|Non-healing, infected leg ulcer in a 60+ year old diabetic man before, and several months after comprehensive nutraceutical, botanical and dietary regimen aimed at quelling "oximation" and reducing Candida albicans. Courtesy of Dr. Roby Mitchell.
Some of the most important things I learned in medical school I learned from an oncologist, Dr. Phillip Perriman. He stressed the importance of keeping up with medical research by reading journals, and gave me my first exposure to the power of fruits and vegetables to influence cancer risk.
But the most important lesson he taught was about the necessity of understanding pathophysiology—the mechanisms of disease. If you understand the process of how disease happens, you're better able to prevent, cure or abort that process. It's about learning to recognize the hiss of the lit fuse, rather that waiting until you hear the blast of the bomb.
Wasn't that the ultimate purpose of all the stacks of journals and books in the Harrington Medical Library, in Amarillo, where I studied? To enable us to understand the processes of disease? It is perplexing to consider the vast mass of material written about disease, and compare it to the soaring incidence of major chronic diseases. Somehow, there's got to be a fundamental flaw in our understanding of pathophysiology. You couldn't have that many books and journals about car repair with no one knowing how to fix a car.
The disconnect reminds me of the story of the man who visits his friend and finds the friend searching around the house for his keys. He asks the friend where he was the last time he had them. The friend says he was outside. The man then asks why he's searching inside the house, when the keys are probably outside. The friend replies, "Because the light is better in here."
I think we've avoided really understanding the pathophysiology of many diseases because it has been much more profitable—socially and economically—to search inside the house of pharmaceuticals, radiation and surgery. When we take a diligent look outside the "house" of our conventional explanations and treatment modalities, we do indeed find some keys.
In the Winter 2008 issue of HPC, I discussed some common denominators of disease under the rubric of "Oximation," a neologistic confluence of the words "oxidation" and "inflammation". Under the microscope, this is the fundamental process we observe that leads to chronic disease. Oxidation compromises the structural integrity of cell/mitochondrial DNA and membranes, leading to premature cell dysfunction and death. Inflammation is the net result of an overactive immune cascade, and it is the primary source of oxidation. By learning to mitigate these processes, we can dramatically modulate disease outcomes.
For example, I had a 60+ year-old diabetic gentleman come in and tell me his doctors wanted to amputate his leg. He had a "non healing" ulcerated wound just proximal to his left medial malleolus. As we all know, this type of lesion often becomes infected, sometimes leading to septicemia and death. In this situation, amputation can be lifesaving. That said, if it were my leg, I'd prefer to keep it.
As I stated in the previous article, I've stopped treating specific diseases like "leg ulcers." My focus is on reversing systemic oximation. That's not to say that I totally ignore the ulcer, hypertension, diabetes, Alzheimer's, osteoporosis, asthma or whatever other disease form oximation has taken. But I make it clear to the patient what the real problem is. This is important because the patient needs to be clear that I'm not there to heal him, but to facilitate his innate healing process. His participation is more important than mine.
I assessed this patient's hormonal balance and provided the requisite hormone replacement, in this case thyroid and testosterone, with the goal of increasing anabolic activity and improving conversion of T4 to T3. I also instructed him on some primary nutrient replacement, specifically B vitamins and magnesium. I'm a firm believer that all diabetics should be loaded with magnesium, as it improves glucose utilization. I also recommended he take the VSL 3 probiotic (Sigma Tau).
His most important lesson from me, however, was about the impact of diet on the ability of fungal and microbial pathogens to survive. Organisms like Candida provoke strong and relentless immune cascades, leading to inflammation and oxidation. In the interest of getting rid of existing Candida, I treated the ulcer itself with Germ-a-Clenz (North American Herb & Spice), a broad-spectrum OTC botanical antimicrobial containing essential oils of oregano and cumin that will kill MRSA and Candida. He was also given a round of oral Oregabiotic (also made by North American Herb & Spice), an excellent natural therapy for reducing systemic Candida.
The net result is that the ulcer has healed, we saved the patient's leg, he's a very happy camper, and his allopathic nurse practitioner was impressed enough to tell him to "do whatever Dr. Mitchell tells you to do."
This is not an isolated case. Many seemingly intractable conditions will resolve fairly well, if you focus on treating the underlying disease drivers.
Same Disease, Different Tissues
The oximation process, aimed at destroying pathogens, is therapeutic in the presence of optimal levels of primary nutrients and hormones required for anabolism. In their absence, oximation becomes pathogenic resulting in much collateral damage.
In atheromatous plaques, for instance, oximation leads to erosion of vascular endothelium to the point of plaque rupture with subsequent thrombus formation and infarction. Virchow himself described inflammation as part of his initial description of the "fatty streak" precursor to atheromatous plaques.
