EATING: YOUR COMPENSATION AND DEFINITION OF VALUE

Somewhere along the line you were told you suck. You were parented or “friended” into being something other than yourself. You were told to change who you are, otherwise your mom and dad wouldn’t like you, your friends wouldn’t accept you, society wouldn’t praise you, and without someone’s opinion to tell you if you were doing a good job− you’d never know what your value was. In short, your value is externally created. It has to be earned.

When someone says you’re doing great! They add to your value. When someone judges you negatively, they have the power to take from your value. Think about how you react when someone angrily honks their car horn at you. Do you react by feeling angry and defensive? Does that random stranger have the power to make you feel emotionally threatened? Is that because other’s reaction to you is so important to your perceived value? You are at the mercy of other’s judgment, other’s opinion, and other’s validation in order to define your success, the quality of your soul, and the value of your life.

When this type of value based on external approval is instilled from childhood, you’re doomed to believe that how people perceive you is the truth of your value. You’re judged on your religion, what you wear, how you talk, your education, your job, how much money you make, how many friends you have, how big your breasts are, how big your truck is, your children’s success following the rules, and any other definition of value that isn’t necessarily the truth. So eventually we are all the same, wanting the same exact things in life, and we are waiting for someone or something to tell us what to do.

This is why consumerism has become such a large part of our culture. Businesses tell you what services and products you need to feel better about yourself.  They create the illusion everyone is buying it, they slap their logo on what it is and the more people you see with that logo, the more you feel you need to buy it. Some of the most valuable things that increase value are: money− or buying power,  education, where you got your education, your job, your house, your car, your clothes,  your parent’s/childen’s accomplishments on this scale, and your ability to have and attract sex.   The sad part is that if any of those ideals are taken away or lost, you actually believe your value is less.

Because you’ve given outside influence the power to define your value, that influence has the power to control you, your actions, your spending, you motivation, the way you make decisions, and how you perceive yourself.  You don’t have self-worth but instead, money-worth, clothes-worth, religious-worth, sexual-worth, body-worth,  fill-in-the-blank-worth. Those outside influences are what you think brings you happiness, but also are the influences that can be lost to create stress and sadness.

How much of your life was created for you? Decided for you? Directed by something else you thought was in charge of your happiness? What I’ve noticed is that when the most important dictators of your value judge you poorly, the easy way to feel better about it is to seek out another form of validation. For example, if someone in your family is sick (which tests the idea that you were taught happiness comes when there are no problems) and you have to take them to the hospital, do you eat to feel better about it?

When one level of value is decreased, in order to feel better about it you’re going to need to find something else to compensate. How many of you compensate with food? Do you eat to feel better about all of the vulnerabilities in life? Has eating become the only stable emotional reinforcement that only you control? Finding a way to control emotional stability is why we have behavioral addiction.

The question I have is what if you decided your value wasn’t defined by your parents, religion, spouse, children, job, money, and your body? What is your true authentic value?  If you were the creator of your value and didn’t need an action, object, or person to define you, your happiness would be something you create rather than receive.

If you eat to compensate for the vulnerability of the world, I suggest you start by thinking about the things, people, objects, and actions you believe define your value. Recognize why they’ve become such a large part of your identity. Seek to find your identity without those addictions, and from there, allow the inevitable vulnerability and fear of rejection, when you allow yourself to be authentic. No matter what others judge and what their opinion of your value is. This is the foundation of self-worth and is the only true source of happiness that isn’t vulnerable to anything other than existence of life.

IS EATING YOUR EXPERTISE?

How much energy and judgment each day do you give to your weight, what you are eating, the diet you are following (or not), and to your overall value as a person? If I were to throw out a percentage of people I help who spend over 90% of the day thinking about these things, I would say over 85% of my clients are obsessed with their body, diets, and food. It's a co-dependent nightmare.

I remember when I was obsessed. I was so afraid of being fat that most of my waking time I'd think about the food, calories, my strategy of control, the exercise I'd have to do, and everything that needed perfect order so that I'd avoid gaining fat. Fear of fat gain became my identity and my expertise.  How many of you reading this have the same fear, or have opposite fear?

The opposite fear would be not getting to eat again. Wondering what you will be eating next, when you will get the opportunity to eat, feeling sadness over the foods you think you are entitle to but are being denied of, and also fantasising about what you will be eating the moment your diet is over. Is eating your obsession, addiction, and your expertise?

If we lived even just 150 years ago you wouldn't have the access to food the way you do today and eating/dieting/weight obsession wouldn't exist. So what would you be doing with your time then? What are your natural talents and how would you express your creativity? If eating/dieting wasn't your main talent, then what would all of your energy and time go towards? How would you express your uniqueness? What if the time, education, and studying you've put into diet after diet after diet went towards a college education? How many of you would have a PHD? The sad part of being identified by eating, food, dieting, and weight is that you are wasting your authentic talent, creative gifts, and your life away on something that doesn't give to the world, but instead isolates your unique and special gifts away from being exposed. Have you ever considered the amount of incredible power you've given away to eating that could be harnessed toward creating something magnificent?

Looking back I can see the incredible amount of power I had, that was going inward towards fear, isolation, and control. Now, that same incredible power is going outward, manifesting something creative. Each and every person has unique power that shouldn't be defined by food and your body.

The power you think you are receiving from food is in reality, your own power to create. What are you capable of with that power? It's time you find out.

