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Welcome to OsteoNaturals. We invite you to shop our online store for quality nutritional supplements that promote skeletal health. In addition, our site is full of useful information about osteoporosis and insights about how it can be managed naturally.

Individuals who intend to stay active into retirement will need strong, healthy bones, and a strategy for maintaining muscle strength and overall fitness. Whatever your age or current condition, it is never too early or too late to make a positive difference. The "OsteoNaturals difference" = natural ingredients chosen for quality, safety, purity and potency.

Saturday, January 6, 2018

This is Part XI of a multi-part essay chronicling my personal experience with osteoporosis. In this series I have been taking readers through the diagnostic and treatment phases of my care that began over 18 years ago when I was diagnosed with severe osteoporosis. Over the years, the combination of experiencing multiple fragility fractures along with an intense immersion into the study of bone pathophysiology has given me a unique understanding of this disease. If you are just joining the series, I encourage you to skim through the previous DX Severe Osteoporosis essays on my blog as they provide background to each new installment. It is my hope that this series will provide you with a better understanding of osteoporosis in general, plus a few "pearls" that you may be able to incorporate into your own quest for better bone health. If you have been reading the essays all along...welcome back.    Dr.M

                                          "And now here is my secret, a very simple
                                            secret: It is only with the heart that one can
                                            see rightly; what is essential is invisible
                                            to the eye." 

                                                                         The Little Prince
                                                                         Antoine de Saint-Exupery

Not only was I beginning to discover ways to improve my skeletal and overall health but I was also starting to see osteoporosis through a much different lens—and this lens was projecting multiple images from seemingly divergent rays of medical and biochemical data. For example, exercise signals the body to form bone. Well, I had certainly engaged in enough exercise in my life to build several skeletons if this was the case. So why was my skeleton, or at least its density, so paltry?

Concussive forces and the shear strain (an engineering term for the application of force at a specific angle) from muscular activity send waves of vibration rippling through the body and into bone. Here, cells called osteocytes detect and respond to these mechanical signals, translating them into biochemical signals that stimulate bone-building. Osteocytes start off as osteoblasts, the very cells that build bone. When osteoblasts have finished forming the collagen matrix foundation of bone, each osteoblast then builds a small chamber around itself. This chamber is like a cocoon offering a protected site for the osteoblast's transformation into an osteocyte while the matrix around it is being flooded with solidifying minerals such as calcium, phosphorous, and magnesium. Once the bone is calcified, the now chambered (in an elongated cartilage sac called a lacuna) osteocyte is in place and able to receive those vibrating wave forces—the signals necessary to activate future bone remodeling activity.

Osteocytes in lacunae
Osteocytes have a star-like configuration with appendages reaching out through bony tunnels that radiate from them. These tunnels are fluid-filled corridors extending to neighboring osteocytes, and along them the vibrating mechanical signal is communicated from one osteocyte to the next. Thus, from every movement of the body, there comes the potential to alter the shape of each osteocyte's cell membrane. It is at this point that the signal changes from a mechanical one to a biochemical one. Receivers in the cell's membrane transmit the signal (if the membrane is healthy enough) into the cell where substances that promote bone formation are then released.

Because of this link between physical activity and osteogenic (bone forming) signaling, it makes sense that athletes generally have better bone density than non-athletes. But for athletes who have pushed themselves to excess for years...decades...this positive response to exercise may indeed turn into a negative response. Over stressing the body regularly with excessive, adrenal cortisol-releasing stress, coupled with neglecting to sufficiently refuel the body with important nutrients, puts the active aging athlete at considerable addition risk for osteoporosis. In addition, exercise alone does not necessarily make for better bones. Young adults who take up an exercise program will only gain a small amount of bone density. A post-menopausal woman who starts working out in a gym won't typically gain any density. Her low estrogen causes a continued loss of bone, although her rate of loss will not be as rapid as a post-menopausal woman who does not exercise. So exercise helps to stimulate osteogenic signaling, and it is vitally important for both bone and overall health, but it will not result in increased bone density beyond a certain age—and it is not the primary determinant of bone density at any age.

I was not only seeing that bone was very much alive and amazingly complex but I was beginning to sense that it had a hidden dynamic life. Bone is amazing in that it can undergo change both by remodeling its architecture in response to external mechanical demands, and to internal physiological needs. A hefty percentage of bone is fairly quiescent at any given time. It is just there, doing its job of supporting the body and providing a reservoir for minerals. But in areas in need of repair or when the body is desperate for mineral reserves, metabolic and remodeling activity increases dramatically. Continuous cycles of remodeling are necessary to maintain skeletal health for normal, everyday activity—but when the stresses of life (both physical and emotional) increase, or when the concussive forces of weight-bearing activity are particularly high, micro-fracturing of bone and the need for
repair increases. Weakened bone must be replaced with new, resilient bone. This renewal process is accomplished by coordinated cell groups called basic multicellular units (BMUs).

At any given time there can be millions of BMUs, areas where osteoclasts are actively tearing down old micro-fractured bone and new bone is being formed in its place. Osteoclasts move like predators on the prowl for injured prey. They feast on old microfractured bone, leaving gouged out tunnels and troughs, and then move on. The osteoblasts come in behind, filling the stripped out areas with strong, new collagen matrix. This bone-like substance, called "osteoid," is then mineralized over the next several weeks by osteoblasts. These cells deposit crystalline mineral salts (hydroxyapatite, such as in OsteoMineralBoost) between the collagen fibers to make them rigid and increase their overall strength. Once this biomineralization has occurred and the hydroxyapatite crystals are in place, the bone formation process is complete.

