Inflammatory Bowel Disease – Crohn’s Disease and Ulcerative Colitis, Part 1

Inflammatory Bowel Disease – Crohn’s Disease and Ulcerative Colitis

In anticipation of the upcoming Crohn’s and Colitis Summit, I want to share more about inflammatory bowel disease, Crohn’s disease, and ulcerative colitis. This two-part series will be a deep-dive into the root cause of inflammatory bowel disease, along with a comprehensive look at lifestyle changes and functional therapies that may provide relief. This free summit, hosted by Ravi Jandhyala and Mallika Allu of Gut Heal Protocol, will be held September 21st-27th. I will be speaking at the summit, and I encourage you to sign up if you or a loved one has Crohn’s disease or ulcerative colitis. Please note this summit has already taken place.

Inflammatory bowel disease (IBD) comprises a number of different medical conditions. The most significant of these are Crohn’s disease (CD) and ulcerative colitis (UC). These are chronic, immunologically mediated diseases with periods of relapse and remission, in addition to marked variations in mucosal inflammation from near normal in remission to severe ulceration in relapse.

UC affects only the colon with superficial inflammation, whereas CD affects the entire gastrointestinal tract and leads to transmural inflammation, strictures, fistulas, and abscess formation. 

The etiology of IBD is complex, but intricate dynamic interactions between the intestinal microbiome, host genetics, and external environmental factors all play an interrelated role in the development of IBD and its subsequent outcomes. 

The key mechanisms underlying the pathogenesis of these diseases are a genetically susceptible host exposed to external environmental factors, affecting gut microbiome and commensal flora. This results in a dysregulated immune response to different aspects of the gut microflora and increased intestinal permeability.

In this article, you will learn:

  • The etiology (root causes) of IBD, CD, and UC,
  • How the intestinal microbiome and your body’s immune response lead to IBD,
  • And the risk factors that may make you more susceptible to developing CD or UC, or having more severe flare-ups.

In Part 2, I will discuss our current strategies for diagnosing and treating CD and UC.

What causes IBD?


The health of the intestinal microbiome plays a key role in the pathogenesis of CD and UC. In particular, this is related to dysbiosis and reduced diversity of the gut microbiome. It also relates to protective bacteria subpopulations, such as Firmicutes, and an increased representation of potentially pathogenic bacteria, such as enteroinvasive Escherichia coli in subsets of ileal CD. In these conditions, species richness decreases, although some species seem to overgrow and increase in number. 

Both CD and UC are defined by an abnormal immune response, in which the immune system mistakes benign or beneficial cells and bacteria for harmful foreign substances. When this happens, the immune system, through a process known as molecular mimicry, can damage the gastrointestinal tract and produce symptoms of IBD.  UC is primarily a T-helper 2 (Th2) immune cell response, while CD is primarily T-helper 1 (Th1) cell mediated. 

Starting at birth, the cumulative effects of different environmental exposures, combined with a predetermined genetic susceptibility, is thought to cause IBD. It appears that continuous exposure to the collective effect of dynamic environmental factors, referred to as ‘exposome’ by Christopher Wild, affects the incidence of IBD.  Infancy and early childhood influence the formation of the immune system, whereas adult exposures to environmental factors alter established pathways.

Western lifestyles also seem to play a role, indicated by higher number of cases of IBD in Europe and the USA. The condition affects 1.5 million US citizens and 2.2 million people in Europe. There has been a significant increase in the last five years that’s consistent across several distinct ethnic groups and geographic locations. This increase parallels the Westernization or industrialization of an area’s lifestyle

Immigrants moving from low risk to high risk areas tend to assume the qualities of the high-risk areas within a generation or two. In their new location, the risks are much higher than in their low-risk country of origin. There has also been an increase in the number of cases in developing countries in Asia, Eastern Europe, and Northern Africa, as their lifestyles and living environments change. Onset of IBD in young adulthood is characterized by a relapsing and remitting course with frequent hospitalizations or surgery.

  1. Is irritable bowel syndrome a type of IBD?

Irritable Bowel Syndrome (IBS) is considered non-inflammatory and a syndrome, or a group of symptoms, rather than a specific disease. Symptoms of IBS typically include chronic abdominal pain, diarrhea, constipation, or alternating bouts of both of these. People with IBS are also more likely to have other functional disorders such as fibromyalgia and chronic fatigue syndrome (CFS). IBS doesn’t produce the destructive inflammation found in IBD, so it may be considered a less serious condition. However, it can still cause chronic discomfort and affect quality of life. Research suggests that IBS can be caused by stress and the manner in which the brain and gut interact.