SCARE TACTIC: HAIR LOSS ON THE HCG PROTOCOL

I've observed over one thousand hCG protocols and personally assisted over 500 people through multiple rounds. From what I've observed with patients, daily administering 125 iu of hCG with Dr. Simeons' very low calorie protocol, only 4 people have brought to my attention their hair loss. The first was a trans-gendered woman (male to female). The second was a woman who lost hair during pregnancy and wasn't worried as she knew her hair would grow back. The third patient had a sensitivity to dry climate (after adding back conditioner her hair stopped falling out). And the fourth, started her second round of the protocol while experiencing debilitating stress and depression, she eliminated both proteins from her diet, and she cheated consistently each week with sugar. Needless to say, if we had known the mental state of this fourth patient, we would not have prescribed her a second round of the hCG protocol.

The question I'd like to ask is why are there so many people on the Internet discussing fear of hair loss during the very low calorie protocol? I'm not saying that it doesn't happen, especially when people don't have the appropriate dosage of hCG, when they don't take adequate breaks between rounds, if they don't use nutritional supplementation, if they cheat with sugar type foods, or if they reduce or restrict protein intake to what is less than prescribed. There are great risks for hair loss with such drastic reductions in food intake. However, it is NOT caused by the caloric value of food, but rather abrupt hormonal shifts that may occur, especially when they eat the very low calorie diet without adequate hCG, or if the patient cheats.

There are a couple of issues I will assume happens when someone cheats during the protocol, specifically with a sugar based foods. First, the abrupt rise and fall in leptin would cause a similar reaction to the thyroid and thyroid hormones. This will not help a hair loss matter. Second, the rapid rise in insulin with leptin, creating an increase in testosterone. This might cause androgenic alopecia. Over time, and repeated bouts of cheating during the hCG protocol, the polar shifts in leptin and resulting hormonal dysregulation and inflammation could increase the risk of hair loss for both reasons. On the other side, if hunger is tolerated and persists, sustained drops in leptin causes a rise in cortisol, which would increase the risk for the most aggressive form of hair loss: telogen effluvium.

Because 98% of my observations have been with prescription hCG protocols, I haven't been able to compare the prevalence of hair loss to homeopathic hCG protocols. But one thing I know for sure, because most skeptics of the hCG protocol have no idea how hCG prevents starvation, they assume the typical symptoms of starvation are the risks. However, if hCG stimulates adequate leptin to reduce the risk of starvation, and the very low calorie protocol reduces the risk of problems caused from excess leptin, we could safely assume (when combined with a good multi-vitamin) hair loss associated to hormonal extremes of binging and starving would be minimized.

I've come to believe that in my opinion, people are sensationalizing the risk of hair loss to scare people out of doing the hCG protocol, or they want to manipulate the consumer to do the protocol differently than Simeons suggested. But, I'd like to know what others have observed.  Dr. Simeons discussed the small risk he observed in Pounds & Inches, but I agree with his point of view. The hormonal ramifications of keeping fat are far worse then the risk of keeping hair.

Until we have proper laboratory research we are all speculating, including myself. However, what I do have to use as a reference point are the 4 people who have lost hair, compared to the thousands who haven't.

WHAT HAVE YOU OBSERVED? IF YOU HAVE LOST HAIR, DID YOU CHEAT? DID YOU EXPERIENCE SEVERE HUNGER? DID YOU LOAD PROPERLY? DID YOU ELIMINATE PROTEIN INTAKE? DID YOU TAKE A MULTI-VITAMIN?

Please comment if you've experienced hair loss and what was your experience.

STOP BLAMING FAT FOR BEING FAT

The biggest failure of the weight-loss and diet industry is the fixation on the consequence of fat. Fat causes disease. Fat creates hormonal problems. Fat can make you self-conscious in our superficial culture. WE HATE FAT AND FAT IS TO BLAME. I believe the blame on fat as the problem is very misdirected and is the reason why the majority of people who lose fat, gain it back.

Fat is an organ, not a cancer. It doesn’t release fuel or multiply and create more fat cells without having been stimulated, or demanded to do so. Fat gain is a side-effect, a consequence, a reaction that preserves life and prevents death by continually adapting to maintain fueling balance.

Your fat cells provide the majority of fuel your entire body uses, both at night and during the day. It functions as the body’s most influential fueling source and when adequately provided, fat fuel prevents major drops in blood glucose, which prevents death. On the other hand, when fuel has over-saturated your system, and threatens life, fat provides life saving storage. Miraculously, fat is capable of multiplying to meet incredible stocking demand, adapting quickly to create more storage sites, and preventing death by flooding and drowning in fuel. How does fat know how to do release fuel and stock fuel? Leptin.

The key that unlocks the flood gates to fat fuel is the hormone, leptin. How much fuel is released is relative to how much leptin you have. How much leptin you create is relative to how many fat cells you have. How much fuel you get is relative to how big the fat cells are. The bigger the fat cell, the more leptin produced, which means the more fuel is released. That sounds like a good thing right? Wrong.

The problem arises when there’s more leptin than needed, and fat floods the body with fuel without the need, or demand. This threatens life because of fuel flooding. This is comparable to a clogged drain. The spout releases too much water and the drain can’t remove water as quickly as the spout gives water, which causes a back-up and flooding issue. But the incredible adaptability of the body is capable of creating an overspill hole (the same one you have in your own bathroom sink). The spill hole provides an extra drainage site, and prevents over-flow and drowning. But the overflow fuel must have a place to go and this is where fat’s ability to multiply comes in handy. The more fuel overflow you have, the more fat you create and these new fat cells are bigger and can accommodate more fuel spillage. But let’s not forget, these new and bigger fat cells create more leptin and also release more fuel, creating a higher risk of too much leptin, over-fueling, flooding, and even more fat gain as a life-saving consequence. Remember, leptin doesn’t just seep out of fat without cause. It requires a stimulus.

Leptin is created by fat only when there is a stimulus. Hormones stimulate the release of leptin, but the most influential stimulus daily, is food intake. All food stimulates fat cells to produce leptin, especially sugar. This is where hunger comes in.