My job was to try and find out if this process was going on in my body and if not...why? Intermittently, as I learned more about bone biology and it hidden physiology, I would scan the slide from the biopsy of my pelvis looking for clues. I could see the BMUs very clearly in their lit-up red tetracycline "ink." Instead of the uniform mineralized bone formation typically seen in "normal"
Zebra-striping: red is new mineralized bone
bone, my BMUs were filled with alternating layers of mineralized bone and un-mineralized matrix, giving it a zebra-striped look.

To me, this suggested there may be a mineralization defect of some kind that was involved in my osteoporosis. It really looked like my severe bone loss—bone weakness—wasn't just from over-activity of the osteoclasts breaking down excessive amounts of bone, but that there was something else going on in addition. It looked as though the crystalline mineral salts weren't "sticking" to the osteoid matrix after it was formed. Or that maybe there was something intermittently inhibiting mineralization. Maybe there was a mineral missing?...or a toxin infiltrating and preventing the hydroxyapatite crystal from forming? Maybe the levels of my testosterone and estrogen hormones were fluctuating every few days? Could the vitamin D and parathyroid hormones which are responsible for pulling in calcium from the gut and kidneys, and maintaining its optimal levels in bone and blood somehow be ineffective? Their levels, after all, had been tested several times over the past year and shown to be normal which meant that the calcium should be there in high enough quantities. Maybe my low level of essential fatty acids (that I discovered through lab testing) was involved? Fatty acids are needed for absorption and deposition of calcium into bone. But if the fatty acids were keeping me from bringing in enough calcium, then shouldn't my parathyroid hormone have been elevated in response to low levels of calcium? My questions seemed endless, and my dearth of information was evident and discouraging. I was seeing that this last question, that of parathyroid function, was of prime importance when evaluating the causes of bone loss, and that is where I placed my next investigatory lens.

                                                    "I need to put up with two or three
                                                       caterpillars if I want to get to
                                                      know the butterflies."

                                                                                The Little Prince
                                                                                Antoine de Saint-Exupery

Stay tuned for DX Severe Osteoporosis - Part XII

Sunday, December 24, 2017

DX Severe Osteoporosis: Part X - Impacting Skeletal Health

This is Part X of a multi-part essay chronicling my personal experience with osteoporosis. In this series I have been taking readers through the diagnostic and treatment phases of my care that began over 18 years ago when I was diagnosed with severe osteoporosis. Over the years, the combination of experiencing multiple fragility fractures along with an intense immersion into the study of bone pathophysiology has given me a unique understanding of this disease. If you are just joining the series, I encourage you to skim through the previous DX Severe Osteoporosis essays on my blog as they provide background to each new installment. It is my hope that this series will provide you with a better understanding of osteoporosis in general, plus a few "pearls" that you may be able to incorporate into your own quest for better bone health. If you have been reading the essays all along...welcome back.    Dr.M

                                "It's a good idea to keep at least a vague idea of
                                  where you are, no matter how much you are used to 

Now, with this inflammatory reaction to gluten being such an obvious concern, I began to look at this strand of the web through every lens I could. It didn't take long to find a few more important connections. Glutamine, an amino acid energy source for cells that line the intestinal wall, is often found deficient in professional athletes that train hard every day and I certainly fit into that category. Cells of the digestive tract need glutamine for sustenance, growth, and energy production. In an exhausted body that isn't being properly replenished, glutamine levels drop and cells of the gut suffer, with poor absorption of nutrients the unfortunate result.

Even if absorption is normal, a hard-working athlete piles on both oxidative and adrenal stress producing copious amounts of free radicals and high blood titers of the catabolic, destructive hormone, cortisol. Excessive free radical and cortisol levels places high demand on essential fatty acid supplies. An athlete's body extracts aerobic energy from molecules reacting with oxygen. In this process, the oxygen molecule looses an electron and becomes an unstable scavenger called a "radical." These free radicals are insatiable, stealing electrons from their closest molecular neighbors, which results in cellular damage. It's the phospholipids (made from fatty acids) in a cell's membrane, that often get damaged...and a cell's membrane, as I would find soon find out, is vital for more than just defining the cell's boundary.

Fatty acids and phospholipids are vital for optimal cell membrane function including the transference of signals from one cell to another. If omega 3 fatty acid intake is deficient, cell membranes (and their ability to transfer signals) suffer. Athletes are particularly demanding of omega 3 fatty acids and optimal intake is necessary to achieve high level performance. Without omega 3s, cell membranes loose some of their functional capacity. This loss of function not only alters the normal signaling of important information but it also increases the signaling for a heightened inflammatory response!

Over the next few months, I discovered more strands in this elusive web. Amazingly, there was no paucity of evidence in the literature showing that the cells and substances that the body releases in response to inflammation were also the cells involved in the destruction of bone. As the bone in our body ages, it becomes less resilient and develops microfractures. This old weakened bone must be replaced with new bone. Both bone resorption, the dissolving of the old, microfractured bone, and inflammation in response to injury, are crucial to overall health. But when the body fails to limit these processes, the immune system gets out of balance and the skeleton goes into a spiral of disrepair.

In my case, the inflammation in my hip began as a response to the stress fractures but then something went wrong—the injured tissues didn't heal, and the inflammation became chronic. And the Gilbert's* syndrome...?...The condition where bilirubin (a breakdown product of blood) increases due to a specific genetic enzyme deficiency? Where did that fit in? This "harmless," hereditary liver disorder, I found, interferes with fatty acid absorption from the gut. (Yes, the same fatty acids that are often found to be depleted in athletes.) With 5 to 7 percent of the population having this disorder, it seemed to me that it should be taken more seriously by the medical community, especially when dealing with people with an ongoing disease process...such as osteoporosis. An athlete with Gilbert's is under double the physiological stress and at a higher risk for inflammatory related disorders, including osteoporosis. Combine this with a sensitivity to gluten and we have a condition ripe for severe bone loss.

