Monday, January 2, 2012


“In treating obesity with the HCG + diet method we are handling what is perhaps the most complex organ in the human body. The diencephalon’s functional equilibrium is delicately poised, so that whatever happens in one part has repercussions in others. In obesity this balance is out of kilter and can only be restored if the technique I am about to describe is followed implicitly. Even seemingly insignificant deviations, particularly those that seem to be an improvement are very liable to produce most disappointing results and even annul the effect completely.” -Dr. A.T.W. Simeons, Pounds & Inches

Unfortunately, because most participants and practitioners know very little about the new science of leptin and its role in starvation, the protocol is still misunderstood, and misdirected, and many have attempted to “socialize” it, to make it appeal to the masses.
In particular, new methods that include more food, are now being introduced—and not because of proper laboratory research, but marketed to ease the fears of those who’ve yet to fully understand how the protocol works (and to make money selling a system or product). Unfortunately, the majority of people who have morbid obesity would metabolically benefit less from this type of approach. But on the other hand, those who have less fat, or who are taking a weaker (or non-existent) dosage of hCG, eating more would makes sense, especially when they have hunger that merits more leptin stimulus from food intake.
But until there is sound laboratory research, clinical evaluations, and conclusive evidence, we are all speculating—some more intelligently than others. Claiming effectiveness based on clinical study comparing weight, is very naïve. Any educated and trained person in the field of physiology understands weight is sub-standard evidence for (or against) a hormonal therapy.
One of the main reasons eating less is better for people who have more fat is for improving metabolic rates. New science has shown that the metabolic system can be successfully manipulated, and improved by finitely balancing leptin levels. Centrally administered fatty acid synthase (FAS) inhibitors (such as leptin) combined with high fuel demand, 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. With fuel demand, daily administration of FAS inhibitors over time increases the number of mitochondria in white and red skeletal muscle. This adaptation to demand increases fueling capacity, which explains why most people who properly follow the 500 calorie protocol show increases in metabolisms, when tested through indirect calorimeter.
Here is our initial statistical analysis done for 40 participants, before and after the 500 calorie medical hCG protocol. Since this report was done in 2009, we‘ve collected data for hundreds of participants and the trend is only improving as we’ve understood eating less (relative to hunger) is ideal. Again, eating more could be ideal only if the dosage of hCG is too weak, but the charted acclimation wouldn’t be as sloped or powerful.
Preliminary Statistical Analysis (for the first 40 participants)
This preliminary analysis was done by Lee Hannah of Boise State University-Boise, Idaho.
Lee Hannah, DVM, MS, MPH
Assistant Professor, Medical Epidemiologist, Boise State University

The data set is small, containing only 12 variables. Of interest was the person’s gender (only 4 males to 36 females), weight at the beginning of the hCG protocol, resting energy expenditure(REE) at the beginning of the protocol, calorie/lb/day at the beginning of the protocol, weight at the end of the protocol, REE at the end of the protocol, and calorie/lb/day at the end of the protocol.
Because we have pre- and post-information on the same individuals, I used a paired t-test to look for a significant change from post to pre for both weight and REE.
Weight: For weight, there was a significant reduction in weight across the protocol. On average, across all 40 individuals, weight went from 202.73 pounds to 180.35 pounds (a change of 22.38 pounds). This was statistically significant, with a p-value <0.001.
REE and calorie/lb/day: REE also dropped between the pre and post time periods, with an average reduction of 69.48; however, this difference only reached borderline significance, with a p-value = 0.07. What is more important to the study is the fact that the calorie/lb/day (which is calculated as the REE divided by body weight) increased across the 40 participants. At baseline, the participants were burning 9.51 calorie/lb of body weight and at completion of the protocol the average participant was burning 10.30 calorie/lb of body weight. This was statistically significant, with a p-value <0.001.

Table 1: Paired Samples Statistics

Std. Deviation
Std. Error Mean
Pair 1
post weight
pre weight
Pair 2
Post REE
Pair 3

Table 2: Statistical significance of differences observed

Paired Differences

95% Confidence Interval
of the Difference

Std. Deviation
Sig. (2-tailed)
Pair 1
post weight - pre weight
Pair 2
Post REE - Pre REE
Pair 3
calorie/lb/day2 - calorie/lb/day1

These results were achieved with test subjects who were limited to eating fewer than 500 calories/day, sustained from four to six weeks. 
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 finite control of leptin combined with demand, 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. And even with a controlled leptin stimulus, eating more would decrease the demand, which would reduce the potential mitochondrial biogenesis and improved resting energy expenditure.
By providing this data, I don’t intend to convince anybody of the efficacy of the hCG protocol, but to confirm what others have observed, and to also motivate more data collection by those who are on the front lines of observation. If we could find a point of hormonal balance and stability, the body will do what it does best: adapt. The question is: if we want to improve the overall hormonal adaptation, should the protocol be dynamic? Does increasing food intake for everyone make sense based on this adaptation? Should we take into account the emotional ramifications when more food is added, which would give more wiggle room to justify cheating?
More research is desperately needed. Especially since we have people taking advantage of the hCG protocol as a diet, marketing it with superficial value, and underestimating the protocol as a hormonal therapy.  The sooner we get laboratory research the better.


  1. Do you know where this study was published? Or is there a ID number for this trial? I am having trouble confirming that the study exists. Dr. Hannah is a veterinarian, who also does public health research. There is nothing listed in PubMed nor her bio from Boise State in relation to hCG however.

    1. This was not a published study. After collecting the data, Dr. Lee Hannah did the statistical analysis for me. She was (and should still be) a professor in BSU's statistics department. The stats were done for my own interest and was published in my book, Weight-Loss Apocalypse.