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.
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.
Paul Rezendes, The Wild Within"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."
... Stay tuned for Part X of DX Severe Osteoporosis
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