The doctors had assured me that there was "no connection" between Gilbert's and my hip pain or my osteoporosis. But that was NOT what I was seeing. What I was beginning to see was that in medicine, the term "no connection" really meant "we have not yet made that connection" or "we don't have the time or money to research it right now." In their eyes, if it hasn't been researched, it isn't worth thinking about. (And if pharmaceutical companies don't see a way to make money on it, it won't be researched.)

Of course, it is not only the essential fatty acids that can become deficient as a result of the athlete's frequency and intensity of exercise. Vitamin and mineral deficiencies are common, as are deficiencies in amino acids. Glutamine and methionine are often in short supply in both the athlete and in people with Gilbert's syndrome. Not a good thing considering the almost endless biological functions that these two amino acids are involved in: energy production, muscle building, fuel for cells of the immune and gastrointestinal systems, collagen synthesis for both joint and bone, the production of glutathione (the body's most important antioxidant), etc... These two amino acids are needed for just about everything. I immediately began supplementing my diet with glutamine and methionine, and whey protein which is a balanced source of essential amino acids. I also began to take milk thistle (sylymarin). If Gilbert's was involved in the liver's ability to function, I wanted to cleans and optimize the function of my liver as much as possible. With my chiropractic training and interest in nutrition, I knew that consuming lots of fresh green vegetables and supplementing with milk thistle could help. Milk thistle is known for its ability to fortify the liver and, as I found out, prevent the depletion of glutathione and limit free radical damage. It finally felt like I was not only starting to see patterns in this complex web, but that I was also finally starting to understand enough that I was able to do things to positively impact my skeletal health.

...Stay tuned for Part XI of DX Severe Osteoporosis

Saturday, December 9, 2017

DX Severe Osteoporosis: Part IX - Seeing Specific Threads of the Web

This is Part IX of a multi-part essay about my own personal experience with osteoporosis. I will be taking you through the diagnostic and treatment phases of my care in hopes that it provides you a better understanding of osteoporosis in general, and pearls that you can use to better your own bone health.

                        "We all see mountains. It is how we climb them that is different."

                                                                                Crucibles of Will

When the body is injured, the immune system's inflammatory response infiltrates the area cleansing it with blood and scavenging, destroying invading organisms. In situations of injury, inflammation can be the magic to survival, but in chronic disease, it is the destroyer of life as we once knew it. Chronic systemic inflammation, in fact, is the major cause of osteoporosis.

To initiate the inflammatory response, the body's first step toward protecting and healing damaged tissue is to put out a call for prostaglandins. These are naturally occurring chemicals that relax smooth muscle and cause peripheral vasodilation to facilitate blood flow. The body produces a specific prostaglandin called PGE2 from fatty acids found in abundance in red meat and dairy products. In addition to vasodilation, PGE2 is responsible for the fever we get when we are sick. It can also be responsible for muscle and joint pains, and, even skin sensitivity—one of my symptoms. These sensations can happen when there is an imbalance in dietary fatty acids, such as an excessive intake of omega 6 fatty acids, even when we aren't sick. It sure was looking like my discovery that I was low in omega 3 fatty acids, coupled with Gilbert's syndrome, may not only connect the dots to my symptoms, but also to my elevated bone resorption markers...and to my osteoporosis.

There are other prostaglandins not directly involved in the inflammatory response but which help prevent excessive inflammation. These prostaglandins are derived from the omega 3 fatty acids, ones found in oils from flaxseed, algae, and in cold-water fish. The sources of these fatty acids happen to be less prevalent in the typical American diet, and this is part of the reason why deficiency is common. That is, deficiency from terrible diets, which I was now beginning to see, was mine.

I felt like I was on to something important, or at least my forever positive attitude was grasping for something—anything—to shed some light on this thing. I dug deeper into the research about prostaglandins and as it turned out they weren't just important for the inflammatory response, but they were involved in bone metabolism! Prostaglandins are made by osteoblasts and can stimulate both the formation and resorption of bone. This was certainly another huge clue. Here was something that seemed to link my vague symptoms (skin sensitivity, irritability, and intermittent feelings of weakness) to two different body systems: the immune's inflammatory response AND bone biology. In addition, it was my first indication that the chronic hip inflammation and the bone loss could be linked after all. I kept remembering what an endocrinologist from the Mayo Clinic and the one from California had said, that there was "NO connection" between my persistent hip pain and the osteoporosis. They acknowledged the connection between the hip stress fractures and the osteoporosis but not the persistent hip inflammation. I didn't understand how they could be so sure about something like that.

But why was I deficient in fatty acids? The endocrinologist had told me that he had tested for diseases that could interfere with absorption, but that these tests came back normal. Plus, I had none of the symptoms typically seen with tropical sprue, Whipple's disease, Crohn's disease, Zollinger-Ellison syndorome, or any of the other 20 or so absorption disorders described in the medical texts.

When I began to look more closely at my diet I discovered that even Americans eating a fairly "good" diet aren't getting enough omega 3s. If highly processed foods, especially ones made with hydrogenated oils, are a large part of ones diet, imbalances of fatty acids become even more common. Looking back to my intense training years, I was certainly not as vigilant about eating well or for that matter eating at all. At times when money was tight I may have just let meals slide, and certainly processed foods were part of my diet. Even so, I felt there had to be more to this picture than just diet. Currently I was eating more healthy foods, avoiding junk foods, and consuming salmon and other cold water fish that were good sources of omega 3s. I knew that eating healthily and taking in good quality nutrients was only one part of the complex process of nourishment for life and growth. There just had to be more to this story.

