News for today's 2018

IMPROVED METABOLIC RATES AND "STARVATION" ON THE HCG PROTOCOL

One of the most important life sustaining reactions to under-fueling or starvation is a decline in energy demand. This decrease comes from a decrease in thyroid hormones (T4 and T3). With the discovery of leptin in 1994, we more fully understand why this metabolic decrease occurs. Hypothalamic leptin levels are an integral part of why the thyroid supresses, and metabolism decreases during starvation. The link between leptin and starvation has been discussed for well over a decade. Initially scientists viewed leptin as a hormone designed to prevent obesity, but many studies suggest that leptin also signals the switch from a fed to the starved state, which would reduce fat use for fuel. As leptin levels decline, so does the metabolic signal from the brain as well as a decline in fueling from fat. What we understand today is that as eating decreases and the demand for fuel isn't adequately met, leptin levels also decrease, signaling to the brain that the body isn't fueling adequately.  This decline in leptin in the brain suppresses Thyrotropin-releasing hormone (TRH). TRH is the neuropeptide that controls the release of Thyroid-stimulating Hormone (TSH), which in turn acts on receptors in the thryoid to promote the synthesis and release of T4 and T3. Ultimately, this response tells the body to conserve energy, which would reduce overall need for fuel in an attempt to balance the body's metabolic mechanisms when lacking food. In an attempt to solidify that this metabolic turn-down in response is regulated by leptin, researchers studied the thyroid reponse to starvation, with and without leptin administration. This means that scientists put mice into starvation and gave some mice leptin and others a placebo (water). The mice with leptin administraion didn't have the same starvation induced drop in thyroid hormones like the placebo group. This research indicates leptin as an important influence on the throid during starvation. <a href="http://www.jci.org/articles/view/9725">Here is a link to an easier to read article about this leptin/thyroid/starvation link.</a> In searching for answers to why low dose hCG could possibly prevent symptoms of starvation during Dr. Simeons' 500 kcal protocol, I knew that prevention in the starvation response from the thyroid would have to be necessary.  As science would suggest, eating less than 500 kcal in food for over a month would most likely show significant changes in the thyoid that would indicate reduced leptin levels, then decreased TRH, TSH, and ultimatlye reduced T4 and T3. This would negatively impact overall metabolism. However, the data I've collected shows the opposite: metabolic rates significatly increase after the 500 kcal protocol with low dose hCG administration. The next important piece in sustaining life during starvation is maintaining energy balance through adjustments in fueling mechanisms. In other words, where does the body create it's fuel: muscle, fat, glycogen, or blood glucose? In order for symptoms of starvation to be prevented the body would most definitely have to create fuel out of body storage, but in order to prevent muscle loss, there would have to be adequate fuel supplied by stored body fat. Science has shown one of the most important regulators of fuel release from fat is leptin. Leptin regulates the most importand fat combusting , AMP-activated kinase (AMPK) and more. Could this science explain why most people experience improved resting metabolic rates after eating less than 500 kcals for over a month? Does the body adapt at the mitochondrial level? <a href="http://www.pnas.org/content/101/7/2058.full">Here is a link to not easy to read science that describes how leptin (when in proper amounts) regulates fat use for fuel.</a> If there was a way to keep leptin levels from falling as they do with starvation, could symptoms of starvation be prevented, not only in the brain but in the body? Could fat adequately fuel the body so that muscle and organ tissue could be preserved? That is a very important question, considering thousands and thousands of people are experimenting with starvation through the hCG protocol. One of the most important studies I've come accross describes how there could be a drug created that would prevent all metabolic symptoms of starvation. But, in my opinion, I don't think we need a drug when we have a simple hormone that could be used instead; HCG. <a href="http://www.ncbi.nlm.nih.gov/pubmed/18356287">Here is a link to a minireview that literally describes experimentation with mice to show what our physiology is capable of.</a>  This study discusses the use of a fatty acid synthase ihibitor (similar to leptin). What if the control of leptin could be balanced by the stimulus of leptin through hCG, rather than a drug? Could the very low calorie protocol keep leptin controlled to prevent leptin-resistance?  This could make sense to explain why people aren't experiencing symptoms of starvation, and even better- improved metabolic rates. Until we have laboratory experimentation for why and if low dose hCG can prevent starvation, we are all left to just assume otherwise. For this reason, I have written a hypothesis that can be used to start a more intelligent and scientificially relevant discussion of why Dr. Simeons hCG protocol could work. Is it the hCG or is it hCG's link to leptin? Based on the science that is available to us today, my bet is on the relationships between hCG and leptin. <a href="http://weightloss-stories.blogspot.com/2012/01/scientific-hypothesis-why-low-dose-hcg.html">READ MY HYPOTHESIS</a> and make that decision for yourself. <a href="http://weightloss-stories.blogspot.com/2012/01/hcg-protocol-is-eating-more-better.html">LINK TO STATISTICAL ANALYSIS OF METABOLIC TESTING AFTER THE HCG PROTOCOL.</a> <iframe width="560" height="315" src="http://www.youtube.com/embed/xiqs4MDFQ2w" frameborder="0" allowfullscreen></iframe>

IMPROVED METABOLIC RATES AND "STARVATION" ON THE HCG PROTOCOL

IMPROVED METABOLIC RATES AND "STARVATION" ON THE HCG PROTOCOL

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