and vegetable carbohydrates are all eventually converted to sugar. Which raises insulin. But fat, unlike protein or carbohydrate does not under most circumstances raise insulin. Even better: when eaten with protein and carbohydrates, fat slows down the conversion process, which slows down insulin production. Which means no insulin spikes. Best of all: animal fat not only suppresses insulin, it suppresses hunger.

Ah, but Simeons was not designing his diet in a vacuum. He created it right when Ancel Keys’ “lipid theory” madness was enveloping the ‘civilized world’ and — FAT KILLS — was often the Headline du Jour. Which was also the time (post WWII) when, as Gary Taubes states in GCBC, scientists were moving from the insulin resistance theory of obesity to CICO. And fat, gram for gram, contains twice as many calories as protein or carbs. So no doctor at that time (and not very many now) would tell a patient to eat a lot of fat and few carbs in order to lose weight. In fact, the Fat Phobia of the time could well explain Simeons proscription against lotions and some shampoos — lest some dreaded fat defy human biology and penetrate the epidural layer before invading the blood cells! — which even he knew had to be nonsense.

This restriction against fat, however, left Simeons with a dilemma. If you remove fat from the diet, all that’s left to eat is protein and carbohydrate, both of which in sufficient quantities, even with table sugar (and its ilk) removed raises insulin, especially in the insulin resistant — his patients. And the presence of insulin prevents lipolysis. Which prevents fat loss.

So even had Simeons started with a “prudent” very low-calorie count of, say, 1200 calories filled with lots of protein (gluconeogenesis) and fruit and vegetables (glucose), weight loss — even with his magical HCG — would have slowed to a trickle. Or worse, patients would have gained fat, as the morbidly obese in locked metabolic wards fed very, very low-calorie diets (that contain no fat but mostly protein and ‘good’ carbohydrate) gain fat.

That meant Simeons had to cut calories so low, that although he was left with only protein and carbohydrate as a result, the total amounts of each were low enough to prevent high insulin levels and thus allow for lipolysis to take place. Gary Taubes does the math on this in his new book, Why We Get Fat, and demonstrates that although fat may be cut by as much as 30% when switching from a typical Standard American Diet to a low-calorie diet, carbohydrates are often cut by as  much as 50%.

What happens to an insulin resistant or Type 2 Diabetic patient who eats such low (in absolute amounts) protein and carbohydrate in the short-term? This: low protein and carbohydrate require less insulin to process their converted glucose into fuel. Lowered  insulin, especially overnight, allows the process of lipolysis to take place. It wasn’t accidental that Simeons dropped breakfast (except for coffee and a tablespoon of milk) altogether. As Dr. Bernstein and other diabetic experts have shown, carbohydrate ingestion during the first meal of the day wreaks more damage to the insulin resistant than at any other time. And of course, by delaying food consumption from dinner the night before until the afternoon of the following day (that is, allowing for a long/er period of time when insulin is not called for), lipolysis can last longer and burn more fat.

So we have two major problems with believing that HCG liberates fat: the nutrient make-up of the calories are as important, if not more so than HCG — and the time frame for ingesting those calories is as important, if not more so. Simeons says:

“The diet used in conjunction with HCG must not exceed 500 Calories per day, and the way these Calories are made up is of utmost importance. For instance, if a patient drops the apple and eats an extra breadstick instead, he will not be getting more Calories but he will not lose weight. There are a number of foods, particularly fruits and vegetables, which have the same or even lower caloric values than those listed as permissible, and yet we find that they interfere with the regular loss of weight under HCG, presumably owing to the nature of their composition.”

This is not the first time Simeons says this. When he speaks of Vegetarians losing weight at half the rate of non-vegetarians (who drink milk instead of eating meat), he says again:

“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.”

If the “nature of the caloric composition” even in a VLCD controls weight loss (that is, fat liberation or not), then HCG simply cannot be the active factor. That would be like saying there’s a magic pill that absolutely, positively liberates and burns fat no matter what — as long, that is, as the moon is blue, you wear purple, and stand on your head in the garden at night when you take it. Oh, and as long as you don’t eat more than 500 calories a day. Oh, and as long as the 500 calories contain no sugar or starch. Oh,  and as long as what you do eat doesn’t spike your insulin. Oh, and …. many more caveats must apply in order for that ‘magic pill’ to work for anyone.

