Rewiring The Leptin Rx Reset

Evolutionary strategy is based upon finding an environmental niche and exploiting it. Evolution is based upon change and the natural adaptations to it. Today, we are going to explore how some environmental triggers might open a “biochemical trap door” that will allow me to add a new recommendation for you to consider adding to the Leptin Rx reset protocol for those who are LR.

I am beginning a series on circadian biology to show you how this all ties in together. Today, I will give you a very cursory review of why circadian biology, leptin, and environment are critical to using the Quilt to obtain your Optimal life.

Why is circadian biology critical to humans?

For evolution to work Optimally, a cell first must adapt to its environment. The first situation any living cell would be subjected to in an earth day is a period of day and night. Over time it would also be subject to the seasons in our environment because of the earth’s revolution, tilt, and angulations of the sun. As time continued on, further life would have been subjected to solar variations and would have had to account for it. It also has to find food to make energy (ATP) to survive, and it also has to control its own cellular division. The epic battle for the cell is to have the regularly expected circadian cycles found in our environment and ”yoke” those signals to its metabolic cycle and to its growth cycle. Most people know that the suprachiasmatic nucleus (SCN) in the brain is where the circadian pacemaker lies in humans. It monitors this dance between darkness and light, and the seasonal cold and hot temperatures in our environment to help control and monitor our own growth and development. Evolution apparently agreed to use these signals in all living things because this is what it uses for all life on earth today. What most people do not know is how leptin plays a massive role in regulating it. Many people and physicians think it plays a small role. Recent research has revealed that leptin can induce expression of a neuropeptide called vasoactive intestinal peptide (VIP) through the VIP cytokine response element. This is an epigenetic modification from our environment directly signaling the master hormone in our body. So what does VIP actually do?

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So You Completed The Leptin Rx? What’s Next?

Once you have added the Leptin Rx to your paleo/primal template and you have successfully experienced all the “small wins” that I mentioned in the Leptin FAQ’s blog, what should you do next? If you recall reading the blog on how the leptin Rx works, it basically is a plan to make your gastrointestinal tract perform visceral exercises that it is not accustomed to performing, in order to cause neuroplastic changes in your hypothalamus’ arcuate nucleus. It uses the vagus nerve as the “stimulator” to send these new messages to the brain. After a period of time, the inflammation will slowly dissipate at the median eminence, and these afferent signals will force expression of certain genes that have been repressed since we were in utero. These genes and pathways are hardwired into our DNA at conception, and used until the child is 12-24 months old. After this time, they are not expressed any longer, because transgenerational epigenetics favors instead the use of the leptin receptor from an evolutionary perspective. This occurs because the leptin receptor in the arcuate nucleus is far more sensitive and accurate in accounting for electrons from food than was using older circadian and ultradian cycles that we used in uteri during morphogenesis. The human brain learns “what neural circuits” to use by repetitive firing. We have a saying in brain surgery, nerves that fire together wire together. This is the basis of the theory of Hebbian learning.

These exercises I told you about in the Leptin Rx signal hypothalamic neurons to adapt to these visceral responses to food in a new way, to sensitize the leptin receptor in order to account for electrons from food in precisely how it was designed to do by evolution. In essence, we are altering the genetic expression of the genes in our arcuate nucleus. I describe it to my patients as “performing brain surgery on them without using a blade.” The visceral responses to the Leptin Rx are transcribed by the vagus nerve, and this information is sent to the brain. This message is dramatically different than the one the patient is used to giving the leptin receptor, and the new message induces changes to the neuropeptides in the brainstem. After some time, (6-8 weeks for most) changes will be induced. These can be followed by the clinician or the patient. Those clinical signs are outlined in the Leptin FAQ blog post. In doing this, we force the neurons to see neurochemical signals that radically confuse the leptin receptor and the brain. The brain’s response to a signal it does not understand is to revert to an older known pathway or to learn a new way to tackle on old problem. I would suggest you watch How your brain re-learns from 2007 by Dr. VS Ramachandran in a TED talk. He exquisitely explains how this type of learning is stimulated in the brain for phantom limb pain and its treatment. One need not use expensive technology to induce gene expression. It is possible to do without an NIH grant too. It requires some synthesis of thought and experience. When you understand the essence of how the brain works, you just need to design a program and force it upon the brain to decipher what to do. That is the essence of the Leptin Rx reset.

