Diagnosing MCAS – Ask Your Doctor for Lab Work

Ask Your Doctor for Lab Work

MCAS can be difficult to diagnose because lab test results may fluctuate as symptoms wax and wane. Many tests may need to be repeated during times of symptom flare-ups. Poor handling of specimens by the laboratory is also a real issue affecting results. Lab testing may thus result in false negatives despite a clinical history highly consistent with MCAS. Furthermore, MCAS doesn’t always cause abnormalities in lab work, adding to the complexity of diagnosis. Positive lab work is obtained only 20% of the time.

If you’re interested in getting lab work done to check for MCAS, I recommend the tests listed below. The top five, in bold, are the most important and necessary to establish a diagnosis:

  1. Histamine – plasma – Quest 36586 – must be chilled. Normal range – 28-51 ug/l.
  2. N-Methylhistamine – 24-hour urine – must be chilled. Normal range – less than 200 mcg/g.
  3. Prostaglandin D2 – plasma – must be chilled. Must be off NSAIDS (Motrin, Advil), aspirin, ASA, anything containing aspirin, for 5 days.
  4. Prostaglandin D2 (PGD2) – 24-hour urine – chilled. Must be off NSAIDS (Motrin, Advil), aspirin, ASA, anything containing aspirin, for 5 days.
  5. Chromogranin A – Quest 16379 – must be off proton pump inhibitors (PPIs) and H2 blockers (Pepcid and Zantac) for 5 days before tests, since they can falsely elevate chromogranin A.
  6. Prostaglandin 11-beta F2 Alpha (PGF2alpha) – 24-hour urine – chilled. Must be off NSAIDS (Motrin, Advil), aspirin, ASA, anything containing aspirin, for 5 days.
  7. Serum Tryptase – Quest 34484. Rarely elevated in MCAS. NR less than 11.5 ng/ml. Positive if increase over baseline of 20% or baseline greater than 15.
  8. Leukotriene E4 – 24-hour urine – chilled. Must be off NSAIDS (Motrin, Advil), aspirin, ASA, anything containing aspirin, for 5 days.
  9. Plasma heparin Anti-XA (must be off heparin products) – chilled. Degrades quickly.
  10. Blood clotting profile – Thrombin/PT/PTT/INR.
  11. Anti-IgE Receptor antibody.
  12. Neuron Specific Enolase – Quest 34476.
  13. Plasma pheochromocytoma workup.
  14. Porphyria workup.
  15. Factor VIII deficiency.
  16. Plasma free norepinephrine – Quest 37562.
  17. Urinary metanephrines – can b done in normal Calgary labs.
  18. Immunoglobulins – IgG, IgM, IgE, IgA
  19. Bone marrow biopsy looking for the following markers: CD117/CD25; CD117/CD2.
  20. Gastrin
  21. Ferritin
  22. CBC – eosinophils, basophils.
  23. Antiphospholipid antibodies.
  24. Genetic testing looking for Phase 1 and Phase II liver detox and methylation defects.
  25. Dunwoody Labs – test zonulin, histamine, DAO enzyme deficiency.

Many of these tests require specimens that are chilled by using a special centrifuge as the mast cell mediators are fleeting and degrade very quickly if not handled properly.

Further tests that may be of help:

  1. MTHFR gene mutations
  2. MAT gene mutations
  3. DAO gene mutations
  4. HNMT gene mutations. The liver plays a role in histamine intolerance. Histamine is not just disassembled in the gut by diamine oxidase (DAO). It is also disassembled in the liver, where it is in high concentrations, by HNMT. Learn more about histamine here.
  5. Glutathione levels. If glutathione levels are depleted, the inflammatory mediators released by mast cells may not be adequately neutralized by glutathione, the master antioxidant. This can lead to a vicious circle where oxidative stress results in mast-cells releasing inflammatory chemicals, which need to be detoxified by Phase 1 of the liver. If glutathione is low, the liver will be unable to neutralize them, resulting in further inflammation and oxidative stress.

These tests can help you identify whether MCAS is the cause of your mysterious and seemingly unrelated symptoms.

Depression, SSRIs and Self-Advocacy

Becoming an Advocate for Your Health

Depression

A recent study has concluded that SSRIs, when treating for major depressive disorder, are not that much better than placebo. Depression as a symptom and as a formal diagnosis, is too simple a label to attribute to a person who feels and experiences life without joy or pleasure and who may have real physiological changes that render his/her life unpleasant, if not unbearable. By attributing a diagnosis to a person such as “depression,” the patient and the diagnosis become frozen in time and separated from all possible antecedents, mediators and triggers. All further enquiry into the timeline of causation comes to an end and the patient (and the doctor) now objectify and identify with the diagnosis, as if some foreign entity, called “depression” just mysteriously fell out of the sky.  Add to this scenario the fact that ones entire medical school training is not aimed to enquire as to upstream causation. In the truest N2D2 tradition of medicine (name of disease, name of drug), we are trained to thread together a constellation of symptoms, arrive at a diagnosis and prescribe a treatment1; all under the 15 minute timeline and the approximately $40.00 fee that the Canadian health care system provides for a consultation. It does not take much to deduce that this is a hopelessly inadequate scenario and not one to foist onto ones worst enemy.

Depression, as a diagnosis, has a litany of possible antecedents (ancestral and genetic predispositions and inheritances), triggers (events that trigger the manifestation of the constellation of symptoms that coalesce to form a diagnosis) and mediators (lifestyle events and behaviours – diet, sleep, food, stress, exercise – that continue to contribute to the diagnosis). From ancestral trauma (that we now know to be epigenetically inherited), to early conception and birth trauma, to adverse childhood experiences and complex trauma, to head injuries, to genetic weaknesses in detoxification and methylation (creating scenarios of over and undermethylation) nutritional and hormonal inadequacies, to toxic insults such as mercury, lead, copper toxicity, mold, Lyme disease and co-infections, to sleep apnoea, to relationship struggles, workplace difficulties, transition from first half of life ego demands to second half of life soul demands; the list is long and complex.

Self-Advocacy

Unless doctors/healers of the future are trained in a new paradigm (Functional Medicine is putting up a valiant effort to educate future health care providers in this methodology), have sufficient life experience and have spent a large portion of their learning years investigating and researching the multiple layers and levels of complexity (7 Stages to Health and Transformation) that may contribute to the origins and continuations of  symptom or disease processes, you, as a health care consumer, will always be at the mercy of their experience (or inexperience) along this continuum. That is why it is imperative that all patients, as much as they can muster the lifeforce to do so, become advocates of their own health and treatment protocols. Patient self-advocacy, combined with a serious intent to do what it takes to get well, is always at the root of successful health outcomes. Or, if faced with a depressive illness or episode, we can hand over all power to the physician/healer we have consulted, take an antidepressant and hope for the best. Your choice.

Resources

  1. https://www.ncbi.nlm.nih.gov/pubmed/28178949

Treatments for Lowering Histamine and Reducing MCAS Symptoms

Treatments for Lowering Histamine and Reducing MCAS Symptoms

Now, you might be thinking, “Why can’t I just take an antihistamine?”

Antihistamines don’t actually reduce histamine release. They only block histamine receptors, preventing you from feeling the symptoms. You may need a round-the-clock blockade of the H1 and H2 receptors, every 12 hours.

If you want lasting relief for MCAS:

  • Histamine 1 blockers – hydroxyzine, doxepin, loratadine, fexofenadine, diphenhydramine, ketotifen, and cetirizine.
  • Histamine 2 blockers – famotidine (Pepcid, Pepcid AC), cimetidine (Tagamet, Tagamet HB), ranitidine (Zantac). Famotidine is chosen most often as it has fewer drug interactions than Tagamet).
  • Mast cell stabilizers – cromolyn, ketotifen (both a mast cell stabilizer and an H1 blocker), hydroxyurea, quercetin.
  • Leukotriene inhibitors – montelukast (Singulair), zafirlukast (Accolate)
  • Tyrosine kinase inhibitors.

H1 and H2 blockers must be taken every 12 hours for maximum effect. It may take up to 12 months to achieve maximum therapeutic effect. The doses may need to be increased to up to three times the recommended over-the-counter dosing.

Here is how I approach treatment with my MCAS patients:

  • Eat a low-histamine diet: Remove alcohol, smoked and cured meat, tinned fish, pickled and fermented foods, berries (strawberries being one of the worst culprits), citrus, nuts, chocolate, dairy, spinach, yeast, soy sauce, tomatoes and tomato products, preservatives, and vinegar. Stop eating leftover food. This will only reduce the incoming histamine and won’t affect the mast cell overactivity within the cells of the body. A comprehensive guide regarding the low-histamine diet can be found here.
  • Promote good gut health: Cut back on gut-damaging and inflammatory foods, and increase probiotics. Use a DAO enzyme, which goes under the generic name Umbrellux DAO – two tablets, 20 minutes before each meal.
  • Stabilize mast cell release of histamine with quercetin and vitamin C 500 mg – two tablets three times daily. We use a product called Natural-D Hist from Ortho Molecular Products.
  • Use H1 and H2 blockers every 12 hours – I use, on average, levocetirizine 5 mg twice daily and famotidine 20 mg twice daily.
  • Block nighttime histamine release with ketotifen or zaditen – 0.25–1 mg at night. Excellent sleep aid, mast cell stabilizer, H1 antihistamine. Excellent treatment for eosinophilic esophagitis.
  • Treat any existing infections: Have a thorough examination done to identify and treat any potential infections in the body which are powerful mast cell triggers. Stool testing by Genova labs and Cyrex Lab Pathogen Testing (array 12) can be of assistance in identifying pathogens.
  • Identify and remove toxins and allergens: This could be heavy metals, mercury fillings, cosmetics, and household cleaners.
  • Nutrients that assist in the treatment: This includes vitamin B6, alpha lipoic acid, vitamin C and E, selenium, omega-3s, N-acetylcysteine (NAC), methylation donors like methyl-folate, SAMe, and riboflavin.
  • Herbs: Nigella sativa, butterbur, turmeric, ginger and peppermint.
  • Get into a solid routine: Getting high quality sleep and staying on schedule helps keep mast cells in check.
  • Reduce stress: Stress, through the action of corticotropin hormone, can activate your mast cells and cause them to destabilize and release mediators.
  • One of the best resources for how to deal with histamine and mast cell activation through nutrition and supplementation is the website and Facebook posts by Yasmina Ykelenstam www.healinghistamine.com.