Risk factors of IBD


Well known risk factors for IBD include:

  1. Cigarette smoking: reduced risk of UC, increased risk of CD
  2. Appendectomy: reduced risk 
  3. Western diet: increased risk
  4. Stress: increased risk 
  5. Depression: increased risk 
  6. Low vitamin D levels: increased risk
  7. Estrogen replacement therapy: increased risk of UC
  8. Left-handedness: increased risk
  9. Mycobacterium paratuberculosis infection: increased risk of CD

Breast-feeding, appendectomy, and smoking, surprisingly, are all associated with reduced risk of UC. 

The effects of some of the risk factors outlined above appear to differ between CD and UC. Despite shared genetic and immunologic mechanisms, distinct pathways of pathogenesis exist.

There’s a substantial body of research that’s available regarding risk factors, but limited evidence for the treatment of these environmental triggers to modify disease outcomes or prevent relapse. There have only been a few controlled clinical trials for modification of risk factors resulting in an improvement in patient outcomes.

Risk loci, or specific gene locations within your chromosomes that appear to alter IBD risk, highlight several key pathways in pathogenesis. These include the following:

  • Innate immunity
  • Adaptive immune responses
  • Abnormal glycosaminoglycan (GAG) content of the mucosa
  • Maintenance of intestinal barrier function with increased intestinal permeability
  • Pathogen sensing 
  • Endoplasmic reticulum stress
  • Response to oxidative stress
  • Decreased oxidation of short chain fatty acids  
  • Increased inflammatory mediators 
  • Increased sulfide production
  • Decreased methylation
  1. Genetics

Everyone is born with a certain genetic susceptibility to IBD. Following exposure to a Western lifestyle, diet, and certain environmental triggers, a specific threshold is reached and IBD may develop. This explains the low concordance rate in twins, suggesting that genetic influence, while important, is only one piece of the IBD puzzle. The exposome, or the total coherent effect of all environmental factors from birth to death, plays the determining role.  

A positive family history of IBD is the most important risk factor for the development of the condition. Whole genome scans have found susceptibility genes for UC on chromosomes 1 and 4. A concordance rate of 19 percent for UC and 50 percent for CD in monozygotic twins has also been established. 

Genetics have shown 204 distinct genetic risk loci for IBD, with the majority of risk alleles being shared between both diseases. However, 37 CD-specific and 27 UC-specific loci have been identified. Known loci account for only a third of the risk for either disease. 

  1. Childhood exposures

Breast-feeding appears to confer a protective effect on both UC (1.8-fold) and CD (2.2-fold), in keeping with known protective effects for other immune-mediated diseases such as eczema and asthma, allergic rhinitis, and type 1 diabetes. This is thought to be due to protective maternal antibodies and the induction of immune tolerance to specific food antigens and gut microbes.

Antibiotic exposure is associated with an increased risk of adult and pediatric-onset IBD. Exposure during infancy or early childhood is associated with the greatest increase in risk. Use of antibiotics between the ages of five and sixteen, through the effect on the microbiome, appears to increase the incidence 1.6-fold. If antibiotics are used in the first year of life, the risk of CD increases 5.3-fold. 

The strongest risk increase is linked to the use of broad-spectrum penicillin (3.1-fold), pen V (2.9-fold), then cephalosporin (1.9-fold).

It’s been hypothesized that by altering the gut microbiome composition, pathogenic bacteria colonize while the normal process of tolerance, which is crucial for immune development, is disrupted. This leads to an aberrant response of the host immune system to its microflora.

On the other hand, early childhood Helicobacter pylori infection is associated with a decreased risk of CD of 1.7-fold and UC of 1.3-fold. H. pylori increases Fox-3, the transcription factor of T-regulatory cells, which down-regulates the inflammatory response. 

  1. Hygiene

A high hygiene level increases the risk of IBD. Living in an urban environment increases risk by 1.2-fold.

Having a smaller number of siblings increases risk 2.6-fold. The more siblings you have, the lower your risk for IBD.

Sharing a bedroom decreases risk of UC by 2.1-fold and CD by 2.3-fold, while a hot water tap in the home increases the risk of CD by 5-fold.

Animal contact decreases risk of UC and CD, with similar effects seen regarding asthma and eczema.

The implication is that the more hygiene measures employed, the fewer helminths (worms and parasites) you’re exposed to, and therefore less induction of dendritic cells maturation and ability to drive the T-cell immune system occurs. This results in decreased protection against autoimmunity. 