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How Does The Leptin Rx Work?

Many people have contacted me about “why” the leptin Rx works and “how” does it work. Many people in the blogosphere have made some claims that much of what is in the leptin Rx is a rehash of the work found in some diet books. Well, today’s post is being done to show you the science underneath my recommendations were formulated and made. None of the underlying science I will mention to you about neuroplasticity will be found in any diet book mentioned in any blog post that I know of. Most of you know I am a neurosurgeon, and as such, I was dramatically influenced by two world famous neurosurgeons named Wilder Penfield and David Kline. Dr. Penfield was the first neurosurgeon to use electrodes on the brain to map it prior to surgeries to avoid neurologic damage during tumor removal. Dr. Kline was and still is the pre eminent world expert in peripheral nerve surgery. I happened to train with Dr. Kline in New Orleans, and got turned on to his work, Dr. Penfield’s work and the work of Dr. Merzenich in the early 1990’s before leptin was even discovered. Dr. Michael Merzenich work on sectioning the median nerve in the hand and seeing how the brain remapped its sensory territory in the cortex via micro-electrodes was brought to my attention by Dr. Kline while I was a resident.

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Intermittent Fasting and Leptin

Today, I decided to blog about Intermittent fasting (IF). Since I wrote the Leptin FAQs, I have been bombarded with requests about IFing and how it relates to leptin signaling. I mentioned in the FAQs that I love IFing, but not when someone is LR. The reason for this is how the AMP-activated protein kinase pathway (AMPk) works. THe AMPk pathway is best described as a fuel sensor for lipid and glucose metabolism. In humans, the control of glucose homeostasis is governed by the balance between intestinal absorption and endogenous hepatic production by the liver and the uptake done in the muscles. Intermittent fasting is a behavioral modification that specifically alters feeding behavior to cause disruptions in glucose and lipid metabolism in humans. It also has specific times when exercising is done as well. When it is practiced well is can lead humans to shred body fat and really control their ability to generate muscle with workouts and re-feeds. I would strongly recommend that you take a look at the leangains protocol sometime on Martin Berkhan’s site. The key question many have asked me is how does it work and why can’t I do it right off the bat regardless of my leptin status. This is a loaded question with an answer that may make your head hurt but you will understand why IFing won’t work if you are LR.

The reason why it is counter productive in LR is the AMPk pathways requires really optimal leptin sensitivity and signaling to be occurring between the brain, liver, and muscles. At its core, when one IF’s it creates a “temporary” cellular stress due to lack of food at certain times. AMPk is specifically upregulated in times of cellular stress. Some examples, are nutrient deprivation, ischemia, hypoxia, exercise, glycogen depletion and oxidative stress. When one fasts, this also counts as a cellular stressor.

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The Leptin Rx: FAQs

What should I do before I start The Leptin Reset? Before you start, take a picture of yourself from all angles. Don’t be bashful or you’ll be sorry in 18-24 months. Next, weigh yourself naked. Let your significant other or a family member take this picture. Go to the store and buy a piece of clothing that does not fit you now, but will when you have met your goal. Remember, calories are important when you’re LR (leptin resistant) and mean nothing once you are LS (leptin sensitive). Macronutirents count when you’re LR and mean nothing when you’re LS.
How do I determine if I am leptin resistant? Remember, you can be LR (leptin resistant) if you’re fat or skinny. If you’re overweight by more than 30lbs, it is a lock you have some degree of LR. If you’re underweight by 20 lbs, you are likely LR, too. If you had an eating disorder, you’re likely suffering from a serious leptin issue.

