HCG Diet Analysis, Part I


Dr. Simeons, a British physician practicing in Rome, first wrote Pounds & Inches (more like a pamphlet at forty-nine pages) that outlined his diet in 1954. The book went through seven more editions, the last published in 1971. The inspiration for the diet, according to Simeons, was the work of  Austrian-American pharmacologist and neurologist Alfred Fröhlich, who treated young patients (with Fröhlich’s Syndrome) with HCG (Human chorionic gonadotropin) in 1901. Thus this diet, if you include its roots, is 110 years old. Yet although its popularity has risen and fallen over the decades, and although physicians have panned it or sold it, there has been very little analysis of it from a scientific point of view.

Certainly enough Gold Standard tests (controlled, random and double-blind) were conducted on HCG as it applies to Simeons’ diet to prove that it does nothing whatever to “liberate abnormal fat” in the people taking it (more about which later), so that anyone who believes in science (rather than anecdote) must trust those conclusions. Worse: an In vitro study published in the 2007 Journal of Endocrinology (In vitro effects of chorionic gonadotropin hormone on human adipose development) shows the very alarming adipogenic (adipose fat building) tendency of the drug, and discusses the newly discovered pathways by which this happens. But. There is an 800-pound gorilla in the room who begs to differ, and it is that gorilla who has been ignored or mocked by the medical-nutritional complex.

Many tens of thousands of people (but a portion of the total diet-following population) report being able to eat only 500 calories a day for up to forty days at a time without hunger. All while losing pounds, and more importantly, a lot of inches around the middle. That is, while losing a lot of adipose fat, and very quickly. Although it’s easy to dismiss the weight loss as the direct result of starvation-level calories, that doesn’t tell the whole story, since lack of appetite (or absence of ravenous hunger) is nowhere taken into account except by inference of a placebo effect. A few thousand people may perhaps have an innate ability to survive on so few nutrients and still have enough energy to get out of bed. A few thousand more might lie about not being hungry to themselves or friends and family. But when we instantly dismiss tens of thousands of people who report the same experience as being liars or fools, it is we who are deceiving ourselves.

It is my hypothesis that there are three or four other processes and variables at work in this diet, unrelated to HCG, which are the true cause of adipose fat release and lack of hunger. I will attempt to show those through logic and through the workings of human biology as it is known today, but which was unknown in Simeons’ time. I also hope to show how Simeons’ made the reasonable leap that it was HCG which was the ‘active’ factor, based on the science known (or not known) at the time he wrote and practiced, but which was also based on his own brilliant deductions of how the human body becomes obese, even though he would not be proven right until many decades later. And I will show where Simeons’ implied, in two different places in his manuscript, that it is not HCG, and could not be HCG that “liberates abnormal fat” and also where he came close to grasping what does, though he probably did not realize his own implications. The science he would have needed to do so — and the tools to measure it — had not yet been discovered.

Finally, I hope to provide not just a newer, more powerful version of this diet, modified only by current scientific knowledge, but also few real tools that people can use in conjunction to the diet to “look inside” themselves to see how they’re doing, without having to rely only on external measurements like mirrors, scales and tape measures. With that will come a simple test I’ve devised (based on one of Simeons’ own observations) that anyone can use at home to prove to themselves that it is neither a placebo effect nor the HCG at work, but something else entirely. Armed with that knowledge, they will then be able to control how fast and how well the modified diet works for them. And since I want to practice what I preach, I will go on that same diet myself and report the results, good or bad, here. Yes, that is n=1, but it will at least be based on how the human body works in regard to food intake, and not the common medical wisdom of the last fifty years. Which has done nothing but given us the rapidly rising twin epidemics of obesity and diabetes.


Dr. Simeons said: “The tendency to accumulate abnormal [adipose] fat is a very definite metabolic disorder, much as is, for instance, diabetes. Refusing to be side-tracked by an all too facile interpretation of obesity, I have always held that overeating is the result of the disorder, not its cause.”

Over half a century later, Gary Taubes said: “Obesity is a fat accumulation disorder. We don’t get fat because we eat too much and exercise too little. We eat too much and exercise too little because we’re fat.”