Hunger is an alarm signal from the brain, forewarning that there isn’t enough fuel being released from fat because of a drop in leptin. If we use our example of the sink and the water spout, hunger is a sign that the water is almost completely drained, and the sink almost empty. Eating would stimulate leptin to turn on the spout and for fat to release more fuel. Once enough fuel has been released and the sink comfortabley filled, the brain turns off the warning signal, and hunger subsides. The problem occurs when hunger isn’t used, and eating continues. Then there is a risk of fuel overflow, the need for a spill hole, and accommodation for the excess fuel with new fat cells. Fat is miraculous! The real problem isn’t the fat, but is any stimulus that forces fat to release fuel, without need. This is like turning on the water when the sink is already full.  In other words, eating without hunger.

Have you ever been told by a diet to only eat when you are hungry and to stop when hunger subsides? Probably not. That would eliminate your need for whatever they are selling. By telling you when and how much to eat, you are dependent on them, and need to pay them for their information. If you actually relied on your own body, and used the built in mechanism that perfectly gives notice for when and how much to eat, you wouldn’t need anybody.

The problem is that most people in our culture have lost touch with hunger, don’t know what it feels like, don’t know when it goes away, and have no idea how the body communicates it’s need for food. Why? Our emotionally driven food culture, and emotionally driven diet culture. We emotionalize eating excessively, and emotionalize the need for control. To make matters worse, we blame fat for being the problem.

Until we stop blaming fat for excess fuel release, and start pointing the finger at the unwarranted stimulus caused by eating without hunger, we’ll never take personal responsibility. We’ll continue to be at the mercy of our cultural gluttony, and under the control of the diet industry.

Fat isn’t a cancer, it doesn’t just appear out of nowhere. It requires a stimulus to release fuel, and a cause that forces the need to create new fat cells. If you eat without hunger, you are the problem. If you eat until you are full, you are the stimulus. Stop blaming fat, and start taking personal responsibility for putting food in your mouth before the brain tells you it’s necessary.

IF YOU ARE NOT HUNGRY, DO NOT EAT.

LEPTIN RESISTANCE: NOT DURING THE HCG PROTOCOL

I have been asked on numerous occasions why I don't discuss leptin resistance, or even mention the fact that all science speculates that the more leptin you produce the less it works. First, I am not an expert. I am a motivated person who really appreciates explanation for why and how things works. If there isn't an answer I'm not afraid to work to find one that might make some sense of things. Second, the idea that there is leptin resistance is because scientists are still not quite sure why the body is doing what it's doing because there is still an incredible amount of research to be done, and leptin resistance is an easy way to explain that something changes from what we'd expect, which creates a point of diminishing returns. To make this easier to understand: leptin resistance = more doesn't function the same as less.

I see leptin from two angles:
1) Leptin within the endocrine system,
2) and leptin within fat cells for fueling purposes.

The science of leptin began in the brain, observing the function of hunger. When obese mice have elevated leptin levels they won't eat, even when they have an abundance of food available. The feeding behavior of mice is very predictable based on their hypothalamic (brain) leptin levels. Because the method of thought has been (and for most still is) to assume "calories in vs. calories out" all fat people, based on this concept, have to eat more than they expend in a day (which could total more than 4000 calories per day). Scientists have assumed fatter people must be hungry all the time and therefore must be eating, all the time. NOT TRUE. They first hypothesized the more fat a person had, the less leptin they have which is why they must eat all the time. Well, that turned out to be false. The more fat you have, the exponentially higher your leptin levels are.

In order to eat as many calories it requires to gain fat, they speculated there must be a problem with leptin that would force Americans to eat so much. They have to be hungry all the time, so there must be some resistance. Now this is where I have observed the opposite.

The more fat a person has the less hunger they have, and the less they eat relative to their expenditure. Per calorie burned they eat less then their leaner counter parts! (ready why skinny b*tches eat more) Mice may not eat when their leptin levels are elevated, but put a bunch of Americans in a room with food, and there is no discussion of hunger but instead, how good the food must taste, how deserving we are to eat it for whatever reason, and it's free! Eat up! Eating in our culture has NOTHING to do with hunger. NOTHING.

Here's what I've observed: the more fat a person has the less hunger they experience- whether they are on the protocol or not. More fat = less frequency of hunger.  (read my blog on why breakfast isn't as important as we thought it was)

Where leptin resistance does make complete sense is within the endocrine system and team of organs that directly work for and against leptin. As fat cells multiply, and new fat cells are bigger and more explosive than the original fat cells, the amount of leptin a person is capable of producing grows at an accelerated rate. A serious problem occurs when corresponding organs can't grow in size and cannot create the correlated response at the same rate. For example, as fat accumulates and more and more leptin is produced, the pancreas is challenged to match the output of leptin with insulin. As fat cells get bigger, and continue to multiply, the pancreas hits a rate limit that can no longer match the output of leptin, unless the pancreas were to grow in size. There comes a point where it is impossible for the pancreas to excrete insulin at the level that fat is excreting leptin, because fat cells outweigh and outnumber what the pancreas is capable of.  The only solution would be for the pancreas to grow in size (which is impossible) or to inject insulin to match the output of leptin from fat.

On the other hand, if leptin suppresses an organ, the more leptin you have the more suppressed the organ becomes. For example, leptin in the anterior pituitary suppresses the signal to the adrenals. The adrenals stimulate your fight-or-flight response and produce hormones that help you feel active, motivated, and excited. The more leptin you have the more suppressed the activation from the brain is to the adrenals. However, there is a point where the adrenals can't suppress any lower because those organs would die. My point is that each organ that corresponds to leptin has a limit and the more leptin you have there does come a point where that organ can no longer respond. This would be leptin resistance.