The easiest test is to look in the mirror. The mirror does not lie and it is really cheap. For those people who still can’t be sure after peeking in the mirror, you can order some blood tests. My favorite is the HS CRP (highly sensitive C-Reactive protein) and the reverse T3 tests (but there are others). They are accurate in over 90% of cases.

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Central Leptin Dominance: Part 3 – King of The Hill

So now that we examined Dr. Lustig’s insulin theory of metabolic control we need to take a look at the reward tracts that are located in the human brain. These tracts have been well studied and their neurochemistry is well understood. What appears not to be as well known is how the hypocretin neurons and the leptin receptor control and modulate their activity. The key point here is that the dopaminegic tracts eloquently spoken of Dr. Guyenet’s reward series are the “efferent only” path that is part of the effector arm of the leptin receptor and the hypocretin neurons. This means, in English, they are playing second fiddle to the leptin receptors and are not the dominant cause of obesity. They clearly play a major role in the neuro-circutry but they do not control obesity. They carry out the action but the orders were given by someone else. One of the reasons I had a major problem with the reward series, is because of my “day job” as a neurosurgeon. I have had the opportunity to operate on many brain tumors in the reward tracts and never have I ever seen either preoperatively or postoperatively one patient develop severe morbid obesity. If these tracts were truly dominant causes this would lead neurosurgeon and neurologists to see many patients with this problem. Well, we do not. That was a big issue for me with the theory. The second issue I had with it was that when we neurosurgeon’s have patients with brain tumors involving the hypothalamus we see tremendous effects on feeding, obesity and on anorexia. This is well documented and I have personally seen this in many cases. Dr. Lustig pointed this out in his AHS 2011 talk when he showed some clinical cases of craniopharyngioma’s and of hypothalamic trauma’s that resulted in morbid obesity.

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Central Leptin Dominance: Part 2

Continuing on in the Central leptin series we will resume in Orlando, Florida. In Orlando, Dr. Myers, went on to say, “In addition to examining the molecular details and importance of specific LRb signals, we are dissecting the regulation and function of individual populations of LRb-expressing neurons and examining the role of leptin in the development of neural circuits. By understanding the totality of leptin action in this way we hope to decipher the mechanisms by which leptin regulates the predisposition to diabetes and other aspects of the metabolic syndrome.” This statement carries huge implications. He has found that not only is leptin neurons somatotopically organized in the brain, but the leptin receptor also appears to be somatotopically organized into certain regions that wire and select certain neurons in the brain that modulate all parts of the obesity physiologic response. It also appears that this organization is different in men and women at the parvo-cellular nucleus in the hypothalamus. Certain parts of the receptor control total body glycemic control, others body weight and size, and others power the para-mammillary neurons to directly control fecundity, placental growth and oocyte maturation. The receptor even codes for gender differences! Men and women really are from Mars and Venus when it comes to obesity and fat deposition, and this explains why the endocrine response is different in men and women. We have known men and women have different leptin levels as adults but did not know how or why this happens. Now we do. We now are beginning to understand why it is the case as well. It helps explain why we see can see PCOS and stubborn weight gain together and why fat is distributed differently in both sexes.

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Central Leptin Dominance For Health: Part 1

Today, we are going to cut deeper into the leptin story. We need to look at the leptin receptor because its biology will explain why studying macronutients at a dietary level just becomes a confusing mess with seemingly multiple paradoxes. I recently commented on this in Paul Jaminet’s blog on August 24th 2011. The comment was very detailed but not written well so I am going to lay out the reasoning in the next few blogs. As most of you know leptin is the lynchpin in my Quilt and sits at position two. Many people might not realize how important it is for health, in sickness, and for optimal endocrine function. It is the dominant factor in obesity and this series is out to show you why this is the case based upon the data coming out of some labs who specialize in this neurobiology. This series is going to be laser like biochemistry on a 30 foot level. When we talk about this type of lab science it is very easy to lose perspective of the larger story I am trying to unveil to you.