Nearly the same inflammatory process occurs in rheumatoid arthritis, as eloquently described in a 2002 article from the Annals of Internal Medicine:
"The natural history of the disease in most patients involves chronic, low grade inflammation. The clinical manifestations of rheumatoid arthritis are initiated by lymphocytes that localize to synovial tissues where, when activated, they cause pain and swelling. These lymphocytes produce protein mediators (cytokines) that initiate inflammation, attract other immune cells to the site, activate resident cells, and cause excess synovial fluid production. After the T cells have arrived in the synovium, they can interact with resident macrophage-like type A synoviocytes. … As a consequence of this interaction, the T cells are activated and various cytokines are produced." The authors add that, "… this process is not specific to rheumatoid arthritis or synovial tissue. Migration of immune cells into areas of tissue inflammation is a nonspecific phenomenon, with specific activation occurring at the site."
Note the similarity of that description with this depiction of psoriasis found in the New England Journal of Medicine:
"Pro-inflammatory cytokines induce the expression of adhesion molecules on endothelial cells and keratinocytes, allowing them to interact with leukocytes. This results in leukocyte extravasation at the site of inflammation, along with migration through the cutaneous matrix toward the epidermis. Numerous studies have identified tumor necrosis factor alpha as a particularly relevant cytokine regulating this complex inflammatory cascade."
The process is recapitulated across the spectrum of specialty journals. Another NEJM review on multiple sclerosis reads: "A central mission in multiple sclerosis research has been to determine he sequence of events underlying the development of the inflammatory plaque." Journal of Alzheimer's Disease (2004) echos this oximation pathophysiology: "Injury begins as local micro-inflammation that can trigger localized, self perpetuating cytokine cascades."
In regards to obesity, an article from the December 2003 The Journal of Clinical Investigations reads: "… adipose tissue macrophages are responsible for almost all adipose tissue TNF-alpha expression and significant amounts of iNOS and IL-6 expression. Adipose tissue macrophage numbers increase in obesity and participate in inflammatory pathways that are activated in adipose tissues of obese individuals."
Whether you're reading about sinusitis, asthma, autism, osteoporosis, cancer, diabetes, glomerular nephritis, hypertension, both types of thyroiditis, depression, most auto-immune diseases, pregnancy dyscrasias, etc., the "usual suspects" of inflammation and oxidation appear. They represent a fundamental, systemic response—to something.
The question is, why is the immune system so over-active in all these diverse diseases? The immune system has an innate intelligence, and it is not likely that it suddenly loses this, and decides to start destroying normal cells, tissues and organs. Something's driving the process.
The immune system normally becomes activated when it detects antigens from pathogenic microbes. The cascade is set off when macrophages digest microbes and then project microbial antigen particles onto their cell membranes via the major histocompatibility complex (MHC). These antigens are presented to T cells, setting off the humoral and cellular cascades.
Part of the cellular cascade is production of reactive oxygen species (ROS), better known as "free radicals." They are responsible for damaging cell/mitochondrial membranes and DNA. These are fundamental breaches of cellular integrity that domino into many different diseases.
There's ample reason to believe that in most patients, the most likely organism inciting the immune cascade is Candida albicans. Candida should normally be a symbiont in the GI tract. Given certain biochemical cues, it morphs from being a benign unicellular organism into a pathogenic, predatory, filamentous one. (See September 5, 1997, issue of the journal Cell and a paper from Cold Spring Harbor Laboratory, December 12, 2000, "Biological Program Prevents Development of Pathogenic Form of Fungi," by Dr. Martin Schroder.)
Like vultures seeking out dead or dying animals, filamentous Candida seek out cells that have been compromised by low ambient oxygen or low nutrient levels. The immune system will try to prevent this invasion. This is what we see histologically and biochemically in diseases associated with oximation.
If you really grasp what's going on beneath a patient's surface symptoms, you'll be better able to help the body move toward normal physiology and restore health.
I'm often able to accomplish this by focusing on restoring the body's ability to maintain what I call "autonomic homeostasis," the ability to maintain a healthy environment. This is done with bioidentical hormone replacement (including thyroid hormone and vitamin D3), and replenishment of key vitamins, minerals, essential fats, and amino acids. I also try to bolster levels of natural antifungals such as stomach HCl and iodide/iodine. A big part is in teaching patients not to throw gasoline, in the form of grain-based, refined-carb, and sugar-rich foods, on the inflammatory fire.
No doubt, some of you were practicing many of these methods while I was still learning how to focus a microscope. What I've tried to do is galvanize the concepts and come up with a catchy name. One of the tests of validity of an hypothesis is whether practitioners, operating independently, come to the same results, repeatedly, by following protocols dictated by the hypothesis. While more work needs to be done, I know I'm not alone in finding that a lot of disease states clear up when I can help patients eliminate Candida, reduce inflammation, and restore healthy hormone levels.
The accompanying pictures are typical of what I see everyday. They reflect the body's ability to heal if we restore its ability to maintain a healthful cellular environment.