Even before Simeons’ spoke out against the prevailing medical belief at that time as to the cause of obesity (Gluttony and Sloth! Gluttony and Sloth!), Ancel Keys (a nutritionist, not a scientist) had appeared on the scene. He not only reinforced the mantra, he added the one scary ‘fact’ that would encase Gluttony and Sloth in amber and make it untouchable for the next sixty years: Fat Consumption Brings Death by Heart Attack. The new slogan to incorporate that ‘fact’ was simple, and very effective in making us a nation of  obese, chronically ill, diabetic fat-phobes: “Gluttony, Fat and Sloth Will Kill You!”

In the intervening sixty years we’ve been buried under millions of tons of sugar, corn and grain, which is what you eat when you remove heart-healthy saturated fat from the diet. After all, you must eat something, and since carbohydrates and protein contain about half the calories per gram as fat, if you remove 270 fat calories per day from your diet, or 30 grams, you must add nearly 70 grams of carbs to your daily intake to reach the same calorie level. That’s a lot of additional glucose! And the USDA, a (non-health-based) organization formed solely to represent the interests of the sugar, corn and grain industries, and not the population, was happy to tell us it was precisely what we should do –and what we needed to do. Disregarding science and twisting biology beyond recognition brought rewards: an ever-growing mountain of profit.

A single man, Ancel Keys, lied about his own data, which changed the nature of research grants and government policy on nutrition forever. And in the last half century, though thousands of well-designed and funded studies have attempted to “prove” he was right (that eating fat, specifically saturated fat, raised overall cholesterol, which in turn clogged arteries, which in turn produced heart disease and increased mortality), in spite of rigorous attempts to show this in every way, shape or form, all of these studies in fact showed the opposite. Eat more fat, especially saturated fat and, in the absence of a surfeit of carbohydrates and the elimination of PUFAs (Polyunsaturated Fatty Acids/Vegetable oils), your lipid values improve, your arteries stay soft and flexible, and mortality numbers improve compared to those who are eating the ‘recommended’ diets.

For more on this see: Jan 13, 2010, ajcn.2009.27725, Am J Clin Nutr, a meta-analysis of saturated fat studies done world-wide, that followed 347,747 subjects in twenty-one studies. A huge cohort by anyone’s estimation.

Result: “Intake of saturated fat was not associated with an increased risk of CHD, stroke, or CVD.”

Conclusion: “A meta-analysis of prospective epidemiologic studies
showed that there is no significant evidence for concluding that dietary
saturated fat is associated with an increased risk of CHD or CVD. More
data are needed to elucidate whether CVD risks are likely to be influenced
by the specific nutrients used to replace saturated fat.”

CVD risks are influenced by the specific nutrients used to replace fat? The answer to that query is: yes, indeedy. As scores of controlled random studies have now shown, when you replace saturated fat with carbohydrates, CHD and CVD risk increases. Exponentially, if those carbohydrates are processed sugars, fructose, and particularly HFCS or even worse, agave syrup. Close readings of P&I indicate that although Simeons wasn’t aware of  fructose problems (hence the suggested fruit in the diet, which does its bad work not by raising glucose, but by raising insulin resistance via non-alcoholic fatty liver disease), which were not discovered until later. NAFLD was exceedingly rare then, but is quickly becoming another epidemic, especially in children. But Simeons was very aware of the connection between carbohydrates and insulin resistance, as I’ll try to show in Part II of this post.

You can, and hopefully will read the details of how and why this happened in Good Calories, Bad Calories, about the politics and money behind the details above, and the actual science and biology of obesity. Followed by Barry Groves’ Trick and Treat, which goes into even greater detail on these issues. Since there’s no way I can recapitulate what both authors have brilliantly stated and conclusively proved, I won’t try. The closest I may come is to create a brief “Cliff Notes” that will hopefully provide a useful synopsis until then.


Why do humans get ‘fat’ at all? Not individual humans (the books I’ve listed discuss that at length), but the species. After all, no animals in the wild, herbivore or carnivore, ever suffers from a “metabolic fat accumulation disorder.” You may be a hippo, but you can still shop at mainstream hippo clothing stores. No abnormal accumulation of adipose fat, no plus sizes required. Ditto for elephants, lions, parrots and the great apes. So how did humans get so lucky?