Lets discuss leptin and it's function in fat cells. Each fat cell produces over six hormones! Leptin has been the main focus of science because of it's influence on the entire endocrine system, and also because of it's control over fueling from fat cells and energy homeostasis. This is where I believe there is no leptin resistance. Why? Because fat cells can increase in size and can multiply and spread, so there is no limit with the function that leptin has within fat cells for fuel. The more leptin you have the more fuel is released.

THE MORE LEPTIN YOU HAVE THE MORE FUEL IS RELEASED!

There is no cap, no rate limit, no resistance. Otherwise, every obese person would be in continual starvation with severe hunger, have severe drops in blood glucose uncountable times daily, would have muscle wasting, and would have difficulty gaining fat. If there was leptin resistance in fat cells, there would be a limit to how much leptin is created, how much fuel is released, there would be a limit to how much fat is gained, and there would be a bell curve graph to fat's function as more fat is accumulated. This is NOT the case. The curve is an exponential curve, that shows only acceleration. As fat increases, leptin levels increase even more. If fat cells were "leptin resistant" there would be a point of deceleration within the function of fat and this is not the case.

If leptin resistance does not apply to the function within fat cells and energy fueling, then the body has the ability to adapt, to create more fat cells, and to and store more fuel, which would make sense based on the human body's need to survive chronic famine. I believe, based on what I've witnessed and observed through thousands of hCG protocols, fat metabolism doesn't have resistance to leptin which is why hunger is not resistant to leptin either. Hunger is in direct proportion to fueling and is communicated in response to maintain fueling balance. This is why I never force anyone to eat breakfast, meals, or pre-portioned food  because hunger is a better assessment of fueling needs then anything else.  The more fat you have the more fuel you get, the less frequent you experience hunger, and the less hormonal need you have for food. It is that simple.

So I speculate that corresponding organs that cannot grow in size to match fat's growth will absolutely have leptin resistance. Fat on the other hand, has no resistance to leptin due to the fact that as leptin increases so does fat cell count, and so does fat's fueling function.

I COULD BE WRONG, BUT IF I WAS- THE HCG PROTOCOL WOULD NOT MAKE SENSE.

IS EMOTIONAL EATING YOUR NEW RELIGION?

Have you ever attached to something so intensely that you modified your character for it? Did it change the way you talk, dress, act, behave, the people you allow yourself to engage with, and change the direction of your life?  Maybe that something was your parents, your religion, your friends in Jr. High or high school, a boy/girl friend, your spouse, or even drugs, work, education, a hobby, etc.  

When you made the decision (or was forced) to change who you were to match that “something” did you have to memorize or conform to a certain dress code, like specific things, was there a certain music you listened to in order to be liked by others with the same label, or to avoid being different?  Did you give yourself a name such as a “hippie”, “religious name”, “EMO”, “athlete” or any title that lets people know the general list of character traits they should expect from that label? I have− in many areas.

I was raised religious from the day of my birth.  I memorized character traits, language, and uncountable times even called myself by the name of the religion. In other ways, I conformed to my siblings, what they liked− I liked. How they dressed− I dressed.  My sisters played volleyball− I played volleyball. Then in junior high I remember changing the way I held my posture to match the other girls that I thought were “cool”. If I was with a group of people I would change the music I liked to match what they liked, so they’d approve of me. Changing who I was to please other people and to gain acceptance, began the moment I learned about positive and negative reinforcement. And the boundaries I were to follow were blunt and the enforcement was pretty extreme. It makes sense that my self-worth became “others”-worth.  My entire childhood was to please others, which required I define who I was to match other people, so they’d like and accept me.

When I got to college this completely backfired. That’s when my toddler like self-esteem was put to the test. Pre-marital sex in the religion my identity was molded around, was deemed “the next closest sin to murder”.  Within weeks I was propositioned to have sex.  I was so afraid of causing a problem, making the other person mad, hurting the other persons feelings, and fearful that if I rejected to proposition that they wouldn’t like me or wouldn’t continue to be my friend, that I passively accepted. It felt like rape.

I worried that the sex was awful for the other person, and if I did have sex maybe they’d want to be my boyfriend.  It was over in minutes, and the same boy never put the same effort into talking to me again. You could imagine the rejection I felt, but worse, the complete trauma over the fact that I was going to Hell. If my family found out I’d be judged, scorned, and shamed. The event was extremely traumatic and even worse− I felt profound guilt and anxiety over what a bad person I was.   This was the beginning of a downward spiral that ended up in a severe mental illness.

In short, instead of relying on others to define me, I decided I would find a way to feel good about myself and I chose my body. My body became my new religion, family, and friends. I could define what was good and bad and no one else could give or take from my new security. I obsessed over the way I looked, would measure my stomach at least 5 times a day.  I’d exercise an hour on top of the three hours of collegiate volleyball training. I counted calories precisely so at the end of the day, the exercise and caloric intake would end up at zero.  Within three months I lost physical strength to play volleyball, checked out of college, and lost a full-ride scholarship. All for my new “body” religion.

Here I am today, writing about emotional eating rehab, and what do I know? I’m not a therapist or a psychologist. But I do know this: if you’ve been defined by other people, objects, actions, or a belief system, you might want to rethink when that identity was created, why and who defined it for you, and if it came from a place of fear, vulnerability, rejection, or need for acceptance. 

If you could go back in time, could you imagine the person you are that isn’t defined? If you weren’t in a body, what does your soul feel like? If you were reborn into a new body with a new life, would your soul feel the same?  Would you, by choice, recreate the same life you have knowing what you know? Most people would love a do-over, but feel chained to what they’ve already been defined by, and can’t see a way out.