I went back to thinking about problems that could interfere with the absorption of nutrients, like poor digestion or malabsorption. The more I read about osteoporosis, the more celiac disease popped up in the writing. But the endocrinolgist had ruled out celiac disease. Or had he? I went over the prior lab work from over a year before and found the test results for anti-tissue transglutaminase IgA (tTGA) (the blood test for celiac disease). The result: 19 U/mL with a reference range of less than 20 units as negative, 21 to 24 units as borderline, and 25 units and over as positive for celiac disease. Yes, it looked like I was negative for celiac disease. But I got to thinking, how can this be a pregnancy "yes/no" type test? It didn't seem like that at all. What was this tTGA test testing for anyhow? When I found out that transglutaminase was an enzyme released by gluten damaged enterocytes (cells lining the intestinal tract) and their microvilli (small appendages for better absorption of nutrients) in the gut it clicked! If my test result was 19 U/mL and 20 is borderline positive, well, there MUST be some kind of damage to my gut taking place. Maybe not total damage to the extent that my gut's microvilli 
were totally atrophied (flattened) (which is what happens in Celiac disease) but damaged none-the-less.

Celiac disease is an intolerance to gluten in wheat, barley, and rye that causes all kinds of abdominal symptoms. Bloating, diarrhea, constipation, these are all symptoms of celiac disease. The more I read about the disorder the more intrigued and excited I got—especially when I came upon the term, silent celiacs. These are people who have celiac disease but have few or no symptoms at all when they eat food with gluten in it. Now I was really thinking, maybe my 19 U/mL for tTGA was significant after all.

I had none of the typical bloating, constipation, diarrhea, kind of symptoms seen with celiac. But I did have intense abdominal pain after hard runs that I was now relating, at least in part, to Gilbert's syndrome. With this elevated tTGA test result it occurred to me that although I may not have full blown celiac disease I sure could have a sensitivity of some kind to gluten. A sensitivity severe enough to cause some loss of absorption or an influence of some kind on my bone health. I knew I needed to do some more testing on my own. The next two tests I did were the antibodies for gliadin (gluten), IgG and IgA. The results: 36 and 42 units respectively. With a reference range of less than 20 units being negative and 20 or more units indicating that antibodies to gliadin were detected, I knew this was significant. I may not have celiac disease with microvilli flattening but there was enough sensitivity to gluten that the enterocytes were "leaking" transglutaminase. These cells were certainly not happy and indeed were causing an immune inflammatory response.

With these results, the possibility of nutrient malabsorption was a concern. And even if the damage from gluten in my diet wasn't severe enough to cause severe malabsorption my research uncovered a little known fact. One that most doctors have no idea exists. Bone loss caused by gluten sensitivity is not simply from the malabsorption of nutrients. A person's sensitivity to gluten can lead to bone loss through two completely different physiological mechanisms. Besides causing damage to enterocyte microvilli which leads to malabsorption, gluten sensitivity triggers a systemic rise in proinflammatory cytokines. These cytokines, along with the release of a protein called zonulin by the enterocytes, causes the tight junctions between the cells to separate forming the condition of "leaky gut". Gluten and other huge molecules enter through these large openings setting off a systemic inflammatory response (thus the elevated anti-gliadin IgG and IgA tests). When this occurs for months and years at a time, it can produce a chronic systemic inflammatory response. Yes, I was now seeing real, specific threads in this entangled web of bone loss. It was one of the most powerful aha moments in my life.

"Hang out with your fear when you're feeling afraid. Follow its movement. Become intimate with it. Fear is an opportunity. Approach it like a tracker in the forest — watch where it goes, what it does, what it eats, where it eats, where it rests, where it turns, where it stops, where it hides. Embrace it. Stay with it."
                                                                                Paul Rezendes, The Wild Within

 ... Stay tuned for Part X of DX Severe Osteoporosis

Sunday, November 19, 2017

DX Severe Osteoporosis: Part VIII - Implicate Medicine

This is Part VIII of a multi-part essay about my own personal experience with osteoporosis. I will be taking you through the diagnostic and treatment phases of my care in hopes that it provides you a better understanding of osteoporosis in general, and pearls that you can use to better your own bone health.

                              "So the relationship of each moment in the whole of all the
                              others is implied by its total content: the way in which it "holds"
                              all the others enfolded within it."
                                               David Bohm, Wholeness and the Implicate Order

My constitution was fire, according to the acupuncturist. Looking back over my life and the intensity with which I approached things...well, I could relate to that assessment. But the smell of being "scorched"...that was just embarrassing...

Bone has three main functions: it supports the frame, protects organs from hard knocks, and acts as a reservoir for energy (fat) and minerals. I had a hunch that it was the last that would hold the most clues to the cause of my osteoporosis, especially since the biopsy showed that my bones were gaunt, with thin, disconnected trabeculae. They looked totally spent—scorched from years of, well, that was the question. Years of what? Malabsorption of nutrients? But the doctor had said I didn't have any absorption issues. Could it have been all those years of training in athletics? With my eyes focused on making the US Olympic Team since I was 13 years old, I had certainly stressed my body to the core. Had it been all those years of stressing my adrenal glands, stressing the overall functions of my body, that had sucked the energy out of me. Could those years have sucked the reserve function right out of my bones? There are lots of athletes who train hard for years and years and don't end up with osteoporosis. So that, at least by itself, wouldn't make sense either. But there was no denying, from the biopsy, it certainly looked like my bones had given just about all that they could give. And now, at the age of 45, all that was left was just empty chambers. And it looked as if they had been running on empty for quite some time.

The endocrinologist had ordered over 30 lab tests but everything was coming up normal, or at least that was his interpretation. At first I just went along with what he said; after all, his expertise on the subject was obviously considerably greater than mine. But, by a year into this mess (of being diagnosed with osteoporosis) my understanding of the technical aspects of bone loss improved and I began to look back over the lab tests more closely. While they were mostly pretty good, I noticed that some of the results were just a little off, just a little out of the normal reference range. I began to wonder, could these have meaning, as they relate to osteoporosis, that the doctor may not have understood?