Because adipose fat helped us survive during our evolution. Yes, survive. Many diseases that we now think of as bad first arrived as an adaptive evolutionary process that helped the species survive under specific conditions, and which ended up being so successful in keeping humans alive that the traits and/or genes for these passed down through the generations. Where they proceeded, some of them, to go seriously awry in individuals as conditions changed. For fascinating detail on why diabetes for instance, and hemachromatosis (which produces excess iron in the blood and kills people in midlife if left untreated) first showed up as a disease that saved lives, read Survival of the Sickest: A Medical Maverick Discovers Why We Need Disease by Dr. Sharon Moalem. It’s a page-turner.

Dr. Moalem doesn’t discuss adiposity, but the principle he outlines for other current ‘ills’ that began as survival traits is the same. If you’re out hunting prey for as long as a week, running flat-out without stopping thanks to your new genetic ability to sweat through your now denuded pores, you need fuel to keep going. No point in having that mastodon finally trot by the cave if you’re so weak from hunger you can’t chase it, bring it down, then haul its ten thousand pounds back to the fire to be cooked. And when the pickings have recently been slim, you cannot afford to be weak from hunger. You need a mini-fridge to haul with you on the run, that won’t get in the way and will just be there when you need it. Preferably internal, since you need both hands free for throwing spears and rocks. Enter adipose fat. That is, energy which can be stored as a lipid, then easily converted back to fuel to be burned upon need. No other fat humans acquire in adulthood have precisely those characteristics.

Nature and biology being what they are, the design is simple yet stunning. The one nutritional element that has the capability to store in a fat cell is glucose, a byproduct of carbohydrate consumption. Fat is almost never converted to glucose. Excess protein will be converted to glucose when required by the brain during sleep (in very small amounts) if the body the brain inhabits consumes little to no carbohydrates on a regular basis. That process is known as gluconeogenesis (glucose-newly made), and in a healthy body it’s used for a single, healthy purpose.

But glucose is toxic to humans in the bloodstream. If you can’t get the glucose out in a timely manner, you will die. Enter the pancreas, which produces the hormone insulin, which removes glucose from the bloodstream by shunting it up as fuel to the very muscle cells that are crying out for it. (Man, those mastodons weighed a ton. Four to five tons. Didn’t they know about the “Calories In, Calories Out” theory? If they’d gotten on a treadmill more often they’d probably still exist.) Muscle cells, which hold 80% of the body’s glucose, have receptors designed precisely to allow all the insulin to enter and feed them. But wait, you may be asking, if you use up all the glucose at once, what’s left to store?

Good question. Nature took care of that too. The usual process in a normal metabolism works like this: when the glucose in our blood stream drops completely, the brain sends out signals that we’re low on food. That’s about the time of day when even though you weren’t hungry an hour ago, you begin to ‘wonder’ what you want for dinner. The hormone that starts sending the hunger signals is ghrelin, the counterpoint to the hormone leptin.

Once you start thinking about food in earnest, and maybe start cooking (or sitting in the restaurant) insulin begins to rise. Glucose is so toxic that insulin must already be there waiting for it to arrive. You eat. Conversion of your food to energy starts. If you’re eating a healthy diet: high fat, modest protein, fairly low carbohydrates that are starch, not sugar, only a small amount of insulin is required to remove the glucose in the meal and carry it up to the muscle cells waiting to be fed.  During this process adipose fat cells produce leptin , which crosses the brain-blood barrier and reaches the hypothalamus, which in turn suppresses ghrelin signals, indicating satiety. That’s when you put down your fork, or at least that’s the general idea.

The specifics are a bit trickier. For one thing, in young men with Fröhlich’s Syndrome (not a disease), which I’ll discuss in-depth in Part II, ghrelin levels remain disastrously high, and hyperphagia (the continuous desire to eat) results. The satiety signal never arrives. But in healthy people about a third of the carbohydrate gets immediately shunted off to the liver, where it is converted into triglycerides and temporarily stored as adipose fat. Without going into detail about glycogen and glucagon, the processes that direct and control this, what matters most is that if the insulin carrying the converted glucose to the cells is rejected by them, that ‘energy’ is also sent down to the liver for conversion into fat. Adipose fat. Which is then locked away with the earlier part of the meal, and cannot be accessed or used as fuel. This is insulin resistance, a precursor to diabetes.