But that isn’t true. The moment I chose not to commit suicide, I realized that the only other way out was to live the same life that existed, as if I was getting a do-over. I had the same family, parents, husband (I got married at 20 during my psychological illness− my poor parents!), and instead of killing myself, I’d be authentic, let go of all definitions they created for me, and allow the incredible atomic bomb of vulnerability,  as they might reject me.  I recognized that allowing that horrific vulnerability was no different than suicide, so I might as well let the world know the real me, and accept any rejection, before I ended this life altogether. 

Who would I be, and if I gained fat− would that make me worse of a person? Would being fat lessen the value of my soul? If not, than my extremist body-religion was misdirected and wrong. I was going to have to find out. That’s when I left the severe safety my body-religion, the religion my parents enforced me to be, the idea that sex made me a bad person, and all that traumatized and falsely defined the value of my soul. I gave nothing the power to define me, because the value of my soul had to existe with nothing. No person, clothing, action, music, hobby, education, and nothing of this visible world could completely define what I felt of myself. That moment of realization, awakened me to a level of consciousness that instantly changed my perception of life forever.

My point− find happiness and love for who you are with nothing. Seek who you are that isn’t definable by the way you look, how you act, what your job is, nor from what you see, hear, or feel.  Recognize that losing weight won’t improve your life (accept that the body you have won’t be so uncomfortable, and may last longer). And if you think once you achieve that thin body that it improves your value, you’re now define by that, and will have intense fear and vulnerability of gaining the fat back. WHAT A NIGHTMARE! This is why I exercised for hours on end, and why I now have severe arthritis at age 34.

 Being thin doesn’t make you a better person, nor should being fat make you less valuable.  The liberty to eat excessively may be your means of gaining freedom from a constraint you really don’t like. The need to restrict food may be a way that you are seeking a new outward definition rather than accepting authenticity.  Think about who you are, move past the superficial definitions, and find what is indefinable.  This is where unconditional love and self-worth starts and where emotional eating or “eating-religion” loses value.    

STARTING OVER WITH FOOD--WITHOUT YOUR PARENTS!

How many of you link your over eating and emotional eating to your parents? There must be some memory you have, sitting at the table, being forced to eat. Or you accomplished something they approved of, wanted to give you positive reinforcement, and rewarded with a cupcake or some other food of their choice. Or maybe you grew up in a large family like myself (9 siblings) and remember the scarcity of food and the frantic feeling when the dinner bell rang. As soon as the blessing was said we were hyenas, fending for ourselves.  I was number 9 of ten children so eating dinner was pretty intense.

Today I’m 34, have three children and a mild mannered husband who eats methodically and slowly. There is no threat of hunger, and no panic over how much food we have to share, and no need to continue to eat so quickly.  Then why do I continue to eat as if I’m an 8 year old girl competing for food with an 18 year old brother, and everyone in between? The more I observe other adults and their eating habits, much of their eating habits started when they lived at home with their parents, and they’ve never considered if those same habits would still apply today.

For example, one woman started eating excessively at 25. It all started after her parents forced her to get an abortion, which was extremely traumatic for her. She chose to go along with the abortion, not because she wanted to, but to avoid disappointment, criticism, rejection, and possible abandonment from her parents. Although when looking back, she realizes her parents would never have abandoned her if she had kept the baby. However she believed because of their intense opinion as to what she should do, that in order to please them she’d have to go through with the abortion. So she did. Not because she made the decision out of her choice, but out of a reactive emotion to please them.  All along, feeling traumatized by their control and the incredible fear of their rejection.  Immediately she started drinking alcohol and spent the next 5 years drunk. Once drinking became a problem she stopped, and immediately turned to food to replace what was hiding those traumatic emotions. She thought she was an alcoholic, and by letting go of her need to drink, she thought everything was fixed. But instead of drinking she turned to food-- without understanding the behavior that drove her need to hide her emotions.  She would hide in her basement with large amounts of candy and she’d watch TV and movies for hours on end, to distract her from the trauma. The obvious result: obesity.

She sat in front of me 17 years later. She was happy, content with her life, and was in a loving marriage. We discussed her eating history, she became aware that her need to eat emotionally began after she stopped drinking. She’d never made that connection before. Once she realized that  was an obvious behavioral and emotional lateral move, she began to cry. She recognized that the emotional trauma she thought was fixed when she stopped drinking, had continued, but instead of drinking she ate. She was once again being challenged to process the trauma that started when she felt emotionally forced to get an abortion.

I asked her, “Knowing what you know now, and how your life has turned out, would you go back in time and make the same decision? Would you choose to get the abortion, or would you take the risk of your parent’s disapproval, and keep the baby?”  She sat and thought, and to her own amazement, she said, “I am content with my life today. I am deeplly in love with my husband, and if I was given the choice to go back? Robin, I would go through with the abortion again.” She was surprised by that thought, but I could see the calm and peace in her expression. I could feel and see the incredible emotional weight lifted off of her. I asked her, “Going back in your mind and making that decision regardless of your parents fears, does it still feel traumatizing?” She started to cry in relief. The trauma was over, simply by going back in her mind and processing the decision from a new place of self-worth.

From that moment forward, her need to eat emotionally began to diminish. She recognized that her behavior today, was continued based on the trauma she felt at 25, which didn’t make sense any more. If she could go back with the level of self-worth she values today, her choice would be the same, but her response to the situation would have been very different. The outcome: less trauma and need to emotionally compensate.

My point with this example is to show how many of us in adulthood continue to eat based on what was appropriate and defining in the past. But if you stop to evaluate those decisions and why they made sense to you in the past, would those reasons to eat still make sense today? Stop and think about why you eat and ask yourself if your relationship with food is still appropriate.

DO FAT CELLS GO AWAY?