Doctors focus on body parts and body fluids to help them understand a disease. But it's really impossible to understand everything...every slight variance in lab test and every "minor" symptom a patient presents with. And even if a doctor did understand these variances, would they try to put all those bits of information together, like pieces of a puzzle, in an effort to understand the patient as a "whole?" For example, I had told my endocrinologist that my skin was sometimes extremely sensitive, at times I was irritable (for me that was really unusual), and my stomach often hurt after long intense runs. I had also told him that I sometimes felt a slight overall body weakness. I couldn't really describe some of these feelings very well and I guess my ability to compete on a high level in road races and triathlons put him at ease that these vague symptoms weren't from something terrible brewing. In fact, he didn't seem to be interested in any of these symptoms, and as for the slightly-off lab work, that was quickly tossed aside.

After my biopsy, several months passed when I thought things might be better, but then I sustained several more rib fractures from very minor traumas. I was getting frustrated. I didn't see any progress in the investigation and now I was breaking again. We didn't seem to be any closer to finding answers to why I had osteoporosis than we were at the beginning. With each visit to UConn there was just a repeat of all the lab tests that had already be done...nothing new and no focus on what lead to follow next. In fact, there just didn't seem to be any leads at all. The only thing that was happening was just a reiteration that I needed to take a bisphosphonate medication which I did not want to do.

With my greater understanding of osteoporosis and my closer look at the lab work (especially those results that were just outside of the normal reference range), I noticed some interesting connections. The "normal" comprehensive metabolic profile (CMP) for example, showed an elevated level of bilirubin, a breakdown product of red blood cells.

My hunch was that each of my symptoms and the "slightly off" lab tests could have some significance. Each of these might hold clues to understanding the "whole" of me, or at least to the source of my severe bone loss. I felt that implicate* within each symptom, within each slightly-off lab test, there could be some view of the whole answer. Like cells that each hold the same DNA map of the complete organism within them, my symptoms had implicate within them the wholeness of my body's dysfunction. In other words, the biology of each symptom was part of the biology of the disease, which was part of the biology of my whole body's functioning. Each symptom was significant to some extent or another. But like DNA, which is nothing without the cell that cradles it, each symptom and slightly off lab test by itself had no meaning. Even the low bone density (bone quantity) meant little without a vision of the whole structure: what my risks for fractures were, what my bone quality was, what my muscle strength was, and how my organs were functioning. Everything had to be, or at least should be, looked at together.

In addition to the high calcium in my urine and the elevated N-telopeptide indicating a high rate of bone loss, I was now aware of this elevated level of bilirubin in my blood. Could this have meaning? When I thought back to the first weeks after my diagnosis, I now remembered that the endocrinologist had said that I had a mild disorder called Gilbert's Syndrome. In retrospect I saw that he was referring to this elevated bilirubin. But I also remembered that he said it didn't have any bearing on my osteoporosis and we had both quickly dismissed it.

Now, a year later, the elevated bilirubin** and my renewed interest in a possible malabsorption issue prompted me to run some lab tests on my own. One of these tests was for fatty acids and the results were startling. I was extremely low in polyunsaturated fatty acids. I didn't understand it, how could I be deficient in these? My diet included oils such as corn and safflower; I ate peanuts and fish and lots of other foods that contain high amounts of essential fatty acids. They were in my diet...but maybe I wasn't absorbing them? The endocrinologist said there was no connection in this either. But I started to think that maybe the fatty acid deficiency was somehow keeping the inflammation going on in my hip. After-all the hip was still hurting, a year now since the hip pain first began and since I had initially been diagnosed with osteoporosis.

Could the low blood polyunsaturated fatty acids and the Gilbert's Syndrome have something to do with the lingering hip pain—or the osteoporosis—or both! Maybe, I was beginning to see what could be the head of a faint trail. All of a sudden it felt as though I had stepped into nature's complex biochemical laboratory where life's continual transformations are fueled and formed. I began to understand chains of biochemical interactions that I never knew existed, and these chains, like strands in a spider web, were being woven by all the biochemical influences of every organ system in the body. The biochemical trails through this web were confusing and seemed infinite.

In an effort to uncover more strands to this yet completed web, I began to think back to the days in high school and college where I had so much abdominal pain after runs that I had to curl up on the floor and wait for the pain to go away. And then I remembered that this pain, although not as frequent or intense, but there none-the-less, sometimes occurred into my 30s...and, into my 40s. Not all the time, but just after hard runs I would sometimes have intense abdominal pains. It had actually just become part of me and I really didn't think about it any more. But now, reading about Gilbert's—nausea, abdominal pain, weakness—especially after the stress of intense exercise and dehydration...well, now things were starting to make sense. The web was starting to take shape.

                              There are things we can only learn about an organism by taking
                              it apart—but to understand that organism we must fully engage
                              with it as a dynamic, interconnected whole. It is no wonder that
                              different parts of the body—the skin, joints, spine, organs—may
                              all be affected by a disease process even when they have no 
                              obvious or direct physical, chemical, or neurological 
                              connection with each other or the process itself.

* "Implicate" (order) is a term developed by David Bohm, a theoretical physicist, who developed a mathematical and physical theory that explored the concept that everything is connected.

** (For more on bilirubin and osteoporosis visit my blog.)

Monday, October 30, 2017

DX Severe Osteoporosis: Part VII -- In Search of the Whole Skeleton

This is Part VII of a multi-part essay about my own personal experience with osteoporosis. I will be taking you through the diagnostic and treatment phases of my care in hopes that it provides you a better understanding of osteoporosis in general, and pearls that you can use to better your own bone health. 