What is crucial to know at the moment is that in humans, particularly our early ancestors, this accumulation of adipose fat (from easily and quickly converted carbs, like honey or berries) was highly beneficial. And leptin — the master hormone that rules all other metabolic hormones and functions — played a role in storing some of that carbohydrate as adipose fat. It sent the signal from the fat cells to the hypothalamus, which signals the liver, which controls thyroid hormone conversion. The signal would allow the liver to bump up T4 (metabolically inactive), instead of converting most of it to the metabolically active T3. More T4 than T3: slower metabolism. Some food is stored, not burned. More T3 than T4, more food is burned, not stored. There’s Reverse T3 as well, but that’s a topic for another day. Leptin controls all this (and more), and will be an item of focus in Part II. But the result is that the higher T4 allowed some adipose fat storage to take place in those hunters. A bit of a belly ensued. Just a bit.

So when the hunt was on, and the run required fuel not otherwise available, another process took place: Lipolysis. In the absence of insulin, lipolysis opens the adipose fat cells and allows the fat to come out and be reconverted from triglycerides to free fatty acids so they can ultimately be burned as fuel. And that meant our bit of adipose storage equaled survival. We could chase food down even without food to eat, and have the energy to catch it. We could go without food for a fairly long time and not die of starvation or burn muscle tissue to use as fuel. That was a good thing for our ancestors, but there are a few not-so-good implications for us. It means a hard-wired sweet tooth, for one. And 99% of the time when you fight your brain … you lose.

More bad news for us: To the brain, especially the reptilian section of our brain, adipose fat means survival. It means living just one day longer in the face of starvation, and one more chance to pass down our genes. Adipose fat is precious. And the body is not willing to let go of it easily. At all. In the presence of lipolysis, however, the body has no choice. Even if you are leptin resistant (more about which in Part II) and your brain thinks you are starving even when you’re fat, those adipose fat cells must open when lipolysis takes place. What makes lipolysis take place? The absence of insulin in the face of otherwise insufficient fuel.

This is important to understand. More details in Part II, but the take-away for Dr. Simeons’ work is that without lipolysis, fat can not escape the fat cells. Not even with HCG. And lipolysis can not take place in the presence of insulin. Ever. Not even with HCG. Here is one of the times I’m willing to use the word “fact”. For humans, this is a fact: in the presence of insulin, lipolysis can not take place. Without lipolysis, fat cells will not release their fat.

Is there something in the HCG diet itself that allows lipolysis to take place even where other diets — very low-calorie diets — have failed? Yes! Hint: it’s not HCG.

On to Part II.

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17 Responses to HCG Diet Analysis, Part I

  1. Mary asked:

    I’m about to start hcg round 2, please tell me if I should cut out natural sugar too (the fruits) to see better loss on hcg? I’d like to modify this round to see a bigger drop in the scale. I’m aiming for 35 pounds in 45 days!

    Also if you’re eliminating all natural sugars that come from veggies and fruit (during weight loss attempts) what vitamins do you recommend to replace the nutrition?


    It’s not just a case of cutting out sugars, unfortunately. What I intend to talk about in Part II is (in part) about the tools and tests you need to use before you start the diet. These tools (free or cheap) will allow you to see where you are in terms of insulin resistance. One of the reasons the diet didn’t work for me (aside from the fact that HCG isn’t the active factor in the diet) is that I was already eating low carb yet I was still insulin resistant. The diet provided more sugar than my body was already eating — or could handle — so not only wasn’t I not hungry (I was ravenous), but my blood sugar spiked and I didn’t lose but a trickle of weight. At the time I didn’t give a thought to whether HCG ‘worked’ or didn’t, I only knew the diet itself — as is — would not work for me. It wasn’t until several years later that I came back to it and began to understand (with a lot more biology under my wing) exactly what was going on.

    If you’d rather not wait, go ahead and start. Once my new posts go up you’ll be able to use the tools to see exactly how you’re doing, and then if you want to make any changes. Good luck with reaching your goal!

    • Alicia says:

      ‘Is there something in the diet itself that allows lipolysis to take place even where other diets — very low-calorie diets — have failed? Yes! Hint: it’s not HCG.’