You can always tell when someone really understands what they are talking about. The first sign is by how humbled they are by the astronomically large amount of information we don't quite understand yet. The more they know, the more they realize they know very little. These individuals want to know more, want a deeper understanding, and are willing to dig deeper for information to questions unanswered.

On the other hand, there are others who think they know everything, have no desire to seek new information and continue to believe there is nothing more to learn. The less they know, the more they think there is nothing else to learn. They only discuss the superficial information, and never go deeper to understand the human body. In this case, because they know very little they are naive to how complex the body really is, so they can't go deeper than memorized statements. The more you know, the more complex the body becomes, and the more information you seek to learn.

Here's an example. How many "experts" profess that once you have a fat cell they only shrink, and will never go away? This is one of the most naive, and quite sad, claims about the body. Once a cell loses it's function, it will go through natural cell death, or apoptosis. When fatty acids are depleted from an adipocyte, the cell has lost it's primary function and will go away. This is a "use it or lose it" situation. In the case of hCG, does hCG "unlock the hypothalamus"? Does hCG convert fat into energy? No. Not at all.

This was written in Dr. Simeons' "Pounds & Inches" in 1967. Let's get updated into 2012. You'd think that by now, self proclaimed  hCG protocol "experts" would have looked deeper into the human body, but because most people selling hCG products or programs don't really know that much about human physiology, they continue to proclaim Dr. Simeons' theories as fact. Without thought to the idea that we understand the human body more profoundly than we did in 1967.  These protocol experts don't realize that they look naive and superficially motivated to others who study the human body and physiology.

The most interesting observation I've made is that I've yet to meet a doctor or physiologist who wasn't interested in a modern hypothesis. These doctors may have written books, workbooks, and created an entire program based around Simeons' theories, and yet they still were thrilled to know the modern science that might relevantly explained why hCG prevents starvation. Where have a met resistance? Self-proclaimed experts who don't understand human physiology. People who don't have the education or understanding of the human body to a level that is necessary in order to comprehend the complexity of the endocrine system, and the hormonal influence on energy homeostasis would rather repeat Simeons' theories. The more the listener knows about the human body the more they appreciate the profound explanation. The less the listener knows, the less valuable a complex explanation is.

In writing a hypothesis for why hCG prevents starvation, I did the best I could with what I could understand. My hope is that another person who may have a deeper understanding than myself, will take what I've started and will describe it to an even deeper level. I look naive to a micro-cell biologist, similar to how others seem naive to me. Why am I writing this? Because the standard "expert" in the hCG diet industry doesn't really know much at all. Really? Fat cells don't go away? Now that's naive.

It's time we set the bar quite a few levels higher and it's time for many of these "experts" to go back to school. Until then, the hCG diet industry will continue to look naive, stupid, and money hungry, just like the rest of the diet industry.

THE SCIENTIFIC HYPOTHESIS: WHY LOW DOSE HCG PREVENTS STARVATION

 “I have never had an opportunity of conducting the laboratory investigations which are so necessary for a theoretical understanding of clinical observations, and I can only hope that those more fortunately placed will in time be able to fill this gap.”

– Dr. A.T.W. Simeons, Pounds & Inches

DR. SIMEON'S HCG PROTOCOL: A NEW HYPOTHESIS

 By Robin Phipps Woodall, Author of Weight-Loss Apocalypse   http://www.mindbodyhcg.com/

HCG injections of between 100IU and 150IU might stimulate, from fat cells, sufficient amounts of leptin to prevent symptoms of starvation imposed by the very low-calorie protocol (VLCP), as described by Dr. Simeons. The controlled hCG/protocol environment should stimulate enough leptin to minimize hunger, to maintain a normal and healthy thyroid signal, and to prevent significant reductions in lean body mass by effectively maintaining energy homeostasis through fatty acid oxidation of leptin-sensitive fat stores.

The controlled demand imposed by participant adherence to the VLCP will prevent fat gain by offsetting the susceptibility to over-stimulate leptin. This controlled demand with optimized fat utilization should, with time and physical adaptation, up-regulate mitochondrial biogenesis. During the second phase, as energy demand on fat is significantly reduced, new smaller mitochondria might progressively increase oxidative power, measuring an increase in resting energy expenditure (calories, per pound of body weight, per day).

Using this hypothesis as the basis of future research might explain what is observed during the protocol.

The following material is meant only to start new discussion about how hCG might influence energy homeostasis when food is removed.

ENERGY HOMEOSTASIS

To start, let’s acknowledge the inherent difficulty of understanding the body’s integrated system of organs, each requiring its own nourishment and energy demands, in addition to understanding the systems of tissues dependent upon these organs. The energy needed to sustain our organs and tissues is a system that feeds and depletes. It gives and takes from one organ to the next, all while accommodating the complex influence from both physical activity and food. This balance of energy demand and energy sharing is called energy homeostasis, and maintaining homeostasis sustains these integrated systems during both feast and famine.

All systems integrate fuel and energy demands not only daily, but over a lifetime. This constant striving for homeostasis is what stimulates the feelings of hunger that prompt us to eat, and to stop eating when we’re satiated. Perhaps the most critical element in achieving homeostasis is maintaining a stable blood glucose level.

We are fed from many sources other than food; some sources of fuel are fat, muscle and liver glycogen, body protein, and blood glucose.  These “tissue” fuels are not stocked equally. Some have more reserves than others. Fat and body protein by far surpass the fleeting amount of energy reserves held in both glycogen and blood glucose. The total integration of these fuel systems for short and long-term metabolic homeostasis is vital to life, hourly, and over the period of our body’s life.

The energy our body captures is powered not only by food, but also by our tissue reserves. However, these substrates must be converted into what can be captured before the body can use it as energy. As you eat, the food you consume is not yet in a form that can be captured as energy, so tissue reserves are readily available to meet immediate demands. But for tissue reserves to be released, key hormones that determine when and how much energy is needed must be accessed.