If that’s the case, it’s clear that the pill is no more effective at liberating fat than Dumbo’s feather is effective at helping elephants fly. Is there something else that can explain what truly liberates fat when someone follows the Simeons protocol … even if calorie intake is increased above 500 calories? I believe there is. Lipolysis.

Lipolysis is the true ‘active’ factor in liberating fat from excess adipose fat cells. That’s what it was created to do: open the cells that insulin locked (and in whose presence the cells must remain locked), liberate the fat, convert that fat to ATP (the form of fuel the muscle cells can use), which allows it to be burned rather than stored.

When the fat is burned, the patient feels full even on 500 calories (or none at all, providing sufficient water intake). This is why people who have tried other low carb diets without long-term success can succeed on Simeons. While Atkins induction is very low carb, it is often very high in protein (gluconeogenesis!) — and then after only two weeks more the carbohydrate count is raised. Gluconeogenesis — the creation of glucose from protein, will raise insulin. Which will prevent lipolysis. Which will prevent fat liberation and loss of hunger.

But is lipolysis both necessary and sufficient to this process of fat liberation and loss of hunger? Can it alone explain both, even when more than 500 calories a day are consumed, unlike HCG? Even in the face of higher or lower protein and carbohydrate intake (calorie composition), when that intake is dependent on the particular level of someone’s insulin resistance, unlike HCG? Indeed it can.

Take those morbidly obese folks on the locked metabolic wards of hospitals. Feed them not 800 calories of protein and carbohydrate (which makes them ravenous, and often makes them gain weight, much to the mystery of the researchers who study them, but not you, gentle reader), but 1000 calories of mostly fat with a little protein — and they will lose, not gain weight/fat. Without hunger, since their fat cells would open and “feed” them, just as Simeons stated. Depending on their weight, 2000 calories would likely work as well, though perhaps not as rapidly. No HCG required.

It is to demonstrate these points that our experiment, begun on April 25th, was designed. For the first few days (Stage One), participants (all on HCG),followed Simeons’ protocol as strictly as they could. Some succeeded a bit better than others, but all of them got closer as the days went on. Those with the highest readings on the glucose meter struggled most with hunger and lack of weight/fat loss; those with the lowest readings struggled least and had the most weight/fat loss (as predicted).

Stage Two will begin on Friday, April 29th and will, I believe, demonstrate that with a simple change in nutrient composition (the idea for which came from Simeons’ own experience with Vegetarians), HCG will fail utterly. That is, I predict that even with a very low-calorie diet of only 500 calories, and even with HCG injections, the following will occur:

1: Fat will not be liberated. At all.

2: Weight loss will cease, and pound/inches gain may be seen.

3: Hunger will return in such force as to be nearly unmanageable.

4: All the above will likely show up as changes on the participants’ glucose meters as well as on their scales.

A THING MAY NOT BE BOTH TRUE AND NOT TRUE SIMULTANEOUSLY

Either HCG does ‘liberate fat’ as it did for the Fat Boys of India, regardless of their caloric and nutrition consumption — OR IT DOES NOT. If it does not, if it fails to liberate fat even in the presence of starvation level calories, and if it fails to reduce hunger (as Simeons absolutely declared it did even for the Fat Boys) then it will be proven to do nothing at all. I believe this is exactly what I believe Stage Two will demonstrate: that as with the Vegetarians who lost weight half as fast as meat eaters, fat liberation and lack of hunger are dependent only on caloric composition. Which, as it turns out, Simeons himself clearly stated.

Stages Three and Four will test my lipolysis hypothesis. Will it, and it alone liberate fat and reduce hunger even in the presence of higher calorie consumption (and without HCG)? Will this process produce even faster fat loss than Simeons protocol as written? We’ll all find out in the next few weeks.

Part V in this series will be published then.