The universe is made up of individual particles that "flow within a continuous energy field encompassing a wholeness much greater than the thought processes which attempt to break the particles from their sea of wholeness."
                                                                                 David Bohm

When I first opened the door into the world of osteoporosis research, it was like walking into an anatomy classroom filled with lots of skeletons. Half of them were broken, missing parts and scattered about, and there was no teacher, just a huge pile of books dumped in a corner. About the only thing I knew was that you were supposed to take calcium supplements and eat lots of dairy. But
it didn't take long, the first book or two on the pile, to make me see that popular ideas about osteoporosis were far from accurate. I had a long way to go and I knew it.

Conventional Western medicine looks for certain signs and symptoms in a patient to match with what are considered the characteristic signs and symptoms of a particular disease entity. The doctor can't consider every physical manifestation that could be a clue to what is really going on because there just isn't time. Where do they draw the line? What physical, mental, or emotional conditions in a patient are significant, and which are not? Western medicine tends to select a small number of symptoms to consider. For each general complaint--headache, back pain, insomnia--there is a brief checklist of questions and a list of diseases to match with the symptoms. In my case, the initial list at the endocrinologist's office was twenty in length. The doctor's objective was not to discover my individual pattern, but to figure out which of a few disease-categories my bones might be dropped into. Having a specific diagnosis, even if it is just called "idiopathic" (meaning "we don't have a clue as to what the cause is...") or "primary," gives us the satisfaction of labeling--satisfaction that the ills are now neatly categorized, ready to be boxed and shipped out for treatment. To categorize is simply a way to feel in control.

The problem is that once we diagnose, it's easy to stop thinking, stop observing. We stop looking for other answers, other possibilities and connections. The pressure is off; the diagnosis is there. But are we really under control...? With a diagnosis, the physician has a ticket to enter the medical superhighway with its trailer-loads of information, and thousands of other physicians and researchers traveling in the same direction. The superhighway feels safe, it's familiar and well marked; but there's lots of country that it passes right by.

I'm not saying we shouldn't diagnose. But there are shortcomings in our way of doing it. Other healing practices approach the analysis of symptoms quite differently. In traditional acupuncture, as in my own chiropractic practice, listening to the patient is extremely important. The acupuncturist relies on the patient's description of the problem that brought them in and on observing the patient--noticing how they move, how they hold themselves, the feel of their skin, their smell, their affect, their energy, even the tone of their voice. As the patient describes symptoms, they are encouraged to mention anything that strikes them as characteristic of their normal pattern, and everything they associate with their current problem.

I didn't feel we were ready to label my loss of bone density with a diagnosis yet. I had no idea what the cause of the bone loss was, but I did know that there was an imbalance spurred by something... somewhere. One of the first tests the Dr. from UConn and I had ordered was the bone resorption marker N-telopeptide (NTX) and the results had come back abnormally high. A reading of 123 nmol/BCE/mmol creatinine with a reference range of 4 to 64* showed that I was loosing bone rapidly. What could cause the osteoclasts, the cells that break down bone, to be so aggressive? Was it diet, stress, over-training, or was it hormonal? Was it toxicity from chemicals or heavy metals? After all, the bone biopsy had shown that strange "zebra striping" appearance that the pathologist had said looked similar to cases of heavy metal toxicity that he had observed before. My biopsy slides hadn't stained positive for iron, and blood and hair analysis' didn't show heavy metals...but tests can be wrong. Or, could it be that my kidneys or my intestinal tract were not functioning properly. I felt TOTALLY fine...I did not FEEL sick. How could my bones be crumbling? How could they be loosing so much density so rapidly and I not feel ANYTHING? Had my genetic makeup just written it that way?

The possibilities seemed endless. The endocrinologists wanted to stick my symptoms in the box labeled "idiopathic" with alendronate as the treatment of choice. But I didn't understand. What did they expect me to do?...take a bisphosphonate drug for the next 45 years? I was only 46 years old, and I might live to be 90 (give or take a few). That just seemed ludicrous!

I wanted a doctor who could look at me as a whole, look at both my inner and outer self as one, not just a case of low bone density. It seemed that an acupuncturist trained in the Chinese healing tradition would be a good person to start with. When I asked the acupuncturist what she thought after her initial examination, she said that of the five elements that make up the body--water, wood, fire, earth, and metal--my constitution type was "fire" and that my smell was that of being "scorched." I wasn't quite sure what to make of this information, I didn't know if it was significant in terms of my efforts to track down the cause of my disease and to make a treatment plan, but I added this information to what I had already found out. At this point in the process, it was just another clue as to how the different systems of my body were working...or, more accurately, not working.

          "The whole may actually organize the parts."
                                                                  David Bohm

* With almost 20 years now of observing the bone resorption markers of hundreds of patients, it is my opinion that this reference range is totally useless. A better reference range for NTX (urine) would be 20 to 45. If a person's NTX gets below 20, osteoclastic activity is probably too low to keep bone quality in the healthy range with minimal microfracture accumulation. If NTX gets over 45 then we run the risk of excess bone resorption and a net loss of bone density.

Sunday, October 29, 2017

How Much Calcium Should I Take?