Leptin is one of the most important energy-controlling hormones. Since its discovery in 1994, we more fully understand leptin’s key role as a fatty acid synthase (FAS) inhibitor, and most notably as an anorexigenic hormone affecting the signal of hunger, the function of the thyroid, and fat metabolism. ^{2 15}

Similar to insulin, leptin levels fall and rise in coordination with blood glucose, signaling to the body and brain when and how much energy reserve is available. ³ Leptin helps maintain blood glucose levels by regulating fatty acid use in skeletal muscle for energy, and preserving blood glucose for other more important organs to use. ⁴

Leptin is primarily found in white and brown fat cells, but could also be produced in the mouth, placenta, ovaries, skeletal muscle, stomach, mammary cells, bone marrow, pituitary and liver. ^{5 6} The rise and fall of leptin levels influence hunger, thyroid stimulus, fat metabolism, and fat gain.  To successfully apply the modern science of leptin’s functions to Dr. Simeons’ protocol, I will discuss leptin as it relates to four areas; the hypothalamus, skeletal muscle, fat, and the thyroid.

LEPTIN: BRIDGING THE GAP BETWEEN THE HCG PROTOCOL AND HUNGER.

As a diet begins, and food is restricted, blood glucose levels fall. As blood glucose levels drop in the body and brain, leptin also depletes. ^{7 12} As leptin levels fall, there is a reduction in malonyl-CoA, a recognized intermediate, in the hypothalamic-signaling pathway that controls feeding behavior and energy expenditure. ¹⁵ Recent evidence suggests that food deprivation, and the associated decrease in hypothalamic malonyl-CoA, increases the expression of neuropeptide Y (NPY) and agouti-related protein (AgRP), which produces the sensation of hunger. Conversely, as blood glucose and leptin levels rise after eating, the resulting increase in malonyl-CoA reduces the expression of NPY and AgRP, producing feelings of satiety when hunger is alleviated. ^{7 10}

Studies have shown administration of a fatty acid synthase (FAS) inhibitor (such as leptin) to the central nervous system in obese mice, dramatically reduces feeding behavior, with the increase in hypothalamic malonyl-CoA concentrations.^{13 25} These findings show that during very low-calorie diets, a stimulant of a FAS inhibitor like leptin, would raise malonyl-CoA levels, and decrease the expression of NPY and AgRP. Theoretically, this should sustain feelings of satiation for longer periods of time with less food.

LEPTIN: BRIDGING THE GAP BETWEEN THE HCG PROTOCOL AND FAT MOBILIZATION.

Leptin is primarily expressed and secreted by fat cells. As fat mass increases during energy surplus, blood leptin increases and interacts with its receptors in the central nervous system (CNS), leading to increased malonyl-CoA expression in the hypothalamus, and decreased hunger. ²² Although there could be fat loss due to lack of hunger with a FAS inhibitor, studies have shown central administration of FAS inhibitors transmitted to the skeletal muscle from the CNS, increases fatty acid oxidation and, with time, increases resting energy expenditure. ^{16 23} 

As FAS inhibitors increase in skeletal muscle, the result is a decrease in muscle malonyl-CoA.  This outcome essentially determines whether or not fat is used for energy. ⁴ Muscle malonyl-CoA is a potent allosteric inhibitor of muscle carnitine palmitoyltransferase (CPT-1). CPT-1 is like a doorway on the mitochondrial membrane, opening or shutting access for fatty acids to enter and be converted into fuel for the body. When CPT-1 is deactivated by muscle malonyl-CoA, entry of fatty acids into mitochondria for β-oxidation is inhibited. ¹⁵

Muscular malonyl-CoA formation is catalyzed with increased activity in the enzyme Acetyl-CoA carboxylase (ACC). ACC is strongly inhibited by AMP-activated protein kinase (AMPK), which is stimulated by leptin. ¹¹ So, as leptin levels decrease, AMPK is deactivated, which activates ACC. ACC creates malonyl-CoA, which inhibits CPT-1, and thus reduces fatty acid oxidation. ^{13 15}

This happens as a response during starvation when blood glucose and leptin levels fall, preserving fat for longer periods of time, and forcing muscles to use other tissue substrates instead.¹² However, eating has the opposite effect.

After eating, when blood glucose and blood leptin levels increase, the activation of AMPK deactivates ACC, which decreases muscular malonyl-CoA. As muscle malonyl-CoA declines, CPT-1 activates and opens access for fat into the mitochondria, where energy can be supplied through β-oxidation. ^{4 11} This might explain how eating food that is not yet in a form that can be captured as energy, stimulates the use of stored fuel for immediate use.

New science has shown that this system can be successfully manipulated, not only to counteract symptoms of starvation, but to improve metabolic rates. Centrally administered FAS inhibitors during food restriction, rapidly increases the expression of skeletal muscle peroxisome proliferator-activated receptor-α (PPARα), a transcriptional activator of fatty acid oxidizing enzymes, and uncoupling protein 3 (UPC3), a putative thermogenic mitochondrial uncoupling protein. ²³¹⁵ Daily administration of FAS inhibitors over time increases the number of mitochondria in white and red skeletal muscle. This could explain why studies show increases in metabolisms tested through indirect calorimeter. ^{23 26 27} 

This evidence shows that if there was a way to safely increase a FAS inhibitor such as leptin, as well as create energy demand with food restriction, the response over time should be to acclimate with more mitochondria, resulting in a higher caloric-burning capacity. But without a FAS inhibitor, one should expect with the same food restriction to see a slowed loss in fat, increased loss of lean tissue reserves, and a resulting decline in resting energy expenditure.