      This is what I don’t understand, I thought the best diet for lipolysis would be high in fat, low in carbohydrate and moderate protein. Simeon’s diet is very low in fat and includes fruit as well as melba toast, admittedly in small amounts but the diet is so low in calories that proportionally it is a fair amount of carbohydrate.

      • Alicia, you’re right. Proportionately the diet as it is contains a high amount of carbohydrate. But the total amount of carbohydrate, relative to a standard diet (which is where many, if not most, users originally start from), it is very, very low. This matters. There are biological ways to ameliorate this, and my suggested modification will do just that.

    • Angela Witham says:

      I would like to know the answer to being on Simeon’s Protocol but replacing fruit with healthy fats as well. I would rather eat less fruit and more of that if I could.

      I cannot wait for Part II. I am so interested in this for when I go into Phase 3/4. Very interesting.

  2. LisaAPB says:

    I guess Mary asked the question that I was going to ask. At first I interpreted if someone doing the hcg wanted to maximize their losses, it sounds like they would drop the fruit and incorporate instead, healthy fats like avocado. Now that I’ve read your response, I’m not so sure.

    Is your diet plan different than the Atkin’s type? Would someone who was on hcg, but followed your proposed diet plan, still lose rapidly?

    • Lisa, my suggested modification to Simeons’ plan will be different than Atkins, which I will discuss in Part II.

      However, someone on hcg who follows the modification should lose adipose fat and inches more rapidly. And they will be able to use a modification of the modification to first stabilize their weight (after 3 weeks on the diet), and then to keep on losing until the next ’round’ if there is one. The fat will come off more slowly in this case, but unlike with the original diet, there should be no need to ‘stop’ losing weight for months at a time. The biological reasons for this will be explained in Part II or Part III (if there is one). The modification will take into consideration various individual levels of insulin resistance, which isn’t done in the original diet plan, nor in Atkins for that matter.

      However, a caveat: as I mentioned in Part I:

      “an In vitro study published in the 2007 Journal of Endocrinology, shows the very alarming adipogenic (adipose fat building) tendency of the drug, and discusses the newly discovered pathways by which this happens.”

      This means that although taking HCG doesn’t work as Simeons’ thought it did (in a beneficial manner as the active factor), and although taking it might not slow down your loss on the diet or the modification of the diet, it has very bad implication for fat gain and thus renewed insulin resistance (and thus increased CHD risk) long-term. I will be discussing the article and its meaning in my next posts. But the question I’d have for you is: if you can do the modification, which will improve insulin resistance and help you lose fat just as quickly with no hunger without the hcg … why take it at all? Just wondering…

      • Ann says:

        I’m not a medical researcher, but ‘in vitro studies’ seem to suggest the interaction between adipose cells and hcg, rather than whatever cascade and regulation happen within the body when all cells, organs, receptors, other hormones, etc are interacting. For instance fat cells are secreting leptin under the influence of hcg, so for those not leptin insensitive – and not pregnant – hunger decreases. What if the sudden rise in leptin without other associated pregnancy hormones changes the signals in the body to halt fat cell production. In vitro you would only have the receptors and the hormones secreted by the fat cells themselves plus the hcg, but in the body you’d have access to all kinds of other factors that could regulate cell breakdown.

        I mean I assume that’s where you’re headed in part II, but it would have to include a hormone that also causes leptin production – and one we can induce through diet alone?

        So we’re cautioned against taking hcg and eating more than our allotted 500 calories. My assumption from that was always that the way hcg behaves in a body consuming a normal life-sustaining amount of calories is different than it behaves in a body facing ‘starvation’…. so while hcg might encourage our bodies to produce fat cells while in feast mode, my understanding was that “somehow” it instead acted to liberate energy from fat cells in times of famine. I thought it was the “somehow” explanation that was a mystery in Dr Simeon’s time – was it acting alone? have an accomplice? stimulate the production of something else? So I’ll be interested to see if your experiment suggests that hcg isn’t necessary at all, or maybe that it is not the active factor but still a necessary player in fat liberation.

        • Ann,

          In Vitro” doesn’t suggest any interaction between anything. An In Vitro study simply means it was done in a lab/test tube rather than in a living organism, which is called an In Vivo study.

          “For instance fat cells are secreting leptin under the influence of hcg…”

          This is incorrect. First, hcg doesn’t influence leptin in any way. I intend to discuss leptin at length in Part II. What it is, and how it actually works. Only discovered 17 years ago, leptin still is not well understood and there is a lot of misinformation that is passed around.