It can be incredibly discouraging to feel so sick for so long and not find any answers. It is my hope that we continue to learn more about multisystem conditions such as MCAS and spread useful information so it may end up in the hands of those suffering.

Share this article with friends and family to help spread the word about mast cell activation syndrome. They may discover it’s more than allergies that’s keeping them down.

Kryptopyrroluria (aka Hemopyrrollactamuria) 2017: A Major Piece of the Puzzle in Overcoming Chronic Lyme Disease

Major Piece of the Puzzle in Overcoming Chronic Lyme Disease

[vc_row][vc_column][vc_column_text]Dietrich Klinghardt, MD, PhD, is a practicing physician in Woodinville, Washington with a focus on the treatment of chronic neurological conditions such as Lyme disease, autism, and CFIDS. In the years that he has treated patients with chronic infections, he has observed that, for many, recovery is often elusive. Patients may plateau or find that their recovery is stalled. In other cases, patients may not succeed in their attempts to rid the body of a particular toxic or infectious burden, such as in patients with longstanding or therapy-resistant, late-stage Lyme disease.

In looking for possible explanations as to why some patients struggle more than others to regain their health, coauthor Klinghardt has found a high correlation between patients with chronic Lyme disease and those with kryptopyrroluria (KPU), or more precisely hemopyrrollactamuria (HPU). The condition is alternatively known as the “mauve factor” or “malvaria.”

KPU may be an inherited condition, but it can also be induced by psychological trauma or chronic infections. Epigenetic influences such as intrauterine, birth, childhood, or transgenerational trauma may trigger KPU; other triggers may include a car accident, divorce or emotional trauma, and physical or sexual abuse. Chronic infections, such as Lyme disease, may themselves serve as a trigger for the condition.

The HPU complex is a biochemical marker and neurotoxic substance frequently identified in the urine of patients with autism, learning disabilities, alcoholism, substance abuse, schizophrenia, ADHD, Down syndrome, depression, bipolar disorders, and even criminal behavior. Some estimate the incidence of KPU to be 40-70% in schizophrenia, 50% in autism, 30% in ADHD, and 40-80% in alcoholism and substance abuse.

Based on testing with Klinisch Ecologisches Allergie Centrum (KEAC; http://www.hputest.nl) in Holland,
Klinghardt has found the incidence of KPU in Lyme disease to be 80% or higher; in patients with heavy metal toxicity (lead, mercury, aluminum, cadmium, and others) over 75%; and in children with autism over 80%. These are very significant percentages of the patient population with chronic illness that may benefit from a treatment program that addresses KPU. Healthy controls do not test positive for KPU.

History

In 1958, a psychiatric research program in Saskatchewan, Canada, led by Abram Hoffer, MD, PhD, the father of orthomolecular psychiatry, was looking for the possible biochemical origin of schizophrenia and a lab marker that would make it easier to identify affected individuals. One study involved evaluating the urine for certain chemical fractions and evaluating those of schizophrenic patients and those of normal controls. The effort yielded “the mauve factor,” a specific substance that reliably allowed the examiners to identify the schizophrenic
patients, as it was not found in the normal controls.

Early on, the substance was known as “the mauve factor” due to the mauve color that was observed on the stained paper. It was then termed “kryptopyrrole”, later identified as hydroxyhemopyrrolin-2-one (HPL). The researchers first called the disease associated with this condition “malvaria,” but it was renamed by Dr. Carl Pfeiffer, MD, PhD to “pyrolleuria” which was, for no obvious reason, consistently spelled “pyrroluria” in later publications. Today, the condition is generally referred to as “pyroluria.” In the 1970s, Dr. Pfeiffer created an assay for the condition and was able to show clinical improvement in positive patients with high doses of zinc and vitamin B6 (between 400 mg and 3,000 mg B6).

Associated Conditions

A partial list of conditions where KPU may be a factor includes ADHD, alcoholism, autism, bipolar disorders, criminal behavior, depression, Down syndrome, epilepsy, heavy metal toxicity, learning disabilities, Lyme disease, multiple sclerosis, Parkinson’s disease, schizophrenia, and, substance abuse. The items listed in bold are those in which Klinghardt has observed a connection to KPU in his patient population.

Symptoms

The KPU condition results in a significant loss of zinc, vitamin B6, biotin, manganese, arachidonic acid, and other nutrients from the body via the kidneys. There are many symptoms of KPU, which may result from deficiencies of these nutrients. Those in bold are tell-tale signs of the condition. Klinghardt finds that depression is often a leading symptom of the condition. Symptoms may include the following:

  • Abdominal tenderness
  • Abnormal fat distribution
  • Acne, allergy
  • Amenorrhea, irregular periods
  • Anxiety / Nervousness
  • Attention Deficit / ADHD
  • Autism
  • B6-responsive anemia
  • Cold hands or feet
  • Constipation
  • Course eyebrows
  • Crime and Delinquency
  • Delayed puberty, impotence
  • Depression
  • Emotional liability
  • Eosinophilia
  • Explosive or episodic anger
  • Familial
  • Hypoglycemia, glucose intolerance
  • Knee and joint pain
  • Light, sound, odor intolerance
  • Mood swings
  • Nail spots (Leukodynia)
  • Obesity
  • Pale skin, poor tanning
  • Paranoia / Hallucinations
  • Perceptual disorganization
  • Pessimism
  • Poor breakfast appetite
  • Poor Dream Recall
  • Poor short-term memory
  • Stress intolerance
  • Stretch marks (striae)
  • Substance abuse
  • Tremor, shaking, spasms
  • Withdrawal

Impact of Nutrient Loss

Elevated levels of HPL found in urine are the result of an abnormality in heme synthesis. Hemoglobin is the substance that holds iron in the red blood cells. Heme is also the principal building block of many enzymes involved in detoxification (cytochromes), enzymes involved in healthy methylation (MSR and CBS), and NOS – a significant enzyme in the urea/BH4-cycle. HPL is a byproduct of dysfunctional heme synthesis and can be identified in the urine. HPL binds to zinc, vitamin B6, biotin, manganese, arachidonic acid (omega-6), and other important compounds that, as a result, are excreted via the urine.

This leads to a significant depletion of these nutrients throughout the body and to the synthesis of non-functioning or poorly functioning enzymes. Turning to the importance of zinc, vitamin B6, biotin, manganese, and arachidonic acid in the body, it becomes clear how widespread the problems may be that are created by this condition.

Zinc deficiency may result in emotional disorders, food allergies, insulin resistance, delayed puberty, rough skin, delayed wound healing, growth retardation, hypogonadism, hypochlorhydria, mental lethargy, short stature, diarrhea, stretch marks or striae (which may be misinterpreted as Bartonella in some patients with Lyme disease), white spots on the fingernails, reduction in collagen, macular degeneration, dandruff, skin lesions such as acne, hyperactivity, loss of appetite, reduced fertility and libido, transverse lines on the fingernails, defective mineralization of the bones leading to osteoporosis, and many others.

Zinc is a powerful antioxidant, and lower levels lead to an increase in oxidative stress. Lower levels are correlated with lowered glutathione, an important part of the detoxification system. Zinc is required to support proper immune function. “White blood cells without zinc are like an army without bullets,” says Klinghardt.

Vitamin B6 deficiency is thought to be a rare occurrence. However, in those with KPU, this is not the case. B6 deficiency may lead to nervousness, insomnia, irritability, seizures, muscle weakness,
poor absorption of nutrients, decrease of key enzymes and cofactors involved in amino acid metabolism, impairment in the synthesis of neurotransmitters, impairment in the synthesis of hemoglobin, seborrheic dermatological eruptions, confusion, and neuropathy. Like zinc, B6 is an antioxidant and correlates to levels of glutathione.

Biotin deficiency may be evidenced by rashes, dry skin, seborrheic dermatitis, brittle nails, fine or brittle hair, and hair loss. More importantly, however, it may be associated with depression, lethargy, hearing loss, fungal infections, muscle pain, and abnormal skin sensations such as tingling. Biotin is an important co- factor in the production of energy in the mitochondria. Biotin is essential for a healthy brain and nervous system. Biotin deficiency is associated with many aspects of the aging process.

Manganese deficiency may be associated with joint pain, inflammation, and arthritis. Deficiency may result in a change in hair pigment or a slowing of hair growth. It is essential for normal growth, glucose utilization, lipid metabolism, and production of thyroid hormone. It may be associated with diseases such as diabetes, dyslipidemia, Parkinson’s disease, osteoporosis, and epilepsy.

Arachidonic acid (from omega-6) deficiency may lead to the impairment of white blood cell function, primarily the leukocytes, which may lead to one being more vulnerable to infection. It may lead to neuropathy, neural and vascular complications in preterm babies, skin eruptions, behavior changes, sterility in males, arthritic conditions, dry eyes, growth retardation, dry skin and hair, slow wound healing, hair loss, kidney dysfunction, heart beat abnormalities, and miscarriages.

When one considers the magnitude of potential health problems that may be present when a single condition leads to a deficiency in zinc, vitamin B6, biotin, manganese, arachidonic acid, and other nutrients simultaneously, the negative implications on health are almost endless.

KPU and Lyme Disease

Three possible origins of KPU are discussed in the literature: genetics, trauma, and chronic infections. The connection between KPU and many of the illnesses previously discussed has been known for quite some time. However, prior to Klinghardt’s early work in treating Lyme disease, never before had a connection been observed or published between KPU and Lyme disease. This discovery has been a key for Klinghardt to return his patients to an improved state of health and wellness, and the changes he has observed have been profound.

Klinghardt has found that 4 of 5 patients with chronic or persistent Lyme disease test highly positive for this condition (when tested with KEAC). That suggests that 80% or more of patients with symptoms of chronic Lyme disease may benefit from a treatment protocol that addresses KPU.

Klinghardt finds that it is rare for a patient to have chronic symptomatic Lyme disease as an adult without the patient having developed KPU. He postulates that the biotoxins from microbes block one or more of the eight enzymes of heme synthesis. This leads to a significant loss of key minerals in the white blood cells, which effectively disarms cellular immunity.

In those where KPU was triggered by infection with Lyme organisms, Klinghardt has observed that the KPU is often an unstable form of the condition where there are times of higher levels of pyrroles being excreted and times when this is not observed. If a person has episodes of depression, these episodes generally correlate to times when pyrroles are being released in higher levels in the urine.

