The Leptin Prescription

Osteoporosis 2: The Vitamin K2 Story

In the first blog on osteoporosis, we focused in on how to stimulate bone mass accrual via our diet. This is by far the best way to fight osteoporosis and least used way, but it is not the only way to treat it. Eating a diet that is plentiful in proteins and saturated fats are smart moves to stave off bone loss as one ages. Eating a diet laden in carbohydrates or filled with a lot of fowl like turkey and chicken is not going to help your bone mass in the long run. The last blog demonstrated that vitamin K2 supplementation (for just 4 weeks) will not only increase your insulin sensitivity, but raise your sex steroid hormones as well to support your bone metabolism. Both mechanisms seem to be related to increased amounts of serum carboxylated osteocalcin (cOC), is made rather than just modulating inflammation in our body. The study I mentioned in part one, had too small a sample size to make firm interpretation on β-cell function result for a population, but the implications are huge for T2D with bad bone, bad heart or bad teeth. It is clear that vitamin K2 is biochemically quite helpful to a T2D with bone loss. The results of this study are consistent with previous studies found in the literature that demonstrated improved insulin resistance by treatment with vitamin K1 or vitamin K2, respectively. The preponderance of the research to date, is pointing out to us that cOC rather than uncarboxylated OC, is the endocrine hormone that increases insulin sensitivity in humans and eventually leads to increased bone mass. It appears the underlying mechanism for this uses inflammatory cytokines and involves leptin receptor dysfunction. It appears that cOC and/or vitamin K2 likely modulates several adipokines and inflammatory pathways other than the classic IL-6 pathways to offset bone loss seen in leptin receptor disease states. Since Vitamin K2 is a critical component of arterial, gut, and bone health, we need to spend some time talking about how the human body handles vitamin K2 in part two of this series. Vitamin K2 up regulates testosterone and it helps both sexes remain somewhat hydrated. This will become important when we hit quantum biology in the blog.

Osteoporosis Part 1

In my day job as a neurosurgeon, I operate on a lot of diseased spines. In the last 12 years, I have repaired over 1000 vertebral fractures from osteoporosis. If you remember back to my podcast with Jimmy Moore, I mentioned in the talk that the changes I had seen in osteoporosis incidence and prevalence is what made me look for the underlying cause. This ultimately led me to leptin and our diet. Many people think since bones are hard and used for support that they are not an active tissue. Bone is a very active tissue in the body that is constantly turned over. We constantly lay down new bone to stressors and resorb bone from areas that are not stressed. Since bone is so active, it uses massive amounts of energy. This is where leptin comes in. Any tissue that requires a ton of energy is coupled to leptin biochemistry. The story on bones and osteoporosis, however, is a very complicated one. I am going to give you a flavor of just how complicated. This osteoporosis series will have many twists and turns. Most seasoned spine surgeons wont know much of what you are going to learn here about bone. Most don't know that osteoporosis is caused by leptin resistance. Just ask one and see if I am correct. Most will tell you to take Calcium, Vitamin D, and exercise a bit to treat osteoporosis. They may mention a Rx for a bisphosphonate class of drugs too. I don't use these drugs at all. If you do just that, you can bet you won't cure a thing and you might even make the problem worse. Spine surgeons are taught a law called Wolff's law in reference to bone metabolism. It says the more stressed a bone is, the more bone is laid down and the stronger the bone is. This law is why most spine surgeons don't think that obese folks will have osteoporosis when they come to see us, much less test for it. These are the people who are experiencing a silent epidemic of this condition. Their numbers have exploded over the last thirty years. I mentioned that in my career I have seen a tremendous increase in this disease. In medical school, I think I had a one hour lecture on this disease. Now it is involved in close to 80{a7b724a0454d92c70890dedf5ec22a026af4df067c7b55aa6009b4d34d5da3c6} of the cases I see in my clinic. Few spine surgeons expect to see osteoporosis in our younger patients because most think this is predominantly a disease of old women with low estrogen levels. We are not taught to look for it in its correct biologic context, so it is often missed as a diagnosis, but often found on MRI imaging as loss of mineral content and more fat present in the marrow space. Spine surgeons must be more vigilant about this disease, because if it's tied to the leptin hormone, it points to the fuels we are putting in our Ferrari's! I will show you why diet is a huge factor in the development of metabolic bone disease that you should consider. This is why I treat osteopenia and osteoporosis a lot differently than conventional wisdom you will hear from other sources.

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.

THE “TEETH” IN DISEASE?

READERS SUMMARY: 1. HOW SCIENCE PRESENTS A CURVEBALL YOU DID NOT SEE COMING? 2. HOW YOUR MOUTH MIGHT BE THE KEY TO DIABETES, OBESITY AND INFLAMMATION? 3. IS THERE A HYPOTHALAMIC PAROTID AXIS? 4. IS THE PAROTID GLAND THE MOUTH'S PANCREAS?   Most of you may not know that before I was a neurosurgeon I [...]

WHAT SHOULD HCG/PALEO USERS CONSIDER AS ADJUNCTS?

READERS SUMMARY: ARE THE SUPPLEMENTS FOR THE LEPTIN RESET DIFFERENT FOR HCG USERS? WHAT ARE THOSE SUPPLEMENTS? WHAT DO THOSE SUPPLEMENTS DO? WHAT SHOULD HCG USERS CONSIDER OVER A STANDARD PALEO/PRIMAL TEMPLATE? I decided to add this post for the many readers I have that use HCG. To say that I have been inundated with [...]

HOW TO FIND YOUR INNER MASTERPIECE?

READERS SUMMARY: 1. WHAT IS PPAR-gamma AND WHY IS IT IMPORTANT? 2. HOW DOES IT TIE ARTHEROSCLEROSIS, VITAMIN K2, AND OUR LIPID PANEL TOGETHER? 3. HOW IS A LEAKY GUT, THE LIVER, OBESITY,CHOLESTEROL, BLOOD PRESSURE TIED TOGETHER? 4. HOW IS EXERCISE COUPLED TO THIS COMPLEX WEB? 5. HOW DOES PQQ FIT INTO ALL THIS? 6. [...]

MSG, your GUT, and your BRAIN, Post-Trauma

READERS SUMMARY: 1. How does MSG and aspartame affect you and your brain and your fat loss? 2. What do artificial sweeteners do to a human? 3. How does neuronal injury from diet, trauma, and energy depletion all tie together? 4. What about young humans? 5. What about young humans with injured brains? In part [...]

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{a7b724a0454d92c70890dedf5ec22a026af4df067c7b55aa6009b4d34d5da3c6} of cases.

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.

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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