To prevent the natural decline in fat mobilization with a very low-calorie diet, there must be an alternative way to stimulate leptin to decrease muscular malonyl-CoA, This allows fatty acids to have continuous access into the mitochondria, where fat could provide substantial fuel for the body without significantly depleting blood glucose. This optimized fat utilization would prevent the need for the body to use lean tissue reserves during extreme caloric deficits and, over time, stimulate mitochondrial biogenesis, ultimately increasing the rate at which a person burns energy fuel at rest.

LEPTIN: BRIDGING THE GAP BETWEEN THE HCG PROTOCOL AND FAT GAIN.

High levels of leptin in adipose tissue, without equally sufficient expenditure, have the opposite effect. Studies show that extremely high levels of leptin, similar to those seen in the obese, increase peroxisome proliferator-activated receptor-gamma (PPAR-gamma), which is the master control switch for fat storage.  ^{21 22 14}

PPAR-gamma activates a host of enzymes that promote the esterification of fatty acids to create triacylglycerides (TAG), and advances the formation of lipid droplets from these TAG.  When administered to mice, high levels of leptin increased the cellular expression of PPAR-gamma by 70-80%. ¹⁴ Leptin signals to the brain that there’s ample energy in storage, but also forewarns pre-adipocites to make room for more fat cells. 

The more fat a person has, the more leptin his or her body produces. ²¹ Essentially, if you were to compare two people who have the same exact metabolic rate, but extreme variance in body fat composition, their bodies would have a different response to the same food. If they ate the same exact amount and type of food, the more obese person would have much more blood leptin stimulated, due to their larger amount of body fat.

The excess amount of leptin, without equal excess energy expenditure, can cause an imbalance in energy homeostasis, making the body more sensitive to resulting fat gain as a need to recapture and compensate for the imbalance.  Leptin’s stimulus of PPAR-gamma would complement insulin as a survival mechanism to make room for more fat, aiding in the preparation for more energy storage cells as an adaptation for long-term energy homeostasis. A person with less fat would have less leptin, which might better compliment their metabolic energy balancing system, thus making him or her less sensitive to fat gain—even when eating the same exact meal as a more obese counterpart. Hence, fat gain and loss is not a linear function of calories eaten and expended because fat hormones, such as leptin, greatly influence energy homeostasis, and the body’s resulting compensations.

Both fat-preserving and fat-creating effects of leptin will function to conserve fat during starvation, and to form fat when food is excessive.  Leptin’s fat burning and storing/preserving relationships seem to follow an “inverted U” model. Leptin’s fat-conserving functions are maximum with high and low levels, and its fat-burning functions are optimal in the middle.

If leptin is stimulated by an outside influence, there might be less necessity for food and more sensitivity to over-stimulate leptin production. This excessive stimulus of leptin relative to expenditure would cause an expression of PPAR-gamma and an increase in fat when relatively small amounts of food are consumed.

LEPTIN: BRIDGING THE GAP BETWEEN THE HCG PROTOCOL AND MAINTAINING THYROID FUNCTION.

Leptin’s elevation and depletion in the brain signals a fed or starved state, not only through hunger, but also through the metabolic suppression or stimulus from the thyroid. ⁸ When elevated, leptin stimulates thyrotropin-releasing hormone (TRH) that controls the release of thyroid stimulating hormone (TSH). TSH acts on receptors in the thyroid to promote synthesis and release of the thyroid hormones (T3 and T4), which increases the body’s basal metabolic rate. ⁸ As blood glucose levels fall with very low-calorie diets, the depletion of leptin in the brain inhibits this cascade affect, resulting in a weaker metabolic signal from the thyroid. ⁹

The natural drop in thyroid signal is an essential, life-sustaining mechanism that occurs during starvation. This mechanism slows down the rate at which the body needs fuel, thus preserving energy stores and life for a longer period of time. However, when leptin is administered during induced starvation, the thyroid signals stay strong. ¹⁰ If the thyroid signal stays strong, the body maintains a normal basal metabolic rate, and requires the same amount of fuel as if in a fed state.

To counteract the natural metabolic suppression of the thyroid, an energy-preserving survival mechanism, during sustained very low-calorie diets, an alternative stimulus of leptin would be needed.

BRIDGING THE GAP BETWEEN LOW DOSE HCG AND LEPTIN.

Not only is there clear evidence that the placenta produces leptin, but there’s evidence that hCG might exert a negative feedback loop on trophoblastic release of leptin. ^{17 18 19 20} This means that specific quantities of hCG stimulate leptin production. If there were too much hCG, leptin levels would decline. If there were too little hCG, not enough leptin would be produced. 

Based on these findings, hCG could be a viable stimulant of leptin. But the question yet to be answered is, would injections of hCG with Simeons’ protocol:

·         Stimulate sufficient blood leptin levels to interact with its receptors in the participant’s central nervous system, acting as a potent FAS inhibitor in the hypothalamus, reducing hunger? In the hypothalamus to sufficiently stimulate the thyroid?

·         Stimulate enough leptin production in the skeletal muscle to increase fatty acid β-oxidation? The right amount of leptin in the fat cells to prevent fat storage?  And enough time and constraint for mitochondrial biogenesis to significantly increase resting energy expenditure?

·         Could other forms of hCG administration, including homeopathic hCG, do the same?

Simeons’ findings left many questions unanswered, and science uncharted by the refuting research of his protocol. Based on the evidence I’ve presented, hCG isn’t burning fat, it doesn’t directly reduce the appetite, and it doesn’t stimulate the metabolism. Rather, it is the energy demand of the protocol, combined with how hCG influences leptin, in the brain and body, that allows the body to metabolize fat and function as if fed, when food is not available. 

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REFERENCES

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