One young adult female struggling with Lyme for several years had severe multiple chemical sensitivities (MCS) that were not improved by any previous treatment. After starting the KPU protocol, she noticed improvements in her MCS for the first time since she became ill. Other patients with intractable chronic infections have experienced significant improvements in immune function and a resulting lowering of total microbial burden.

Klinghardt has observed numerous patients that have struggled to rid the body of parasitic infestations. In these patients, regardless of the interventions used, the patient continues to expel these parasites on an ongoing basis. Therapy-resistant infections are a hallmark sign of KPU. Klinghardt has found that once the KPU protocol is put in place, there is often a swift resolution of long-standing infections and infestations. This includes patients who have failed years of antibiotic therapy for chronic or late-stage Lyme disease.

Sandeep Gupta, MD, from Australia has stated that parasites and pyroluria almost always go together. He has observed that almost every chronically unwell individual seems to have both; one opens the door to the other. Chronically low levels of zinc allow parasites to invade the mucosal layer of the gut. Parasites may then move to the liver and gallbladder. They interfere with mood, energy levels, and sleep. Addressing the parasites while restoring zinc and B6 often makes a tremendous difference in his patients.

Chronic Lyme disease patients often suffer from severe jawbone infections that may require cavitation surgery, which often tends to fail in this population. When the clients are pretreated for KPU, the outcome of the surgical procedure is generally much better. In some mild cases, ozone treatment of the jaw may be sufficient to turn things around.

Klinghardt has followed the interest in HLA-DR genetic typing in regards to biotoxin illnesses such as Lyme disease and mold. Prior to KPU, patients with certain haplotypes were considered more difficult to treat as the body could not properly and effectively respond to and remove biotoxins from Lyme disease, molds, or in the worst cases, both. In his experience, once the KPU issue is addressed, these HLA types become far less of a concern in most patients and no longer hold them back on their road to regaining health.

Once bodily systems are back online and functioning properly, a few months after introducing the KPU protocol, patients become less vulnerable to Lyme disease, to mold, and even to heavy metals. Their bodies are now much better equipped to deal with these conditions when they have appropriate levels of zinc, vitamin B6, biotin, manganese, and arachidonic acid to support optimal functioning of numerous bodily processes.

KPU and Methylation

In Klinghardt’s work, if a patient has KPU, treating the KPU condition first is a foundational intervention before pursuing more specific methylation support. Specific enzyme blockages are discussed earlier in this article.

In people with cancer and active EBV infection, EBV triggers a hypermethylation inside the cancer cells that may accelerate cancer cell growth. If methylation support is introduced based on genetic SNPs or other lab testing but the patient has an untreated, active EBV infection (such as is common in chronic fatigue syndrome, Lyme disease, and other related conditions) or an EBV-related cancer such as throat, stomach, breast, prostate, or Hodgkin lymphoma, supporting methylation may lead the patient to an increased risk of cancer or accelerated rate of cancer growth.

This potential makes treating KPU first even more important as balancing the zinc and B6-dependent enzymes indirectly
without the addition of methyl groups is generally a safer way to restore healthy methylation on all fronts as opposed to directly supporting methylation with methyl donors.

When people begin to explore methylation, KPU should always be evaluated and addressed first. Several enzymes in or adjacent to the methylation cycle use the heme molecule which utilize zinc and vitamin B6 as primary building blocks. By supporting KPU, the methylation cycle works more smoothly, both in its ability to methylate and demethylate, and at a lower risk to the patient.

KPU and Heavy Metal Toxicity

When KPU is present and zinc and vitamin B6 are depleted, the detoxification pathways are overwhelmed and ineffective as the heme molecule is an integral part of many detoxification enzymes. Both zinc and vitamin B6 deficiencies, which are important cofactors in the methylationcycle, reduce levels of glutathione in the body. Glutathione is important for the detoxification of heavy metals and other toxins.

Replacing missing zinc and vitamin B6 increases glutathione. This, in turn, increases the rate of detoxification of heavy metals and other body burdening
toxins. Once KPU treatment is introduced with zinc and B6, reducing the metal burden no longer requires heroic measures.

However, it is also the case that incorporating the KPU protocol will liberate additional heavy metals within the body. This aspect of the KPU protocol is discussed later in this article and is important for the practitioner to understand before beginning to treat patients for the condition as additional detoxification support is generally needed. This protocol is intended to be done only with the guidance of a knowledgeable practitioner.

KPU and Porphyrin Disorders

There is a group of disorders related to pyroluria called porphyrias. KPU is one of a group of conditions known as porphyrin diseases. In 100% of porphyrin diseases, the HPL compound is found in the urine.

Porphyrin testing is readily available and is a reliable tool. Klinghardt prefers to send a urine sample to Laboratorie Philippe Auguste (http://labbio.net) in France for testing. Other options are also available in the US, such as through Genova Diagnostics, Doctor’s Data, and Great Plains Laboratory.

In the US, pyroluria and porphyria are viewed as separate conditions. However, in collaboration with the Dutch lab KEAC, it has been established that everyone with elevated porphyrins has pyroluria. When pyroluria is addressed, the porphyrins go down.

In porphyrin testing, uroporphyrin is an indicator for aluminum, coproporphyrin for lead, and precoproporphyrin for mercury. Klinghardt has not seen a case with elevated porphyrins that did not have KPU, and when the KPU was corrected, aluminum, lead, and mercury are excreted
from the body, and the porphyrins go down.

This is, in part, due to the fact that when the body has been deficient in zinc for a long period of time, it may retain heavy metals much more readily. When zinc is missing from the body, it is replaced in our bones with lead. If zinc is supplemented, lead is expelled. Secondly, the enzymes needed to detoxify these metals are heme-dependent enzymes,
and these metals accumulate when heme synthesis is abnormal.

Klinghardt notes that discussions on the topic of porphyria are much more widely accepted than those on pyroluria. In his experience, he finds that almost all of his patients have elevated porphyrins, and that pyroluria is the deeper core issue.

KPU and Histamine

When a KPU patient is having a good day, low histamine levels are observed; on a bad day, higher histamine levels are observed. It is the relative elevation of histamine in response to foods, inhalants, allergens, emotional stressors, and electrosmog that is problematic and causes the allergic phenomena, not the absolute histamine level. When histamine levels rise from a low level to a moderate level, the reactions are often severe. Learn how to control your histamine levels in my guide located here.

When exploring histamine levels in a KPU patient at a time when they are experiencing hives or asthma, the histamine levels are elevated, but not to levels that would create a problem for others. The relative rise in histamine, however, in KPU patients is experienced in a far more significant way.

Klinghardt has worked with biochemists in Germany that are beginning to link KPU with mastocytosis or mast cell activation syndrome (MCAS). They have observed that KPU treatment repairs the heme molecule, which notably stabilizes the mast cells and lowers the response to these relative rises in histamine.

KPU and Multiple Sclerosis

Klinghardt has treated many patients with multiple sclerosis. The MS patients that he has tested have been highly positive for KPU. Over time, he has
concluded that KPU is a frequent cofactor in MS. He has found that patients with MS respond favorably to KPU treatment.

In patients with KPU, absolute histamine levels are almost always low. The treatment for MS patients with KPU may include histamine in addition to the KPU protocol outlined in this article. Treatment with histamine may be either with oral or transdermal products. Prokarin is a transdermal patch which delivers histamine and has been used by some practitioners in the treatment of MS.

Evaluation and Testing

Klinghardt recommends that people start with the HPU Questionnaire (http://www.hputest.nl/evraag.htm). Once the questionnaire is completed, a score is calculated to provide a probability that a person may have KPU. If the score is 10-14, Klinghardt will often recommend proceeding with treatment without the need for confirmatory testing as the treatment itself is generally well-tolerated.

If the score is 0-9, he may suggest testing for the condition using additional lab work.

Pyrroles are impacted by light, temperature, oxygen, and time; and they readily break down. Once they begin to break down, the likelihood of detection is significantly lowered. Ideally, testing would be performed within eight hours after the collection, though this is not practical and rarely possible.

Within the United States, two of the available labs for testing include the following:

  • DHA Laboratory (https://www.pyroluriatesting.com) uses a frozen one-time collection at a cost of $80. They recommend the collection be the second urination of the day. They suggest avoiding all supplements, vitamins, and minerals for 12-24 hours prior to the specimen collection. The lab is testing for hydroxyhemopyrrolin-2-one (HPL).
  • Health Diagnostics and Research Institute (http://www.hdri-usa.com) charges $140 for a 24-hour collection and $90 for a random collection. HDRI suggests stopping zinc and B6 as well as antidepressant medications for 48 hours prior to the collection. They suggest not smoking or consuming caffeine for 24 hours prior. While there is no additional cost for testing the hydroxyhemopyrrolin-2-one (HPL) compound, this must be specifically ordered on the requisition form as it is not part of their KPU assay by default. If you do not specify HPL as an add-on, you will get kryptopyrrole (2,4 dimethyl-3-ethyl pyrrole) only.
  • In Europe, Klinghardt uses the Dutch Lab KEAC (http://hputest.nl) for HPU testing. The lab is guided by microbiologist Dr. John Kamsteeg, a world leader in HPU. The results of HPU testing with this lab align closely with the percentages of patients with chronic Lyme and other conditions that Klinghardt identifies with the HPU condition.
  • In Australia, KPU testing is available through SAFE Analytical Laboratories (http://safelabs.com.au) and Applied Analytical Laboratories Pty Ltd (http://www.apanlabs.com).

Each lab has their own very specific instructions for performing the test. This includes information such as shielding the specimen from light as well as how to handle and ship the specimen. It is important that the recommendations be closely followed to optimize the sensitivity of the test result.

To further maximize the sensitivity of testing, it may be best for the patient to be under stress at the time the test is being performed as HPL excretion is known to increase during times of stress.

In some circumstances, however, patients may still test negative even when the condition is suspected. In those cases, it may be best to repeat the test. In many cases, the result will be positive on the second or third test. In some patients, an empiric trial of the KPU protocol may be indicated despite repeated negative KPU tests, and this often leads the patient to
higher ground. WBC (not RBC) intracellular zinc may be a useful tool for exploring the potential for zinc deficiency where it matters most – in the white blood cells.