I have previously called leptin the master hormone of the brain. Remember that the brain has two ways to control things, one is direct neural wiring and the second is the control over the hormonal secretions body wide. Given these two factors, I think I may have under called it, honestly. This hormone signals the entire body’s nutritional status, metabolic status, and endocrine status to the brain at all times. The brain in turn uses leptin to regulate total glycemic control, energy balance, and all neuroendocrine function in all systems in humans. This means that energy regulation is centrally controlled by our neuroendocrine system. The brain uses this hormone as an afferent and efferent signaling hormone to know precisely what is going on in our 20 trillion cells body wide. The brain does not have direct wiring to all 20 million cells because of space limitations of our cranium and our mother’s vaginas. So it uses hormones and cytokines to extend its power and reach to send signals to those 20 trillion cells.

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My Leptin Prescription

I have been asked by many to put a short post out about how I reverse Leptin resistance in my own clinic for my patients. After reading all of the comments left here, at MDA, and on Jimmy Moore’s forum, I decided that it was a good idea.

1. First make sure you really are Leptin resistant (LR) to begin with.

The easiest way to do this if you are heavy is to look in the mirror. If you’re overweight you definitely are Leptin resistant. If you still have a large appetite and crave carbohydrates, especially at night, these are also signs that you are likely Leptin resistant. If you are fit or in decent shape and not sure based upon the above symptoms, I would tell you to go get a blood test and check your reverse T3. It will be elevated. I also recommend simultaneously checking a salivary cortisol level. With LR, you will always see higher cortisol levels later in the day.

2. To regain Leptin Sensitivity (LS) follow a strict Epi-Paleolithic diet.

To see an outline of a strict Epi-Paleolithic diet, read Brain Gut 6: Epi-Paleo Rx. The type of fuel you eat is important initially in eliminating the foods that cause Leptin receptors to become nonfunctional.

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READERS SUMMARY: 1. Why you should be disgusted with our policy on diabetes. 2. How is one to survive the situation. 3. What can you do to avoid this situation and to thrive?   I read an article this morning in my local Sunday paper that stopped me dead in my tracks and caused me to write this. Majid Ezzati is the chairman of global health at Imperial College of London and his study was just published in The Lancet just last night. The study was based using data from 150 published national studies that followed adults over 25 years in 199 countries. The study used modeling to estimate the numbers for 92 other countries. I am not a fan of this type of science but I have to say, I believe they under-called the problem in a big way. The modeling did not take into account the three youngest generations world wide. More importantly, It failed to include the youngest three generations obesity crisis in the biggest problem country. That country is the USA.   When I was on Jimmy Moore’s podcast this May, I estimated that the numbers in the USA for type two diabetes were north of […]

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Why Sleep and Leptin are Yoked?

