The Osteoporosis Rx
Osteoporosis is a disease in which the bones become weak and are more likely to break. People with osteoporosis most often break bones in the hip, spine, and wrist. If you think this problem is not common, let me pick up the rock you must have been sleeping under. In the United States, more than 60 million people either already have osteoporosis or are at high risk, due to low bone mass. RULE 1. If one is leptin resistant, Wolff’s law is null and void, and you are at very high risk for a fractured vertebrae or hip/wrist. You should stop here and go read EMF-8 Quantum Bone for the pathophysiology of this disease. The key features are to increase your spring water intake to 1-1.5 gallons of non fluoridated water a day and strict avoidance of artifical light and the use of pulsed EMF technology devices. This means that "normal conventional wisdom osteoporotic treatments" and exercise will not heal or strengthen a bone until the underlyig pathophysiology is repaired first. When a person has high levels of leptin, it eventually drives cortisol higher and this stimulates even more inflammatory cytokines from cells. As this occurs, LR develops all over the body. Cortisol is one of the major hormones involved in the sympathetic nervous system. When cortisol is chronically high, as I told you in the Hormone 101 blog, it’s bad news. When someone is leptin resistant, they block osteocalcin’s main function and this causes osteoporosis. This is one major reason why fat people lose their bone. It also definitely proves that Wolff’s law is null and void when you are LR. Even resistance exercise maybe harmful when this occurs. Bone only strengthens when the underlying hormonal terroir is working properly. In LR, it is seriously broken. RULE 2. Andropause and Menopause are associated with osteoporosis, and not caused by it. In both situations the best treatment to overcome it is to change your diet to a high fat and protein diet. You would be a wise patient to avoid all bisphosphonate drugs until it’s too late. This will be hard to do, because most clinicians will push drug treatments over evolutionary medicine treatments. Remember The Seven Dwarfs of menopause: Itchy, bitchy, sleepy, sweaty, bloated, forgetful, and all dried up…and the bones are real dried up!
Osteoporosis 3: Related Drugs and Diseases
What are some of the medical conditions that are associated with osteopenia or osteoporosis? 1. Excessive alcohol intake- greater than two drinks a day consistently will do it. 2. Tobacco use- This causes a 100 fold increase in bone loss. Oral tobacco is worse than inhaled smoke 3. Stress- any cause be it emotional, physical, mental, psychic all raise cortisol chronically and kill bone 4. Lack of physical activity increases obesity risk, which increases cortisol from leptin resistance 5. Low calcium intake or absorption from gastrectomy or low acid production from any reason 6. Reduced strength and activity due to a chronic illness or a sedentary life (checked with a grip test) 7. Small build or leanness naturally – correlates with BMI below 19 for women and men. 8. Asian women have a particular propensity to osteopenia genetically and from their diet. 9. Drug therapy, for example, long-term use of corticosteroids such as prednisone-used to treat rheumatoid arthritis, asthma, celiac disease, autoimmune diseases, Crohn’s disease, IBD, and ulcerative colitis. 10. Low Magnesium, strontium, boron, Vitamin D3, Vitamin K2, elevated PTH levels, low sex steroid levels, high insulin levels, low progesterone levels, any cause of a leaky gut. 11. Menopause 12. Andropause 13. Any cause of chronic inflammation (perimenopause can cause severe acute bone loss) 14. Disuse atrophy from any cause (space travel) 15. Paralysis 16. High carbohydrate diets 17. Veganism or a plant based diet. 18. A diet high in whole grain (carbohydrates) is especially risky due to mineral malabsorption in gut 19. A diet lacking in animal protein and animal fat and cholesterol. 20. Excessive use of statins and thyroid hormone can cause osteoporosis 21. Age and sex: the older one is predisposes to osteopenia. Women lose 1-3{a7b724a0454d92c70890dedf5ec22a026af4df067c7b55aa6009b4d34d5da3c6} of their bone density ever year after their last period. 22. Chronic endurance athletics of any type cause severe bone loss due to chronic cortisol elevations 23. Gastric bypass patients carry enormous osteopenic risks. 24. Severe liver or kidney disease; Renal insufficiency can lead to osteodystrophy. 25. Diabetes 26. People with scoliosis of unknown cause (idiopathic scoliosis) also have a higher risk of osteoporosis. I believe this is because most of these children have severe underlying Vitamin D deficiency and a leaky gut, but this has never been studied in the spine literature. Any time I see a scolisosi patient, I always screen for low sex steroid hormones, low Vitamin D levels, and low Carboxylated osteocalcin levels. Bone loss can be a feature of complex regional pain syndromes.as they develop over time. It is also more frequent in people with Parkinson’s disease and chronic obstructive pulmonary disease as well.
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.
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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.
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.
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.
What Are The Optimizing Labs?
When you finally decide to take total control of you life and optimize yourself I always suggest testing. Many of you have bombarded my email and my twitter account for a blog to a list of those labs. Well, today's post is for you. I was resistant to do this because I felt having the list of labs is a waste of time if you don't have a physician who can decipher what they all mean for you. 7 years ago, I could not tell you what this group of labs meant at all to your optimal health. I learned it by reading and going to classes to optimize myself. After much reflection I have decided to give you what you asked for. I am fortunate because many of the PCP's I work with understand these tests well. I may also update it as I think it needs to be updated over time. The first set of labs are what I call the core lab set for optimization. There are other panels I add to the core lab based upon the history, physical, and the food logs I will have patients give me. This blog is meant to be a resource for you to refer back to when the need arises. Discuss these with your doctor but don't assume they will run out to order them because they may not know what all these tests will tell them. That part takes some time. I recommend starting the dialogue with your doctor to assess their willingness to help you. Most of my PCP doctors are awesome "helpers" to their patients with these issues. This requires a lot of work on the doctors part and the patients part. Do not be surprised if this is not covered by insurance. The time required to optimize someone is unreal. I know how long I spent optimizing myself 6 years ago. It was a tedious process but I was not going to give up because I believed my life depended upon it. For most people, 2-3 years you can expect the changes you want. If you are really in tough shape it may take longer but that should not deter you. I love patients who bring big challenges. They are the most appreciative patients I have had in the last 5 years. We can never settle for a C or D when an A is possible.