Other laboratory indicators that may be suggestive of KPU include the following:

  • WBC < 5000/mcL (due to low levels of zinc)
  • High LDL / Low HDL
  • Low normal alkaline phosphatase (<60U/L)
  • Low omega-6 fatty acids in red cell membrane test
  • Low taurine in amino acid profile
  • High MCV
  • Low glutathione
  • Low ATP
  • WBC and RBC zinc and manganese levels may be normal while biopsies from bone and CNS are completely deficient.
  • Bone biopsies are a reliable predictor of KPU. Severe deficiencies of zinc, manganese, lithium, calcium, magnesium, and molybdenum are often found.

Alkaline phosphatase (ALP) is a zinc and magnesium dependent enzyme. When someone is consuming adequate magnesium and is still presenting with low ALP, zinc deficiency is a likely consideration, and this may represent another indication for KPU. When ALP is below 55, zinc deficiency can be suspected; when below 40, it is likely.

A consequence of KPU is low glutathione and low ATP. In the realm of chronic illnesses, low reduced glutathione and low ATP are common and should alone trigger the suspicion that KPU may be a factor.

Treatment

KPU is a severe but reversible deficiency of zinc, vitamin B6 (or P5P), biotin, manganese, arachidonic acid, and other co-factors. It is important to recognize, however, that treatment with zinc and vitamin B6 does not result in fewer pyrroles being excreted in the urine. KPU orthomolecular treatment does not fix the underlying condition; it substitutes what is being lost as a result of the condition such that the person is no longer deficient in key nutrients needed by the body to move towards health.

The general KPU substitution treatment that Klinghardt uses in his practice is as follows (dosages for 160 lb.) adult and should be adjusted based on weight; may be customized for specific patient needs):

With Breakfast

  • Zinc 25-30 mg (as picolinate, gluconate,sulfate, or zinc l-carnosine). Nausea after zinc supplementation may be a sign of hypochlorhydria or low stomach acid; this often resolves after a few months on treatment.
  • Vitamin B6 50-100 mg (split between pyridoxine HCl and P5P, with P5P being the predominant form)
  • Biotin 3-5 mg for brain, skin, hair, and nails
  • Magnesium 100 mg (glycinate, bisglycinate, or malate) – or titrate to bowel tolerance.
  • Arachidonic acid from omega-6 oils (Ghee such as Mt. Capra Goat Milk Ghee, Evening Primrose Oil, Hemp Seed Oil, Black Currant Oil, Borage Oil, Pumpkin Seed Oil; 4-6 capsules of Evening Primrose Oil per day is commonly used.)

With Dinner

  • Zinc 25-30 mg
  • Vitamin B6 50-100 mg
  • Biotin 3-5 mg
  • Magnesium 100 mg
  • Omega-6 Oils

This is the core treatment Klinghardt utilizes for KPU.

Additional Support

  • Vitamin A 1,500-3,000 IU per day to improve the absorption of zinc in the gut
  • Niacin 40-50 mg per day for psychiatric symptoms. (Abram Hoffer used up to 3000 mg per day.)
  • Taurine 100 mg twice per day (up to 2,000 mg at bedtime) for brain-related symptoms such as seizures, brain fog, and memory loss. Supports elimination of neurotoxins, improves bile quality, increases glutathione, and normalize brain rhythms.
  • Lithium 5-10 mg per day (Orotate or Aspartate); lithium is lost in the urine in some patients with KPU.
  • Manganese 2-5 mg per day (Patients with joint problems may require additional manganese above the dosages recommended here; see additional considerations later in this article on manganese for patients with Lyme disease.)
  • Chromium 250-500 mcg per day
  • Molybdenum 100-500 mcg per day
  • Boron 1-3 mg per day
  • Trace Minerals – As more is learned about KPU, additional elements are found to be lower in those with the condition. Thus, supplementing trace minerals may be a supportive strategy. BioPure MicroMinerals, Quinton Isotonic, or similar mineral products may be helpful

As compared to the first version of this article which was published in 2009, Klinghardt has found that many of hispatients do quite well with lower dosagesof some of these key nutrients than were originally utilized.

In Europe, Depyrrol is one product which provides support for KPU. Additionally, and in the United States, BioPure CORE and CORE-S are available to support those dealing with the condition. Another product in this realm is Mensah Medical’s Pyrrole Pak. These products serve as a solid foundation for KPU treatment; though additional co- factors may be needed for a given patient.

Some patients may not tolerate both vitamin B6 and P5P as contained in some products and may find it necessary to take each component of the KPU program separately.

In terms of BioPure’s CORE and CORE-S, CORE-S is a recent reformulation of the CORE product which has been available for many years. While either may be an appropriate option, CORE-S generally results in less nausea, better absorption, and is often better tolerated by those patients with Lyme disease as it does not contain manganese. While many with pyroluria may benefit from manganese, it may act as a growth factor for untreated Lyme disease, and thus, some may prefer to avoid its use in this patient population. The reformulated CORE-S contains horsetail as people with KPU excrete higher levels of silica in the urine, which leads to higher levels of aluminum toxicity. With either CORE or CORE-S, two capsules twice daily are a common target dose for a 160 lb. adult.

When first starting to introduce products in support of KPU, it is best to start with lower dosages and to take them towards the end of a meal and to gradually work up to the target dosage. Levels of B6, taurine, or biotin may be additionally and individually titrated upwards depending on the patient’s symptoms and needs. With the introduction of zinc, it is best to monitor copper levels after a few months on the protocol as copper replacement may also be needed. Zinc, vitamin B6, and manganese are copper antagonists. Thus, monitoring levels of copper and supplementing where needed is an important part of the treatment protocol.

Copper deficiency can lead to hemorrhoids, varicose veins, fatigue, edema, hair loss, anorexia, skin problems, osteoporosis, cardiovascular disease, aneurisms, and many other undesired conditions. Current nutritional teachings are misinformed on the topic of copper toxicity. The immune system uses copper and iron to fight infections associated with Lyme disease. As a result, oxidized copper is displaced in the connective tissue and may appear as though the patient is copper toxic by some testing methods when in fact copper supplementation may be appropriate. High dose Vitamin C has the effect of reducing oxidized copper to a form that can be reused by the body.

Detoxification and Course of Treatment

As treatment for KPU is implemented, this often can result in toxin mobilization as the body begins to release heavy metals. Symptoms may include muscle aches, bowel problems, or those normally associated with cleansing or detoxification reactions. Additionally, the immune system begins to become more active which can result in a Herxheimer-like reaction as the immune system begins to better respond to the backlog of microbes that it was previously unable to adequately address.

One approach for minimizing these reactions is to start slowly with introduction of the KPU nutrients and work up over time. In most cases, there is no reason that the treatment course must be an aggressive one. Nonetheless, this treatment should always be guided by a knowledgeable practitioner. In addition to the KPU treatment discussed earlier, consideration should be given to detoxification support and to protection of the red blood cells as the treatment is initiated.

According to Klinghardt, many of our metabolic enzymes use zinc as part of their molecular makeup. However, in patients with KPU, there is not enough zinc available to satisfy the need. In these cases, lead, mercury, and other 2-valent metals bind to these sites instead in a poor attempt to fulfill the role of zinc.

Once zinc is reintroduced into the body, 2-valent metals such as mercury, cadmium, aluminum, and lead are liberated. The patient may now have dislodged heavy metals circulating throughout the body.

These may be competing for the already overtaxed detoxification pathways or may be redistributed to places where they may be more problematic. Lead moves back into the blood, which can cause problems including damage to red blood cells. To protect the red blood cells, freeze-dried garlic and Vitamin E are often used.

Incorporation of known toxin binders further supports the detoxification process. Some of the binders that Klinghardt uses in his practice include chlorella, Ecklonia cava, zeolite, and
chitosan. Silica from horsetail supports binding of aluminum, and thus, the use of a high-silica zeolite such as BioPure ZeoBind is often utilized. It is critical to support the kidneys with specific drainage and organ support remedies in order to optimize the removal of heavy metals and to avoid stressing the kidneys.

An interesting observation has been that patients with KPU often get worse when an attempt is made to incorporate detoxification agents or antimicrobial agents prior to having first addressed the KPU condition. Once KPU has been addressed, other treatment options are often much more effective and better tolerated.

Additional Considerations

Many patients with chronic Lyme disease have issues with sulfur intolerance. This leads to a patient being unable to effectively utilize a number of detoxification agents such as alpha-lipoic acid, DMSA, DMPS, and glutathione; as well as supplements such as garlic. This may be related to genetic predisposition, but some of the enzymes involved in sulfur metabolism (CBS and others) are heme and B6 dependent; both of which are depleted in KPU. As patients are treated for KPU, these sulfur tolerance issues may resolve. Klinghardt has found that molybdenum at a dose of 100-500 mcg per day may correct sulfur intolerance in patients with KPU, as molybdenum may also be lost in these patients.

Ammonia is generally high in patients with KPU. As KPU is treated, high levels of ammonia tend to normalize. To bind and excrete ammonia, zeolite may be used.

Resolution of KPU

For most with the condition, supplementation will be required for life. However, Klinghardt has seen complete resolution of the condition after having addressed epigenetic influences, trauma, or unresolved conflicts using tools such as mental field therapy, family constellation work, or EMDR. By resolving trauma in the ancestry, the epigenetics are influenced in a positive way and the condition resolves.

Klinghardt has also observed complete resolution of Lyme-induced KPU when the infection is managed successfully with biological interventions.

Final Thoughts

Once patients are on the KPU protocol and mobilized metals have been addressed, the body begins to respond to backlogged infections and significant improvements in the patient’s condition
are often observed. Hormonal status often improves. Some patients who have been on thyroid medication for years may even become hyperthyroid as the body begins to function more optimally. Other patients may lose weight. Symptoms directly related to low levels of zinc, vitamin B6, biotin, manganese, and arachidonic acid often resolve.

Just as homes are built by first laying a solid foundation, addressing KPU and the deficiencies in zinc, vitamin B6, biotin, manganese, and arachidonic acid are key pieces of the puzzle in addressing the complexities of chronic Lyme disease and many other conditions.

Evaluation for KPU is one of the first things that Klinghardt pursues in working with patients with chronic illnesses. Implementing the KPU protocol often yields progress that had not previously been possible, and patient recovery is accelerated in a very deep and profound way.