To begin to understand how sleep interacts with metabolism, we need to understand a bit about neuroanatomy. In sleep, the cerebral cortex is in a state of cortical synchronization. In wakefulness, several subcortical regions of the brain stimulate the cortex to remove this synchronization. When we undergo slow wave Non REM sleep (drowsiness) there are a small group of neurons in the hypothalamus called VLPO neurons that are GABAergic (inhibitory) and they fire on the subcortical areas that are stimulating the cortex. In doing so, these VLPO neurons bring about cortical synchronization. After sleep begins, NREM sleep gives way to REM sleep. During REM sleep there is a coordination of cross talk between the grey matter brainstem nuclei while cortical synchronization is maintained. This is quite complex coordination of events that occurs in the brain while we sleep. A common disease of dis-coordination of sleep is Narcolepsy. In other words, the tracts that normally control the stages of sleep occur out of sequence and cause people to fall asleep and lose muscle control in wakefulness. Narcolepsy occurs because we lose a specific set of neurons in the hypothalamus that effects this coordination of signals. These neurons are called the hypocretin neurons (HC). These neurons are found in the ventral lateral hypothalamus in a small area that also control appetite and feeding. These neurons also effect loops that effect feeding. There is no set point. When we lose HC neurons we set up the neurochemistry that becomes resistant obesity. The dopamine tracts are the direct targets of the HC neurons. We don’t see obesity as a common phenotype when we see tumors of surgical ablation of these dopamine outflow tracts. This is the main reason many do not believe there is a set point for obesity. The hypocretin neurons sit scattered through many MSH cells (also involved in obesity). The HC neurons make two peptides called (hypocretin 1 and 2)HCrT1 and HCrT2. In the literature, these peptide hormones are also known as the orexins so you do not get confused. These peptides are remarkably similar to gut incretin hormones that help tell the brain what type of foods are present in the gut. Another remarkable trait of the hypocretin neurons is that in the human brain there is only 50,000 total HC neurons in an organ with over one trillion cells. And they appear to be very new in mammalian phylogeny. It appears mammals handle sleep and energy metabolism very differently than the rest of the living. The small amount of HC neurons, however, project widely all over the brain. We now know that the hypocretin neurons control the stability of wakefulness or our arousal. It appears they may also control energy metabolism via leptin function.

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READERS SUMMARY: 1. Why do we sleep? 2. Does sleep control metabolism and cell growth? 3. Do all living things sleep? How long is too long or too little? 4. What are the stages of sleep? 5. Can sleep help prevent degenerative aging diseases and cancer? 6. Is sleep the primordial condition or did it evolve as we did?   Why do we sleep?  Well, most sleep researchers are losing sleep trying to find that out as well right now!  It appears to be an elusive target.  What we do know , is that when you don’t sleep a lot of bad things happen.  Disease propagation is one and psychosis and eventual death are others.  Most people don’t realize that lack of sleep is deadly for humans, but it clearly is.  Sleep appears to most to be a restorative physiologic process.  That is what they say now;  I am not so sure about this as yet.  If sleep is restorative, as they say, what are its targets?  We have no idea what the targets really are as of now.  What we do know about sleep is that it is incredibly important biologically because every animal has biologic sleep requirements.  It seems evolution has strongly naturally selected sleep […]

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READERS SUMMARY 1. Quick overview of carbohydrate metabolism 2. Quick overview of fat metabolism 3. Quick over view of protein metabolism 4. Are all exercises created equal? 5. What exercises optimize us for health and longevity?   The process of how food is turned into ATP is called cellular respiration.  Foods are made from carbohydrates, proteins, and fats. This a quick overview of dietary biochemistry to show how our foods and mitochondria have to interact.  Carbs have four stages of metabolism that allow them to be transformed into CO2, H2O, and ATP.  Stage one is called glycolysis.  It has either 10 or 11 steps.  10 if they occur in the cytoplasm, or 11 if they occur in the mitochondria.  It begins with glucose of glycogen and ends with pyruvate under anaerobic conditions.  It only allows for 2 ATP to be made form glucose and three if glycogen was the source.  It also liberated 2 hydrogens in the form of NADH.  Stage two carb metabolism has no name but it allows formation of Acetyl CoA from pyruvate.  This occurs in the mitochondrial matrix without oxygen, but is an aerobic process.  No ATP is made but two Hydrogen atoms (H) are released to make 2 NADH.  Stage three of […]

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A Leaky Life?