Ninety-nine percent of calcium in the body (and that is 3 pounds of the stuff!) is in our bones. And since bone is in a constant state of being torn down and then being built back (remodeling), let's just say it goes without saying that we NEED adequate calcium for good health. Calcium is important not just for our bones but also for a whole host of other essential functions. Without calcium there would be no nerve transmission, muscle contraction, cell signaling, blood clotting, constriction and relaxation of blood vessels, or secretion of hormones. (1) Studies have consistently found that higher calcium intakes reduce the risk of hypertension, obesity, and type 2 diabetes. (2,3,4). In a 2015 study from the National Osteoporosis Foundation, Weaver, et al. found a "significant decrease in fractures with calcium and vitamin D supplements." (5)

OsteoSustain: three tablets provide 500 mg calcium

The Recommended Dietary Allowance (RDA) for calcium as endorsed by the Institute of Medicine (IOM) is 1,000 to 1,200 mg daily for adults and not to exceed 2,000 mg. (6) People should strive to meet these calcium levels using food sources to the greatest extent possible. A healthful, well-balanced diet should include dairy (especially yogurt and kefir...preferably goat), dark leafy greens, and other calcium sources like sardines, almonds and beans.

Unfortunately, some people are sensitive or allergic to dairy. In addition, although many physicians recommend dairy as a calcium source, high dairy intake may come with other undesirable effects. Besides grave concerns over the dairy industries use of rBGH (growth hormones), milk is acidifying to the body (and not necessarily good for bones as the dairy industry would like you to believe) and casein, the major protein found in milk, has neoplastic (cancer) potential. Also, D-galactose (from the lactose sugar in milk) has been shown to increase inflammation, contribute to neuro-degeneration and reduced immune function. To this point, Michaelsson, et al. observed a link between high milk intake (3 or more glasses per day) and higher rate of both mortality and fracture in women, and a higher rate of mortality in men. "There were positive associations between milk intake and concentrations of markers for oxidative stress and inflammation." The authors concluded, "A higher consumption of milk in women and men is not accompanied by a lower risk of fracture and instead may be associated with a higher rate of death." (7)

We recommend 500 to 800 mg/day of supplemental calcium depending upon your diet. If you have severe bone loss and are sensitive to dairy then a slightly higher dose per day may be indicated.

1) Linus Pauling Institute. Calcium dietary supplemental fact sheet. National Institutes of Health Office of Dietary Supplements website: Updated November 21, 2013.

2) Alender, P.S., et al. 1996. Dietary calcium and blood pressure: a meta-analysis of randomized clinical trials. Ann Intern Med 124:825-31.

3) Bucher, H.C., et al. 1996. Effects of dietary calcium supplementation on blood pressure. A meta-analysis of randomized controlled trials. JAMA 275:1016-22.

4) Villegas, R., et al. 2009. Dietary calcium and magnesium intakes and the risk of type 2 diabetes: the Shanghai Women's Health Study. Am J Clin Nutr 89:1059-67.

5)Weaver, C.M., et al. 2016. Calcium plus vitamin D supplementation and risk of fractures: an updated meta-analysis from the National Osteoporosis Foundation. Osteoporo Int 27:367-376. 

6) Institute of Medicine. 2011. Dietary Reference Intakes for Calcium and Vitamin D. Washington, DC: The National Academies Press.

7) Michaelsson, K., et al. 2014. Milk intake and risk of mortality and fractures in women and men: cohort studies. BMJ 349:g6015. 

Monday, October 16, 2017

DX Severe Osteoporosis: Part VI -- Drug Therapy, Fixing Without Healing

This is Part VI of a multi-part essay about my own personal experience with osteoporosis. I will be taking you through the diagnostic and treatment phases of my care in hopes that it provides you a better understanding of osteoporosis in general, and pearls that you can use to better your own bone health. 

"In this country we are brought up to underestimate the power of our own capacity to heal, to be ignorant of how to support and strengthen our ability to recover from illness, and to rely on external substances to counter disease, discomfort, and inadequacies of all kinds."                                 Crucibles of Will

The first endocrinologist had given me two options: either do nothing until I began to self-destruct, or immediately start taking two drugs--thiazide, a diuretic that makes you urinate more but lose less calcium, and alendronate (Fosamax), a drug that stops bone loss, boosts your density, and lowers the risk of fracture. My new doctor from UConn disagreed about the thiazide, because while it may reduce calcium in the urine it can also inhibit calcium absorption from the gut.* The alendronate though, he was in total agreement with, and said that I should start it immediately.

Medications can be incredibly dramatic and effective gifts. But most drugs don't fix things, they just interfere with bodily systems in such a way as to get a desired therapeutic effect--like taking drugs to improve one's performance in sport. Gold medals are often won with the help of chemicals because for some athletes it is simply the color at the end of the chain that is important, not how you get it. The problem with drugs, besides being illegal in sport, is that the athlete never gets to find out who they really are, what they alone can really do. They are robbed of that special feeling of truly experiencing what it is like to give their whole self to a silence, to the unknown territory of their own potential--to an emptiness into which they bring the essence of who they are and offer it to the world. 

I have always thought that it was important to pay attention to the underlying truth of any situation, and the natural integrity of other beings and of ourselves. That's one of the reasons I went into chiropractic, a drugless profession, which tries to discover the whole truth behind a person's injury or illness, and which respects the integrity of the individual's body, including that body's power to heal. Drugs certainly have their place in health care, but I feel that we should try to help people as naturally and wholly as possible--it seems like less of an insult upon the body--more pure and in harmony with the person's whole being. Growing up, I could never understand how anyone could take a drug to make them something that they were not. So being told to take alendronate before we'd even tried natural alternatives was not only difficult for me to accept as the only answer to my health problem, but my resistance also had a practical side. Once a drug therapy is initiated there is no way of assessing the effects of a natural treatment plan. 

Using bone density as an indicator of success or failure of a treatment regime for osteoporosis is impractical because density builds so slowly. But using specific lab tests to see changes in the body's physiology, changes that would be beneficial in improving bone density, is more practical. If I could see improvement in lab values as a result of natural therapy, then I would know that my biochemical patterns were shifting in a good way, becoming more balanced. Starting the use of alendronate before more information was gathered would eliminate this important guide. 