          “so while hcg might encourage our bodies to produce fat cells while in feast mode, my understanding was that “somehow” it instead acted to liberate energy from fat cells in times of famine.”

          As I explained in Part I, only lipolysis can ‘liberate energy from fat cells’ and it can only do that in the absence of insulin. HCG liberates nothing. I will go on to discuss what in the diet does induce lipolysis in Part II, so I hope you’ll keep reading!

      • LisaAPB says:

        If I could do the modification, and have great losses, and all the other wonderful benefits I’ve felt so far under the hcg diet (no joint pain! no skin rash! no headache! thyroid meds reduced, BP reduced) then heck yeah, I wouldn’t take anything I don’t need.

        • Lisa, the benefits you’ve mentioned in addition to the weight loss is direct result of the weight loss, plus getting your insulin resistance under control. And that will be as good, and most likely better, with the modification. Either way, HCG has nothing to do with it.

          I’m so glad you’re having such success!

  3. Mary says:

    When will u post part 2?

    I have to guess ur talking about a glucose monitor, but when u get the results what do u do then? I mean this should just help u understand why ur losing slow or fast…or are u going to give instructions on how to maximize your loss when the results are low? Vs how to bring it down..

    • Mary,

      I’m writing Part II now. When will it be ready? LOL – when it’s done? Sorry, couldn’t resist. I just don’t know how long it will take, because even when it’s ‘done’ I go back and edit/polish for at least a day.

      One of the tools is (among other things) a glucose monitor, and yes, I will be talking a lot (Part III, maybe?) on what to do with the information it provides — but better still — how to change the readings to something far more advantageous to you. And I will also talk about how to massage the diet so that you do get to maximize your losses when you can.

  4. Ann says:

    I know what in vitro means. It means it is not in the body, and therefore the only thing is studies is the interaction of whatever you use in the experiment – in the case of the paper you cited, they used adipose tissue and hcg. Suggesting the experiment observed the interaction between the two.

    “For instance fat cells are secreting leptin under the influence of hcg…”

    This is incorrect. First, hcg doesn’t influence leptin in any way. I intend to discuss leptin at length in Part II. What it is, and how it actually works. Only discovered 17 years ago, leptin still is not well understood and there is a lot of misinformation that is passed around.

    I’m kind of confused because that 2007 study seemed pretty clear on that.

    Results: “Data in Fig. 9 show a significant enhancement of the amount of leptin secreted into the culture media after a 24-h incubation in the presence of 500 or 5000 mU/ml HCG. In addition, the leptin increase observed with 5000 mU/ml HCG (+120 ± 50%, n=6) was similar to that induced by 10 nM 17ß-estradiol (E2; +160 ± 50%, n=6), used as a positive control in these experiments (Machinal-Quenlin et al. 2002a).”

    Conclusions: “Data in Fig. 9 show a significant enhancement of the amount of leptin secreted into the culture media after a 24-h incubation in the presence of 500 or 5000 mU/ml HCG. In addition, the leptin increase observed with 5000 mU/ml HCG (+120 ± 50%, n=6) was similar to that induced by 10 nM 17ß-estradiol (E2; +160 ± 50%, n=6), used as a positive control in these experiments (Machinal-Quenlin et al. 2002a).”

    • My apologies, Ann, I didn’t realize you were citing that precise study. I intend to cover it, but since you bring it up here it’s important for everyone to realize the study was on why pregnant women get fat (with increased adipose fat, not just the weight of the baby). The increased leptin is not a good thing, it has serious long-term obesity and health implications for anyone not pregnant who takes HCG.

      • Ann says:

        That’s so interesting! I am always so amazed at the complicated cycles of the human body. It’s also comforting to know that my 50+ lbs during pregnancy were only partly from Blooming Onions! Looking forward to part III…

  5. Connie says:

    Seriously excellent points here, many thanks.

  6. vosi says:

    I’ve been looking for information on HCG for a while. After a lot of Google-ing, finally I found your website. I guess I was using the wrong search words, because when I finally got it right I saw your site ranked at the top, just under the commercials. Normally the top sites are full of garbage.

    Now that I found you, great info, thanks!

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