Okay, now that we established that mitochondria leakiness determines our lifespan, what can we say about disease generation? Does leakiness determine disease progression? Well, it appears it does. We know that lower life forms like yeast accumulate mitochondrial mutations one hundred thousand times more frequently than in their nuclear DNA. Most of those occur in the control region of the mitochondrial DNA (mtDNA). The new theory of mitochondrial aging is that leakiness of free radicals at the first cytochrome also helps weed out those mitochondrial mutations as we age. Why? Mitochondria that are sluggish to the signal to divide because of the mutation would be taken out by apoptosis very quickly. Moreover, if the mitochondria were in perfect order, it would divide immediately and through clonal expansion lay waste to its inefficient brethren. This is intracellular natural selection at work. So the more mutations in the mtDNA coding region the more leakiness occurs. That leakiness is the signal to the nuclear DNA to make new mitochondria. This pathway is called the retrograde response. This is how a defective mitochondria signals the nucleus that something is amiss. In theories past, we always believed it was the nuclear DNA that set the tempo for such decisions but now we know that power rests with the mitochondria. This retrograde pathway is found in yeast all the way up to humans phylogenetically.

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Dancing Between Purity and Pollution

Mitochondria can allow life or kill us. Mitochondrial DNA has only 37 genes. From those 37 genes comes just 13 proteins. Those 13 proteins code for the electron chain transport complexes. The remainder of the genes code for tRNA. Mitochondria also cant grow outside the cell. They require the 30,000 genes in the nucleus to make up another 1500 proteins for them to function. Mitochondrial DNA and nuclear DNA have to have precise lock and key fit to generate energy production. If not, the cell eliminates itself by apoptosis (levee 19) fast. If It works well, this combination is naturally selected for future cell division to generate energy. Aging is quantified by how “leaky” our mitochondria are to free radicals at complex ones in electron chain transport. Their own DNA is adjacent to the first complex in electron chain transport. So the more leakage, the more damage is done to its DNA and energy production will fall. Moreover, that is the signal to make more mitochondria or undergo cell suicide! This first complex (NADH) is by far the most leaky to free radicals of all the complexes. This paradox of fate caused evolution to select for 10-20 copies of mitochondrial DNA in each cell to sustain energy production of an organ in question. So mitochondria can breathe life into us and end it based upon how many good mitochondria we have in a tissue.

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Why Does Heart Disease Really Occur?

Let me begin by saying, I think western medicine is ideal for acute diseases. I know this is a dogmatic statement to lead with, but I believe this to be true. And those diseases are the ones that shortened our lifespans most in the first half of the 20th century. Most people I talk with always want to know why I think medicine has missed the boat with respect to chronic diseases? I have thought long and hard about this one and I think I have arrived at my reason. Healthcare, up until the 1940′s, was done anecdotally and by empiric observation. In the 1940′s, the government saw some statistics that showed close to 40% of the deaths in the US were caused by heart disease or stroke. It also appeared that the numbers were accelerating and not slowing down. The real reason they became interested is that no one knew why this was happening. So they decided to study this problem with a long term observational population study that began in 1948. That study was the Framingham Heart study. The bible has the book of Genesis, and physics has Einstein’s theory of relativity and Framingham is medicine’s raison d’etre.

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How to Change Your Doctor and Your Life

Readers Summary 1. Why humans can change their DNA with a thought. 2. Are we mismatched? 3. Motivated by Paleo Hack thread. 4. Why convention healthcare fails us. 5. What we can do together to change that. CHASING CHANGE Humans evolved the attributes of a large brain, the ability to speak, and formed an intricate social networks that can use many aspects of technology. Our biggest attribute is the ability to think. This allows us to radically change the environment that we are ideally adapted to. It has allowed us to dominate all habitats and create havoc in most of them as well. The real human miracle of our mind is not that we can see the world as it is…but that we can see it as it is not and then change it. If we think and act incorrectly, we can quickly recalibrate and overcome it. Conversely, we seem to be a prisoner to our paleo-cortex (older, less evolved brain) and resist change even when we know it must occur. Many times we will subjugate the best interests of our survival to suit our emotional needs or desire. The real paradox of humanity is that often our reasons for […]

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Hormones 101: Clinical thoughts revealed