Alendronate is in the family of drugs called bisphosphonates that work by killing off (or at least making them really sick) all the osteoclasts, the cells that eat old, worn-out, and unstable bone. Normally, after the osteoclasts have resorbed the old bone, other cells, called osteoblasts, come along behind and make new, strong bone, in its place. This remodeling process is what keeps our bones healthy and resilient, and the interaction or coupling between the two cell types is a balancing act that needs to be maintained. It is precisely this coupling that the bisphosphonates disrupt. 

I felt trapped...I knew very little about osteoporosis and even less about drugs. I was concerned, fearful actually, of breaking more bones and I didn't want to fall into what looked like a big dark hole of the unknown. I was 46 years old...what were these doctors asking me to do?...take drugs for my skeleton for the rest of my life?...another 45 to 50 years?! It didn't make sense.

All my life I had tried to respect my body, both to heal and to achieve in athletic competitions, with no help from synthetic chemicals of any kind. The only substance I ever used was what came naturally inside me. Now I was being asked to participate with the doctors in doing something to my body that destroyed part of its natural functioning. If I did this, I felt I would be betraying the body I had always tried hard to respect and improve. 

The problem with bisphosphonates, and the newer drug Prolia, is that they shut down bone resorption but do nothing to encourage osteoblasts to form bone. In fact, it's the osteoclasts that normally signal the osteoblasts to make new bone. With the osteoclasts gone from the scene, new bone just doesn't get made. The overall effect is a decrease in bone remodeling with minimal increase in bone density. The reason bisphosphonates are able to reduce fractures is not from their paltry increase in the density of bone (which, is secondary in other words it isn't primary new bone, just a secondary sprinkling of minerals onto the old weak scaffolding), but from a reduction in the number of small cuts of gouged out bone that the osteoclasts ordinarily make. Like the perforations that make it easy to tear pages from a notepad, these spots are vulnerable to fracture, even though they are a necessary part of remodeling. Where there is no remodeling, there are no temporary weak spots, and no focal areas where a little crack can get started. In normal bone these small cuts pose no problem, but if the overall density and strength of bone is low, these perforations become the ideal sites for catastrophic fractures to begin. 

Older people are typically more sedentary and place less stress on their skeleton. Leaving the old bone in place by stopping remodeling, seems to work well in reducing the risk of fracture, even though the actual quality of the patient's bone becomes arguably worse. How many years can a person go without remodeling before that old bone becomes so old that it's more fragile than new bone would be with remodeling sites? That's a big question and nobody knows the answer. For an 80-year-old it's probably a reasonable risk. For a 46-year-old, it's a question that hadn't been tested much, and I wasn't sure I wanted to volunteer to be a guinea pig. 

The UConn doctor was concerned that I was going to start getting some major fractures. Besides the two ribs from skiing and the new compression fracture from lifting the couch, I snapped two more ribs just leaning up against a horse to pick out its hooves...heard them snap, as easily as twigs on a dead pine. The literature was daunting; it referred to bone loss such as mine as irreversible. That's one really ugly word, irreversible. It's like saying some runner is
My biopsy with disconnected trabeculae there's no point in even point in even entering the race. The bone loss is considered irreversible because once the trabeculae, the small structural supports that give strength to inner bone are resorbed and become disconnected from surrounding bone, there is no way for new ones to reform. And when the new ones can't form, and old ones don't repair, the density just keeps going down and the risk of fracture keeps going up.


But everyone can be beaten; maybe not by me, but by someone. I finished back in the pack in a lot more races than I ever won, but even when it looks like you can't win, you don't know till you put yourself out there and run till you drop. It is sure a lot better to get on the starting line even if you only finish second or third, or last, than it is to just sit and think about it. With osteoporosis, it was even hard to tell who was toeing the line, what I was racing against--but I knew I wasn't going to let this "irreversible" hype make me shy away from trying. I wanted to heal my body, not just take some calcium and hope for the best, and not just take some drugs that killed off some of my cells, interfered with my body's natural processes, and made my bones old. 

I knew no one was going to be committed to this program except me. But I was ready to give it everything I had. It wasn't long before I started ordering a lot of my own lab tests and researching osteoporosis using every source I could find.

One of the first tests the doctor from UConn had ordered was N-telopeptide (NTX), a bone resorption marker that measures how much bone collagen is in your urine. When the osteoclasts tear down old microfractured bone, the shards of bone collagen go into the blood and is then flushed out of the body through the urine. If the lab results for NTX come back elevated, it means the osteoclastic activity is excessive and you are loosing bone rapidly. Rapid bone loss is a major risk factor for fracture and the higher the NTX the greater the risk of breaking something. In fact, if you take two people, both the same age, same build, same everything...and they have the same bone density...the one with the higher NTX will have a greater risk of fracture. 

My NTX test result was 123 nmol BCE/mmol creatinine. (Reference range: 4 - 64 nmol BCE/mmol creatinine)  Uh-oh!     

              "Dont' give up. It is still your turn to be in this world."
                                                                   Crucibles of Will

*  Taking a thiazide diuretic didn't seem like a good idea even way back then when I didn't know much about osteoporosis. Now, with about seventeen years of experience with this disease and working with patients with bone loss for at least ten, using thiazides to limit urine calcium loss seems like an even a worse idea. Thiazides interfere with trace mineral absorption, especially magnesium and zinc. Potassium depletion is very common with thiazides and can cause heart arrhythmias and glucose metabolism problems...not something you would want to have, especially if you are running marathons and competing in Ironman triathlons. Simply adding more vegetables to a person's diet and having them supplement with boron, potassium and vitamin K-2 MK-4 almost always lowers urine calcium losses. A much safer approach.

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