Disclaimer

This article is not intended to provide personalized treatment recommendations or to facilitate self-treatment. Treatment should be done only under the care and supervision of a licensed medical authority. Attempts to self-treat the condition may result in unintended negative consequences.

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Useful Resources

Scott Forsgren, FDN-P, is the founder of BetterHealthGuy.com, a health coach, blogger, podcaster, health writer, advocate, support group facilitator, and LymeLight Foundation board member. He recovered his own health after a 20-year journey through Lyme disease and mold illness. Today, Scott is grateful for his current state of health and all that he has learned on this life-changing journey. Dr. Klinghardt served as a powerful mentor, teacher, and guide as Scott worked to understand the disease which had previously taken so much of his life and moved toward a place of health and wellness. Scott continues to utilize a maintenance pyroluria protocol which he started almost a decade ago. To follow Scott’s work, visit http://www.betterhealthguy.com. His podcast “BetterHealthGuy Blogcasts” is available on his web site and on YouTube, iTunes, Google Play, and Stitcher.

Dietrich Klinghardt, MD, PhD, studied medicine and psychology in Freiburg, Germany, completing his PhD on the involvement of the autonomic nervous system in autoimmune disorders. Early in his career, he became interested in the sequelae of chronic toxicity (especially lead, mercury, environmental pollutants, and electromagnetic fields) and its impact on chronic illness. Dr. Klinghardt has contributed significantly to the understanding of metal toxicity and its connection with chronic infections, illness, and pain. He has developed Autonomic Response Testing, a comprehensive evaluation system that has helped many practitioners to become accomplished holistic practitioners. He founded Sophia Health Institute (http://www.sophiaha.com) in 2012, and is actively involved in patient care at his clinic outside of Seattle. More information on his educational seminars can be found through the Klinghardt Academy (http://www.klinghardtacademy.com; US) and the Klinghardt Institute (http://www.klinghardtinstitute.com; UK).[/vc_column_text][vc_empty_space][vc_row_inner][vc_column_inner width=”1/2″][dt_default_button bg_hover_color=”#dd3333″ border_radius=”6px” border_width=”0px” button_padding=”12px 18px 11px 18px” default_btn_bg_color=”#1e73be” font_size=”16″ icon=”JTNDaSUyMGNsYXNzJTNEJTIyZmElMjBmYS1maWxlLXBkZi1vJTIyJTIwYXJpYS1oaWRkZW4lM0QlMjJ0cnVlJTIyJTNFJTNDJTJGaSUzRQ==” icon_size=”16″ link=”url:http%3A%2F%2Fhoofa.wpengine.com%2Fwp-content%2Fuploads%2F2017%2F08%2FKryptopyrroluria-aka-Hemopyrrollacramuria.pdf||target:%20_blank|” size=”custom” text_color=”#ffffff” text_hover_color=”#ffffff”]Download PDF of this Article[/dt_default_button][/vc_column_inner][vc_column_inner width=”1/2″][/vc_column_inner][/vc_row_inner][/vc_column][/vc_row]

Limitations of Traditional Medicine – Observation Two: It distorts the doctor/patient relationship

Limitations of Traditional Medicine - Observation Two: It distorts the doctor/patient relationship

In our last post, we discussed how most diagnoses don’t just fall innocently out the sky at some point in life’s trajectory and how easy it is, once a diagnosis has been made, for patients to objectify the diagnosis as something separate from themselves, the choices they have made and the life they have lived. This process of objectification of illness has been disparagingly called N2D2 medicine; the name of disease = name of the drug. Dr. Sydney Baker has termed it “name it, blame it. tame it” medicine.

This trend in modern medicine has a further interesting effect on the relationship between the doctor and the patient. By avoiding cause and effect inquiry, it limits the patient’s involvement in their own care and projects the power to heal onto some outer authority. The doctor is seen as all healthy; the patient is often seen as all sick. The patient frequently identifies with their diagnosis in order to derive some form of identity and meaning from this one-sided relationship. It is a means of barter and exchange within the allopathic system.

The implication is that when this transaction occurs, and the patient assumes the illness as an immutable, fixed, objective entity of sorts, the patient’s “inner physician” completely shuts down. Their desire for self-enquiry and self-advocacy for bringing all that it takes for themselves to heal their illness, closes off as the responsibility gets shifted onto the outer authority figure, whether it be a doctor, naturopath, psychologist or some other member of the healing profession.

This occurrence is particularly tragic because it has been my observation that it is the physician within the patient that needs to be activated to result in a true transformation. The inner physician’s healing action is as great as that of the physical doctor/healer appearing on the external scene. Similarly, if the inner healer is not activated by the conscious act of intention by the patient, the possibility of a true healing experience is somewhat dissipated. If nothing shifts in the internal dialogue and the mental field of the patient, if the patient is not fully engaged in cause and effect inquiry and totally committed to changing previous outcomes, then the possibility of something shifting at the level of the physiology is somewhat muted and no true, lasting transformation occurs.

For example, an herb is somewhat inert unless the individual consciously links the physical substance to their intentional mental field, engages their mind in a solution-focused way, and then in some mysterious alchemical process, activates its healing potential. This process is incredibly important to the doctor/healer and patient transaction. It has been much maligned in the traditional research as exerting the so-called “placebo effect,” but if the mind-body connection is real (and the evidence is too overwhelming to ignore), then why do we not factor this into the healing equation and give credit where credit is due? If, as a patient, one is not mentally engaged and in agreement with the outlined therapeutic interventions, it is highly likely that the healing effect will be significantly compromised.

Evidence-Based Medicine in the World of Mold Illness

Evidence-Based Medicine in the World of Mold Illness

The practice of evidence-based medicine (EBM) is held out as the gold standard of practice when it comes to evaluating how best to treat certain conditions. As this article will outline, nowhere is this standard in more disrepute than in the evidence-based practices currently in use on how best to treat mold related illness.

What is Evidence-Based Medicine? The term "evidence-based medicine" (EBM) was first used in 1990 by G.H. Gyatt, a professor from McMaster University Canada, but a broader description of EBM appeared in 1992 when the Evidence-Based Working Group published a new approach to teaching the practice of medicine in JAMA. (1) The article stressed that “evidence-based medicine de-emphasizes intuition, unsystematic clinical experience, and pathophysiological rationale as sufficient grounds for clinical decision making and stresses the examination of evidence from clinical research.(2)” The article emphasized that this would require “new skills of the physician, including efficient literature searching and application of formal rules of evidence evaluating the clinical literature.(3)” Tradition, anecdote and theoretical reasoning based on the basic sciences would be replaced by evidence from high-quality, randomised, controlled trials and observational studies, in combination with clinical expertise and the needs and wishes of patients.(4)

On the Internet, numerous articles discuss other potential definitions of the term "evidence-based medicine"(5). Sackett et al. define EBM as “the integration of best research evidence with clinical expertise and patient values”(6). Another definition states that “EBM is nothing more than a process of life-long, self-directed learning in which caring for patients creates the need for clinically important information about diagnosis, prognosis, therapy, and other clinical and health care issues.” A further definition suggests that EBM is “an evolutionary progression of knowledge based on the basic and clinical sciences and facilitated by the age of information technology.(7)”

Many of the above definitions arose from a BMJ article published in 1996, which stated that EBM is the conscientious, explicit and judicious use of the best current evidence in making decisions about the care of individual patients. The practice of evidence-based medicine involves integrating individual clinical expertise with the best available external clinical evidence from systematic research.(8)

Evidence-based medicine requires asking relevant clinical questions concerning the patient’s issues, performing a literature search for relevant research data to support or refute diagnostic and/or treatment approaches, critically appraising the literature regarding its validity and applications, and then implementing one’s findings and insights in a clinical setting.

Twenty-five years ago, evidence-based medicine, which involves utilizing the medical literature to effectively guide medical practice, was considered profound enough to be described by the initial authors as a paradigm shift in the way medicine was to be practiced. The authors reported Thomas Kuhn’s description of a scientific paradigm as “[a way] of looking at the world that defines both the problems that can legitimately be addressed and the range of admissible evidence that may bear on the solution”(9). When defects in an existing paradigm accumulate to the extent that the paradigm is no longer tenable, the paradigm is challenged and replaced by a new way of looking at the world.

Some of the shift toward evidence-based medicine was initiated due to a loss of confidence in the traditional medical model and the studies that had initiated those practices. Larry Dossey M.D. commented on many of the scandals that rocked the confidence of healthcare consumers at the end of the last century(10). “The uncertainties of medicine are cause for celebration,” Dossey wrote. “Modern medicine is losing some of its invincibility. Many of the rules of good health that have guided patients and physicians for decades have taken a beating from which they may not recover. The almost blind allegiance we once had to the treatments offered has been severely undermined by these studies — some of the absolute certainties are no longer as absolutely certain.”

First, there was the Vioxx drug scandal, in which many people died from heart disease after consuming what were thought to be relatively innocuous anti-inflammatory drugs. Compounding the problem was the fact that this particular drug had been marketed as being relatively safe. Furthermore, evidence emerged that the drug companies had known for some time that the drug had an increased incidence of cardiac side effects, but they had chosen to hide these negative findings to ensure a profit.

In the Women’s Health Initiative study(11), hormone replacement therapy (HRT), specifically Premarin and Provera, once a mainstay of post-menopausal symptom management and considered to be safe, was shown to actually increase women’s risk of heart disease, stroke, thrombosis and breast cancer. The risks of increased cardiovascular disease (CVD) and breast cancer were concluded to far outweigh the benefits of osteoporosis protection and colon cancer reduction. Millions of women, to the fanfare of massive nation-wide news coverage, were immediately withdrawn from hormone replacement therapy as a result of these findings. The sales of these two drugs dropped 50% in one month. The American Association of Clinical Endocrinologists, (AACE), the American Congress of Obstetricians and Gynecologists (ACOG) and the North American Menopause Society (NAMS) recommended HRT use only for short-term symptom control.