Readers Summary Why I use highly sensitive C-reactive protein (CRP) and Vitamin D as biomarker proxies. After Leptin, Cortisol is the next most important domino to fall. Hormone Cascade explained in a paragraph. Unintended consequences of hypercortisolism destroy health. Initial HS CRP signals the genesis of underlying hormonal disruption (First sign Leptin is toast). Now that we have laid some foundation about Leptin at the “30 foot research level” (I know, I made your head hurt at times), let’s zoom out now and look at how this affects the hormones that dictate the things patients see and feel and sense about their bodies. I want to now give you some perspective as to WHY this matters We have established that as one gets fat, Leptin levels rise. Once they get high enough (around a Body Mass Index (BMI) of 20-24), Tumor Necrosis Factor (TNF) rises in several tissues. This also causes a rise of NF kappa beta and IL-6 in the brain.  TNF quickly destroys normal hepatic homeostasis, which sets the stage for fatty liver disease and type two diabetes over time. This rise in TNF also biochemically changes Leptin receptor signaling and changes its quantum properties by changing its […]

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Why is Oprah Still Obese? Leptin Part 3

Now, we know definitely that Leptin controls all energy production by regulating all the hormones in the body. But, do you wonder what happens when that regulation goes awry in the muscles? Well, here is some information about one part of how Leptin works to keep us fit when your body is sensitive to it.

When Leptin was discovered in 1994, no one really had a clue as to its many functions. One function that was particularly murky was how the brain controlled peripheral energy utilization and optimized it. It is awfully hard to realize that the hypothalamus (size of a pea) can control the need for fuel of 20 trillion cells in the human body. Well in the last few years, scientists found out about uncoupling proteins (UCP). So far five have been discovered in mammals. The one we will discuss today is UCP3.

This protein, UCP3, allows Leptin to work inside of peripheral cells like the muscle cell. For UCP3 to work optimally, it requires optimal functioning of Leptin and thyroid hormone simultaneously. In muscle cells, UCP3 is the dominant UCP in humans. So it is vital to maximizing efficiency in exercise and energy use. What UCP3 allows the muscle to do, is to shift out of regular oxidative energy production done at the mitochondria and making energy in the form of ATP, and into making pure heat without generating ATP. This biochemical action decreases ROS (levee 3) at the mitochondrial level, decreasing cellular stress. And therefore the energy is dissipated mostly as heat. Another protein, UCP1, is dedicated to doing this same action when it is activated 100% of the time.

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Leptin Part Deux: Liver

Many people are under the assumption that the thyroid is the real key to metabolism. I can’t tell you how many meetings I have been to and heard this nonsense. It happened today while I was speaking to a dietician and nutritionist in a hospital. It’s just not correct. The liver is the engine of our body’s Ferrari! The thyroid is best described as the gas pedal for the engine and leptin is the electronic chip that controls the entire process. So we need to discuss some biochemistry now. Rub your head a few times before we start to increase your blood flow!

When humans eat a meal about 60% of the calories wind up in the liver to deliver energy to tissues between meals to sustain normal energy production. Another hormone, Glucagon, mediates this release of fuel. The remainder of the energy (40%) is sent packing to the peripheral tissues and the muscles where insulin allows the energy to enter the cells. If those cells are leptin sensitive they use all 40% of the calories with nothing left over. If they are leptin resistant the excess calories go directly back to the liver to be placed into fat storage (or stuck inside the liver cell) in fat cells because of the high insulin levels. The more fat that gets deposited, the higher leptin levels go over time. If the fat gets stuck in the liver it causes a large immune reaction driving up more inflammatory chemicals. When it gets to a critical level (different body fat levels for all people) the fat begins to make the bad stuff. (IL6 and TNF alpha)

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Please Note: The author of this site is not engaged in rendering professional advice or services to the individual reader. The ideas, procedures, and suggestions contained within this work are not intended as a substitute for consulting with your physician. All matters regarding your health require medical supervision. I shall not be liable or responsible for any loss or damage allegedly arising from any information or suggestions within this blog. You, as a reader of this website, are totally and completely responsible for your own health and healthcare.