Later critiques of the study pointed out some bias and manipulation of data, including but not limited to the following:

  1. Many women chosen for the study were not in the typical age range for HRT – they were, on average, 12-15 years past the age of menopause and had significant baseline cardiovascular and coronary artery disease (CAD) at the initiation of the study.
  2. Approximately 74 percent of the women included in the study had never used HRT before and were outside the 3-4 year post-menopausal window of opportunity for HRT, in which cognitive and cardioprotection from HRT was maximal.
  3. Premarin was the estrogen used in the study. Premarin is a conjugated equine estrogen drug with 50 percent estrone (known to increase breast cancer risk prior to the WHI study), equilin and equilenin, both of which have unknown activity on human estrogen receptors. The WHI study was not undertaken with human estrogens (E1=estrone, E2=estradiol and E3=estrone). Premarin is an oral equine-derived preparation and is known to increase liver coagulation proteins, thus increasing the risk of stroke and cardiac events. Transdermal estrogen was not used, which has shown no association with the increased activation of liver clotting proteins. NAMS preaches that there are no randomized, placebo-controlled trials to support the claims of increased efficacy or safety of compounded, bioidentical hormones; however, there is a plethora of studies demonstrating the superior efficacy and safety of pharmaceutical bioidentical hormones over non-bioidentical, synthetic hormones.
  4. Progestin was the chosen progesterone preparation. This is a medroxyprogesterone acetate preparation that had already been shown to have an unfavorable effect on lipid profiles prior to the WHI trial.

Much criticism was levelled against the WHI study when the data were placed within a clinical perspective and further studies reached different conclusions. The results of the WHI and the Heart and Estrogen/Progestin Replacement Study (HERS) trial, when reassessed, were shown to not apply to younger women, specifically those aged 50-60. In most of the subsequent studies, there were no cardiovascular deaths among 6,000 women on HRT, as compared to several deaths in the placebo group (12). There was overwhelming evidence that the anti-atherosclerotic effect of HRT depended on the time of initiation and that early initiation was protective.

With regard to knee surgery, researchers proved that performing arthroscopic surgery on an arthritic knee, once a mainstay of surgical interventions for this condition, was no more effective than administering an anesthetic, making a skin incision, and performing a sham surgery. The outcomes in terms of pain and symptoms after either of these two procedures were virtually the same. The value of mammograms has also been seriously questioned, and it is unclear as to whether or not a mammogram has any influence on the number of women dying from breast cancer each year.

These observations are supported in the literature, which shows that many medical findings and treatment suggestions previously taken as the gold standard do not stand the test of time. John Ioannidis, known as a meta-researcher who has based his career on researching the validity of medical research findings, has shown time and time again in published studies that as many as 90 percent of the published medical information that doctors rely on is flawed (13). Eighty percent of non-randomized studies (the most common type of studies) turn out to be wrong, and 25 percent of gold-standard randomized studies turn out to be wrong, as do 10 percent of platinum-standard large randomized trials. One of his papers (14) discussed his belief that researchers were frequently manipulating data analyses, choosing career-advancing findings rather than good science and using the peer-review process to suppress opposing views (15). In perhaps one of the most ignominious examples of medical science undergoing a dramatic reversal in treatment approach, Dr. Egas Moniz received a Nobel prize in 1949 for his pioneering of the frontal lobotomy in 1936 to treat incurable mental illness (16). Times do change, and sometimes, they change radically.

A Wall Street Journal article written by Ron Winslow entitled Study Questions Evidence Behind Heart Therapies (17) discussed a study that revealed that less than 11 percent of 2,700 recommendations commonly made by cardiologists were supported by scientific evidence. Furthermore, many of the dogmatic recommendations and guidelines created by cardiologists are formed by individuals who are connected in some financial way with the pharmaceutical companies (18). Another study showed that 85 percent of individuals who had stents or angioplasties to treat their blocked coronary arteries did not need them. Furthermore, the group that did have the surgical procedures ended up much sicker than the individuals who treated their condition with drugs alone (19). Thus, more critical evaluation of standards of practice was needed.

The original 1992 Evidence-Based Medicine Working Group set out specific criteria for assessing the strength of evidence that supports clinical decisions (20). Has the diagnostic test been evaluated in a patient sample that included an appropriate spectrum of mild and severe disease, treated and untreated disease and individuals with different but commonly confused disorders (21)? Was there an independent, blind comparison with a gold standard of diagnosis (22)? Was the assignment of patients to treatments randomized (23)? Were all patients who entered the study accounted for at its conclusion (24)? Lastly, were explicit methods used to determine which articles to include at its conclusion (25)?

Evidence-based medicine utilizes specific steps to arrive at conclusions:

  • Ask the right question using an acronym PICO (26). P=Patient or problem, I=Intervention, C=Comparison intervention, O=Outcome.
  • Acquire the best evidence by searching various databases, including but not limited to PubMed, Embase and Cochrane Library. Evidence-based medicine has various levels or grades for use in assessing the strength of studies.
  • Appraising the evidence: Is the study valid and relevant? What were the results of the study? Will the results help in treating the patient?
  • Apply the evidence. Once the evidence is obtained, it must be filtered through the patient’s value systems and the level of the practitioner’s core competencies. Shared decision making is essential once the risks and benefits have been explained.
  • Performance assessment. Whether this approach is helping and assisting the patient to achieve his or her anticipated and expected health goals must be determined. This is done by assessing the four steps listed above.

There are four levels of evidence that are used when assessing the strength of studies via an EBM approach.

  1. Level I – This is considered the top level of evidence, and it is derived from randomized, double-blind, placebo-controlled trials and/or meta-analyses that combine the evidence from these trials. Meta-analyses are considered to be the most eligible for Level I status, but they too have come under some criticism as a means of evaluating critical evidence. Many studies that are combined in a meta-analysis are homogenous and lack sufficient outlying evidence.
  2. Level II – This evidence is not considered quite as reliable as that from Level I. This evidence comes from controlled trials without randomization, cohort or case-control analytic studies and multiple-series studies.
  3. Level III – This evidence is based on expert opinion from those specialized in one particular area under investigation. Most often, there are no control groups, and sample sizes are small. This approach can often lead to a large margin of error unless statisticians compile the evidence from all expert opinions.
  4. Level IV – This evidence is based on personal experience and is the least desirable source of evidence because it lacks statistical validity.
    The original working group emphasised that it would require a specific teaching course and orientation, as taught at the McMaster University Medicine Residency Program, Department of Medicine, in order to critical appraise journal articles and arrive at the bottom line regarding the strength of evidence and how it may bear on the clinical problems in question.

According to the original JAMA article, the residents “learn to present the methods and results in a succinct fashion, emphasizing only the key points. A wide-ranging discussion, including issues of underlying pathophysiology and related questions of diagnosis and management, follow the presentation of articles. They always substantiate decisions or acknowledge the limitations of the evidence and discuss the literature retrieval, the methodology of papers and the application to the individual patient. (27)” This article emphasised that this “new paradigm will remain an academic mirage with little relation to the world of day-to-day clinical practice unless physicians-in-training are exposed to role models who practice evidence-based medicine”. McMaster University recruited internists with training in clinical epidemiology and the “skills and commitment [needed] to practice evidence-based medicine. (28)” This is a tall order for a busy clinically orientated profession, and even this article agrees that practicing in this way is fraught with complexity and difficulty. Furthermore, when first published, the authors asked whether advocating evidence-based medicine in the absence of definitive evidence of its superiority in terms of improving patient outcomes is an internal contradiction (29).

One of the challenges facing a clinically trained and clinically based practitioner who does no in-house research and whose practice is full of competing demands is how to best evaluate the available evidence and make the best treatment decisions for patients who present every day with complex problems. The average physician spends far beyond 40 hours per week in the office, seeing patients, managing staffing issues and dealing with paperwork.

The available paths to researching evidence-based literature and applying that information to complex patients with a multitude of issues are as follows:

  1. Read journal article summaries at night with a critical eye on the quality of the research presented. Many doctors have a strictly clinical background, not a statistically oriented, research-based background, and therefore, they may lack the knowledge to interpret research articles critically.
  2. Read the opinion pieces or position papers of others who have read the original articles and commented on the quality of the research presented in association or interest group publications. Many of the position papers published by specific associations may not have the current best evidence and may not represent the best science available.
  3. Attend conferences where the presenters, one assumes, are leading the field that the conference concerns, have done the necessary research and are presenting information based on Level I and Level II evidence-based research.
  4. Listen to drug company reps who visit one’s office with the details of the research concerning their products, which is presumably biased due to vested interests whether the product in question is a supplement or a drug.
  5. Listen to patients’ summaries of their internet searches and attempt to interpret their evidence into rational decision making.
  6. Read up on what one’s colleagues are discussing and/or referencing in online discussion groups.

From these beginnings, evidence-based medicine has had some major achievements. The Cochrane Collaboration was established to collate and summarise evidence from clinical trials, methodological and publication standards for primary and secondary research were established, national and international infrastructures were built to develop and update clinical practice guidelines, resources and courses were developed to teach critical appraisal and new knowledge bases for implementation and knowledge transition were built (30).

However, since evidence-based medicine was first introduced and adopted, many cracks in the paradigm have appeared that warrant careful appraisal:

  1. The co-opting of clinical trials by invested drug manufacturing and medical device interests and the manipulation of data to suit endpoint outcomes has become more subtle and harder to detect. These companies often set the research agenda, decide what is counted as a disease (i.e., sexual arousal disorder, which is treated with sildenafil), decide which tests and treatments will be compared and choose the efficacy outcome measures (31). In addition, setting inclusion criteria to select those most likely to respond to treatment, manipulating the dosing of both intervention and control drugs and selectively publishing positive studies (while suppressing negative outcomes) in leading peer-reviewed journals, with the assumption that their trials are unbiased, creates serious legitimacy issues regarding the conclusions reached. One review of industry-sponsored trials of antidepressants showed that 37 of 38 had positive findings but only 14 of 36 trials with negative findings were published (32). Psychiatric prescription and drug trials are at the centre of many of these controversies (33). Among the RTC studies in psychiatric journals, those that reported conflicts of interest were five times more likely to report positive results. Large drug companies do not fund and are not interested in treatment interventions that do not support a pharmaceutical intervention.
    Many studies that show the long-term benefits of compounded bioidentical hormone replacement therapy interventions do not make it to mainstream medical journals for these very reasons. A very contentious JAMA-published article, a retrospective observational study, indicated the negative effects of testosterone replacement therapy on cardiovascular disease, and this article changed the way that testosterone therapy was used in male andropause, despite the fact that many prior RCT studies had shown no such impact or favourable outcomes (34).
  2. The co-opting of policy makers (politicians) by the drug industry affects the introduction of certain evidence-based policies (35).
  3. A surplus of evidence results in unmanageable clinical guidelines (36).
  4. Large trials are designed to achieve marginal gains in a saturated therapeutic field and may tend to overestimate potential benefits. After many of the large early gains in research (the use of antiretroviral drugs in HIV and the use of triple antibiotic therapy in H. Pylori), new research has had to shift its focus to marginal gains in often overpowered trials that tend to underestimate harm (adverse effects undetected) and overestimate benefits (effects that are statistically but not clinically significant (37)). GlaxoSmithKline was fined $3 billion for multiple criminal and civil offenses, such as false reporting, the unlawful promotion of medicines and failure to report safety data (38).
  5. The overemphasising of computerised decision support systems and defensive decision-making support technologies, as well as inexperience with complex presentations that do not comply with simple guidelines, may interfere with more experienced and nuanced clinical decision making on the part of an experienced practitioner who is somewhat accustomed to tolerating ambiguity and uncertainty in clinical decision making (39).
  6. Decision making may be driven by non-clinical staff who are incentivised by financial endpoints and not by the nuanced quality of care for complex individual patients. “Patients may often feel tyrannized when their clinical management is inappropriately driven by algorithmic protocols, top-down directives and population targets (40).”
  7. Simple and/or complex algorithms do not fully apply to an aging population with complex presentations and comorbid conditions. Each person is genetically and biochemically unique (as is only too well demonstrated in the CRS population), and although specific guidelines, as outlined by Dr. Shoemaker, must be followed to achieve success, there may still be many comorbid complexities that render the application of these same strict guidelines somewhat problematic, i.e., a patient with CIRS who has had a previous traumatic brain injury, complex early developmental trauma and a borderline personality disorder.

The authors of this critical 2014 BMJ paper, entitled “Evidence-based medicine: A movement in crisis?” suggest launching of a new campaign for what they termed “real evidence-based medicine”. According to them, this is how to best describe what they mean by real evidence-based medicine and the remedying solution:

What is real evidence-based medicine, and how do we achieve it? Real evidence-based medicine:

  • Makes the ethical care of the patient its top priority.
  • Demands individualised evidence in a format that clinicians and patients can understand.
  • Is characterised by expert judgment rather than mechanical rule following.
  • Shares decisions with patients through meaningful conversations.
  • Builds on a strong clinician-patient relationship and the human aspects of care.
  • Applies these principles at community level for evidence-based public health.

Actions to deliver real evidence based medicine:

  • Patients must demand better evidence that is better-presented, better-explained and applied in a more personalised way.
  • Clinical training must go beyond searching and critical appraisal to hone expert judgment and shared decision-making skills.
  • Producers of evidence summaries, clinical guidelines, and decision support tools must take account of who will use them and for what purposes and under what constraints they will be used.
  • Publishers must demand that studies meet usability standards, as well as methodological ones.
  • Policymakers must resist the instrumental generation and use of “evidence” by vested interests.
  • Independent funders must increasingly shape the production, synthesis, and dissemination of high-quality clinical and public health evidence.
  • The research agenda must become broader and more interdisciplinary, embracing the experience of illness, the psychology of evidence interpretation, the negotiation and sharing of evidence by clinicians and patients, and the prevention of harm from over-diagnosis.

I believe some of these revised criteria have been met by Dr. Shoemaker and his co-authors. Dr. Shoemaker has published critiques of what has passed for evidence-based medicine guidelines in the management of mold illness prior to his ground-breaking work. The American College of Occupational and Environmental Medicine (ACOEM) and the American Academy of Asthma, Allergy and Immunology (AAAAI) published in 2002 and 2006, respectively, guidelines reporting that mold exposure was not capable of producing human illness. Much of the ACOEM “evidence” was based on opinion papers by defense consultants in litigation regarding water-damaged buildings (Bruce Kelman and Ronald Gots) and cited no human studies as reference material (41). Dr. Shoemaker cited an article in the Wall Street Journal and an article by Craner that exposed the bias and concealed conflicts of interest of the ACOEM authors: “there is nothing evidence-based in either the ACOEM or AAAAI, as that process begins with the observation of affected patients.” Dr. Shoemaker is clearly using the criteria regarding the best way to practice evidence-based medicine in his criticism of their lack of fulfillment of these criteria in publishing these opinion papers.

I have relied almost exclusively on Dr. Shoemaker and various co-authors of certain papers to understand the complexity of this multilayered condition. Dr. Shoemaker is extremely insistent that the steps to be followed in the diagnosis and treatment of this condition must follow the guidelines set out by his own research, as well as clinical practice and treatment guidelines. It is obvious that he has followed an evidence-based approach in this undertaking. Dr. Shoemaker began his original work with CIRS when he observed that patients with a mysterious disease seemed to improve when prescribed a lipid-lowering drug, cholestyramine. Based on that original observation, he explored the biology and pathophysiology of the disease processes in patients, using the best evidence available at the time, without the influence of financial interests. As he learned, he explored further hypothesises, published numerus studies, wrote books, collaborated with other researchers and lectured on the subject. He continues to utilise the best evidence-based practices in an attempt to understand the genomics that underlie CIRS and how the use of VIP (and the rest of the CIRS protocol) influences the proteomic and Neuroquant findings of affected individuals.

The proof regarding whether an evidence-based approach is effective in managing CIRS patients is whether the patients involved in the study enjoy improved health as compared to controls. At present, there are no long-term randomized trials of the Shoemaker approach to treating CIRS. In other words, his research may not have fulfilled the Level I criteria regarding what type of research best characterises evidence-based medicine. However, his work has nonetheless systematically fulfilled most of the other criteria in that it is patient-centered and documents responses to care that are quantifiable and reproducible.

(*1) Evidence-Based Medicine Working Group. Evidence-based medicine. A new approach to teaching the practice of medicine. JAMA 1992; 268: 2420-5.
(*2) Ibid
(*3) Ibid
(*4) Greenhalgh, T., “Evidence-based medicine: a movement in crisis?” BMJ 2014; 13 June, 348
(*5) http://researchguides.uic.edu/ebm
(*6) Sackett D.L., et al., “Evidence-Based Medicine: How to Practice and Teach EBM.” Edinburgh: Churchill Livingstone.
(*7) Doherty, Steve. “Evidence-based medicine: Arguments for and Against.” Emergency Medicine Australasia 2005; 17: 307-13.
(*8) Sackett, D.L., Rosenberg, W.M.C., Gray, J., Haynes R.B., Richardson W.S., “Evidence-based medicine: what it is and what it isn’t.” BMJ; 312:71-72.
(*9) Kuhn, T.S., The Structure of Scientific Revolutions. Chicago, Ill: University of Chicago Press; 1970
(*10) Dossey, L., Alternative Therapies Sept/Oct 2002, Vol. 8, No.5 32
(*11) Rossouw, J.E.1, Anderson, G.L., Prentice, R.L., LaCroix, A.Z., Kooperberg, C., Stefanick, M.L., Jackson, R.D., Beresford, S.A., Howard, B.V., Johnson, K.C., Kotchen, J.M., Ockene, J. Writing Group for the Women's Health Initiative. (2002). “Risks and benefits of estrogen plus progestin in healthy postmenopausal women: principal results From the Women's Health Initiative randomized controlled trial.” JAMA. 288(3):321-33.
(*12) Family Practice News. (2003). 33(11), 1-2
(*13) Freedman D., (2010). Lies, Damned Lies, and Medical Science. The Atlantic. Nov 2010 Issue.
(*14) Ioannidis, J.P.A., (2005). Why Most Published Research Findings Are False. PLoS Med 2(8): e124. doi:10.1371/journal.pmed.0020124
(*15) Freedman D., (2010). Lies, Damned Lies, and Medical Science. The Atlantic. Nov 2010 Issue.
(*16) Csoka, A., (2015). Innovation in medicine: Ignaz the reviled and Egas the regaled. Med Health Care Philos. Springer Journal, Dec 4.
(*17) Wall Street Journal |Feb 25th 2009
(*18) Rogers, S., (2009). Total Wellness. Aug, p. 1.
(*19) Boden et al., (2007). New England Journal of Medicine. Optimal medical therapy with or without PCI for stable coronary artery disease. April 12, 356; 15:5003-16.
(*20) Evidence-Based Medicine Working Group. (1992). Evidence-based medicine: A new approach to teaching the practice of medicine. JAMA, 268(2420), p. 2422.
(*21) Department of Clinical Epidemiology and Biostatistics, McMaster University. (1981). How to read clinical journals, II: to learn about a diagnostic test. Can Med Assoc J. 124:703-710.
(*22) Godfrey, K., (1985). Simple linear regression in medical research. N Engl J Med, 313, p. 1629-1636
(*23) Department of Clinical Epidemiology and Biostatistics, McMaster University. (1981). How to read clinical journals, V: to distinguish useful from useless or even harmful therapy. Can Med Assoc J, 124, 1156-1162.
(*24) Ibid
(*25) Ibid
(*26) University of North Carolina, Health Sciences Library. (2016). “Forming focused questions with PICO.”
(*27) Evidence-Based Medicine Working Group. (1992). Evidence-based medicine: A new approach to teaching the practice of medicine. JAMA, 268, p. 2420.
(*28) Ibid
(*29) Ibid
(*30) Ibid
(*31) Cohen, D., (2013). “FDA official: Clinical trial system is broken.” BMJ, p. 347.
(*32) Turner, E., Matthews, A.M., Linardatos, E., Tell, R., Rosenthal, R. (2008). “Selective publication of antidepressant trials and its influence on apparent efficacy.” N Eng J Med, 358, p. 252-60.
(*33) Perlis, R.H. et al., (2005). “Industry sponsorship and financial conflict of interest in the reporting of clinical trials in psychiatry.” Am J Psychiatry, 162(10), p.1957-60.
(*34) Vigen, R., MD, MSCS1, et al., (2013). “Association of Testosterone Therapy with Mortality, Myocardial Infarction, and Stroke in Men with Low Testosterone Levels.” JAMA, 310(17), 1829-1836
(*35) Le Couteur, D.G., Doust, J., Creasey, H., Brayne, C. (2013). “Political drive to screen for pre-dementia: Not evidence based and ignores the harm of diagnosis.” BMJ, p. 347.
(*36) Allen, D., Harkins, K. (2005). “Too much guidance?” The Lancet, 365, p. 1768.
(*37) Greenhalgh, T., Howick, J., Maskrey, N. (2014). “Evidence-based medicine: A movement in crisis?” BJM. p. 348.
(*38) Roehr, B., (2012). “GlaxoSmithKline is fined record $3billion in US.” BMJ. 345, p. e4568.
(*39) Greenhalgh, T., Howick, J., Maskrey, N. (2014). “Evidence based medicine: A movement in crisis?” BMJ. p. 348.
(*40) Ibid
(*41) Shoemaker, R. (2010). Surviving Mold: Life in the Era of Dangerous Buildings. Otter Bay Books: Baltimore, p. 310-311.

Limitations of Traditional Medicine: Observation One – Separates Cause and Effect

Limitations of Traditional Medicine: Observation One

Mahatma Gandhi said, “One of the greatest tragedies of modern medicine is that it’s just way too effective.” Put quite simply, traditional medicine works. Dr David Simon gives the following example: Let’s say that before you go to bed at night, you drink a half a quart of vodka with a cheeseburger and wake up at 3 a.m. with heartburn and pain. If you reach over for your Rolaids and within ten minutes, your heartburn is gone, what does that teach you? The lesson learned is to take your Rolaids before you go to bed at night! By taking the drug and suppressing the symptom, it completely separates you from that experience. It provides a short-term solution, but it does very little to link cause and effect in the creation of illness. And it does practically nothing to encourage personal responsibility in the process.

This attitude perpetuates the paradox of immediate sensual gratification versus that of eternal youth. Individuals do not want to feel symptoms they are experiencing; hence they suppress them, yet they also wish to live a healthy life in the absence of disease. Very little thought goes into the link between the two—how each act one performs has the potential to either assist the body in its healing process or hasten its trajectory to entropic disease states.

In an integral model, we are most concerned about how the patients have lived their lives up until this point in time. We want to investigate how the choices they have made, in all facets over the full span of their lifetime—from their food choices to their exercise regimes, to their familial and social relationships, to their work environment, to their spiritual practices—have influenced their symptom manifestation. It is also essential that people be familiar with the content of their thought processes and their internal dialogue, and how their perceptions of reality in the world are affecting them. We will see that all of these factors play a determining role in the kind of health or disease they will experience.

In modern allopathic medicine, individuals have been completely identified by their tissue diagnosis and the stage of disease, which leads to complete objectification of the individual and an absolutely material definition of health. It’s either this diagnosis or that diagnosis; that’s it. The patient is entirely divorced from the rest of their contextual interrelationships and stripped from a cause and effect relationship. Mark Wolynn, author of “It Didn’t Start With You” says: “diagnosis shuts down self-enquiry.” People are instantly transformed into cancer or a diabetes patient and deprived of their multiple interconnecting experiences. This contributes to the unconscious collusion between doctor and patient, based as it is on a faulty assumption that the disease process is entirely physically or biologically based.

There is a Common Misconception Concerning Meditation

There is a Common Misconception Concerning Meditation

There is a common misconception that meditation is concerned with “quietening” or stopping the activity of the busy mind. Nothing could be further from the truth.

While it may downregulate the biological consequences of an active or stressed mental field, (by lowering cortisol and the stress hormones, adrenaline and noradrenaline), the truest and deepest benefit of meditation is the gradual awakening to the reality that we are more than just our physical bodies.

In deep meditation states, we become aware of the many layers of our human experience – the movement of our physical bodies, the fluctuations in our moods and emotional states and the thousands of thoughts that pass across our consciousness. We may also stand the chance of becoming, for the first time, deeply aware of our true, subjective, core nature.

Our body changes year to year, our moods come and go, and our thoughts flit across our consciousness at an alarming rate. We have approximately 60,000 thoughts a day, the majority of which are the same as the day before. But the fundamental question is: to whom are these changing events taking place?

The answer is YOU, the real you, the witnessing subjective sense of oneself. Only in the deepest states of witnessing meditation do we stand the chance of arriving at our true, authentic selves.

While it has many health benefits, the deepest and most enduring benefit of a daily meditation practice is that we may, for the first time, become aware of our core nature, our deepest selves. Like a cloth that we dip into dye every day with a meditation practice, we stand the chance of permanently colouring our daily lives with the qualities of our core, unchanging, authentic selves. We slowly wake up to the realization that our daily waking consciousness and the incessant movement of our internal dialogue do not represent our deepest identity.

If we make meditation part of our daily practice, we may also experience many of the well-documented health benefits of a daily practice. Forty seven studies on meditation were analyzed and published in JAMA Internal Medicine in Jan 2014. Conditions such as anxiety, depression, hypertension, IBS, chronic pain, cancer, HIV, tinnitus and insomnia have all been positively influenced by a meditation practice.

MRI scans have shown that after 8 weeks of a meditation practice the area of the brain associated with fear and the fight or flight response (called the amygdala) shrinks. Mean while, the prefrontal cortex, the area associated with concentration and decision making, increases in size. The scale of change is influenced by the number of meditation hours practiced.

Furthermore, in deep meditation, we may transcend all awareness of a separate, symptomatic self and experience the opening into a sense that my separate, subjective self is no different than anyone else’s. We wake up to the awareness that at the deepest core of the human experience lies the awareness that there are no boundaries between you and me.

Integrative Medicine: What’s Really Going On?

Integrative Medicine: What’s Really Going On?

I have heard the same lament too many times to ignore it any longer. Every day, while interviewing new patients, I hear the same thing. They tell me – often with sadness, sometimes with anger, and most often with regret – that they’ve come to the end of their relationships with their family practitioners. Most often, the reasons are, “He just doesn’t listen to my needs anymore”, or “She chastises me every time I wish to use non-medicinal therapies”, or “She’s a very good doctor, but she doesn’t know anything about the supplements I’m taking”.

This morning a new patient, whom I’ll call Helen, told me that her doctor of 23 years, with whom she had a close relationship and who had delivered her three children, replied to her questions about alternative therapies with, “Oh, come on Helen, get a grip!” She told me their relationship ended right then and there. I find this situation tragic.

I know how hard my colleagues work, how compassionate and dedicated so many of them are and how accomplished they are at the fine art and science of family medicine. So why is there this huge resistance to embracing the healing modalities that so many of their patients are actively seeking out and benefiting from?

ON THE BANDWAGON

In 1998, the American Medical Association (AMA) dedicated an entire issue of their journal JAMA to alternative medicine.1 Their editorial literally gushed with the promise of alternative medical procedures. The question was raised as to why this bastion of conventional medical, which has vociferously opposed alternative medicine in the past, suddenly jumped on the bandwagon?

According to Dr. Julian Whitaker, a well-known US practitioner and spokesperson for alternative medicine, the answer is simple: “It’s because the public is deserting conventional medicine and flocking to alternative health care providers by the millions.”

THE NUMBERS DON’T LIE

While reliable statistics in developing countries such as South Africa are hard to come by, the figures we see in the first world indicate a growing trend towards integrative medicine among educated, high-income social groups. In 1991, Dr. David Eisenberg, MD, published a groundbreaking study on the extent to which the public had adopted alternative medicine. His follow-up study was the lead article in JAMA, entitled, “Trends in Alternative Medicine Use in the United Sates, 1990-1997”.2 Dr. Eisenberg reported that 46.3% of Americans visited an alternative practitioner in 1997. This is a substantial increase from the 36.3% he reported in 1991, with the American public making 427 million visits. By 1997, the number jumped to 629 million, exceeding the total visits to all conventional physicians.

We know that 3.8 million Canadians consult alternative practitioners, spending about 1.8 billion dollars in the process.3 An additional two billion dollars are spent on herbs, vitamins, supplements, books and courses. A Statistics Canada 1998-1999 National Population Health Survey showed that 19% of women use alternative health care versus 14% of men. Some observations have shown that users tend to have post-secondary education and are high-income earners.

One finding of the study, which must surely be alarming to the medical establishment, was that 60% of people who consulted alternative practitioners didn’t discuss it with their doctors. I have found that this lack of consultation is not because people don’t want a conventional doctor’s professional advice. But most people know in advance what their doctors will say, and thus decide to spare themselves the embarrassment of an unpleasant interview.

MEETING DEMANDS

Patients want more from their doctors. Not only do they want them to be informed about the latest research on supplements such as saw palmetto or glucosamine sulfate, they also want them to recognize issues more commonly addressed by alternative practitioners. My advice is not to let any doctor get away with comments such as, ‘There aren’t enough studies to recommend their use,” as there are many good quality studies done on a multitude of non-medicinal therapies that just aren’t published
in journals sponsored by pharmaceutical companies, which doctors usually read. Patients are also expressing a profound need for their family practitioners to hear their concerns about the mind-body connection and all that it entails.

Patients are no longer tolerant of alternative medicine being regarded as light medicine. They are taking their worldviews seriously and are expecting their health care providers to assist them. People are realizing that they are more than just a physical body with a set of symptoms. They’re aware that physical disease is often the end expression of long-ignored minor symptoms, which is why they are searching for advice before the minor symptoms manifest as major diseases.

A QUESTION OF COLLUSION

I suspect that some of my colleagues’ resistance to this new medicine my be due to a genuine distrust in what they see as entrepreneurial zeal on the part of alternative practitioners who exploit the gullibility of a vulnerable and ill-informed public. Some of these colleagues may also genuinely believe that alternative treatments are without scientific merit.

But there seems to be more at play here. Unwittingly, I believe that doctors and patients unconsciously collude in an archetypal relationship whereby doctors see themselves as all-healthy and the patients as all-sick. This model blinds both doctors and patients to the reality of the inner physician, that part of within ourselves that activates healing. The medical perspective often depersonalizes the patient, while treating the disease.

I also suspect that my colleagues are afraid of this new medicine because they have not been adequately prepared or trained to diagnose, let alone treat, the full extent of their own private suffering. Hence, they fail to recognize the full extent of their patients’ cries for help.

Alternative medicine is being integrated into mainstream medicine by a patient-driven, educated consumerism, whether the medical profession likes it or not. Viable alternative solutions for virtually all medical conditions will continue to grow in popularity into the next century. As a result, the entire face of medicine will change dramatically. My colleagues had better be prepared, or face the disappointment of ever-increasing patient dissatisfaction. Or worst yet, extinction.

By Dr. Bruce Hoffman
MBChB