In simpler terms, “germophobes” may be at an increased risk of developing IBD.

  1. Autism

There have been several reports of a link between autism spectrum disorder (ASD) and chronic gastrointestinal (GI) symptoms. Endoscopy trials have demonstrated a higher prevalence of nonspecific colitis, lymphoid hyperplasia, and focally enhanced gastritis in people with ASD compared with controls. Postulated mechanisms include aberrant immune responses to some dietary proteins, abnormal intestinal permeability, and unfavourable gut microflora. 

Wakefield et al conducted one of the earliest studies investigating gastrointestinal anomalies in autistic children in 1998. In this study, twelve children with regressive developmental disorders, nine of whom were autistic, were all reported to have abnormal colonoscopies. The most consistent finding was lymphoid nodular hyperplasia (LNH), which was present in nine of the twelve children. This mild to moderate colitis was deemed nonspecific on the basis of not fulfilling criteria for either Crohn’s disease or ulcerative colitis.

Criticism regarding the ‘normalcy’ of LNH in children prompted Wakefield, et al. to perform ileocolonoscopies in 60 children with regressive developmental disorders and compare them with 37 developmentally normal controls. In this trial, ileal LNH was present in 93 percent of affected children in comparison to 14.3 percent of controls (P<0.001). Chronic colitis was detected in 88% of affected children compared with 4.5% of controls. 

Torrente et al. compared the gastric biopsies of 25 autistic children with those of ten normal controls, ten CD patients, and ten children with H. pylori infection. Eleven of the 25 autistic children had a focally enhanced gastritis, while two had mild diffuse gastritis. Immunohistochemistry results demonstrated the pattern of lymphocyte infiltration was most similar to Crohn’s disease, with the exception of a striking predominance of CD8-positive over CD4-positive cells and a marked increase in intra-epithelial lymphocytes. Another highly specific finding among autistic children was a dense, sub-epithelial basement membrane immunoglobulin G deposition, which was absent in the other subgroups.

ASD patients and their caregivers often report improvement in the patient’s condition after following elimination diets. Improvements occur not only in the GI symptoms, but also in behavioural and cognitive problems such as hyperactivity, communication skills, and attentiveness. Interestingly, 36% of children with ASD have a history of cow’s milk and/or soy protein intolerance in infancy. In addition, while studies haven’t indicated an increased incidence of Celiac disease in these individuals, parents have often reported an improvement in their child’s behavioural disturbances when following a gluten-free diet. These benefits haven’t been seen consistently in randomized trials, although a Cochrane review did report a significant reduction in autistic traits on a gluten-free, casein-free diet.

One hypothesis is that ASD may be accompanied by aberrant innate immune responses to dietary proteins, leading to GI inflammation and aggravation of behavioural problems. One study, measuring pro-inflammatory cytokines in response to common dietary proteins, showed a greater than two standard deviations (SD) excess in tumour necrosis factor-alpha and interferon-gamma production in response to gluten and cow’s milk protein among ASD children, when compared with controls. 

A subsequent study confirmed a higher prevalence of elevated tumour necrosis factor-alpha and interleukin-12 production with beta-lactoglobin and alpha-lactoglobin, but not casein, in autistic children and children with non-allergic food hypersensitivity, compared with normal controls. 

Another theory suggests that abnormal intestinal permeability in children with ASD causes them to absorb fragments of incompletely broken-down peptides such as gluten or casein, which cross the blood-brain barrier and act as endogenous opioids. 

The gut microflora has also been targeted as a potential player. There have been anecdotal reports of the onset of autism following broad-spectrum antibiotics, suggesting that disruption of the indigenous flora may lead to colonization by neurotoxin-producing bacteria. Autistic children have been shown to have higher counts and more species of Clostridia than controls matched by age or gender. A small prospective trial demonstrated a significant but transient improvement in autistic features following a course of vancomycin (antibiotic) therapy, with relapses presumed to occur because of persistent spores that proliferate upon discontinuing the medication.

  1. Yeast

The ratios of yeasts in the gut, such as Saccharomyces cerevisiae and Candida albicans, may be significantly altered by IBD. Normally, yeasts and fungi account for less than 0.1% of the total microbiota population. However, there is often a decreased population of S. cerevisiae and increased populations of C. albicans and other Candida yeasts in the guts of people with IBD.

Antibiotic use can result in fungal overgrowth, especially of the Candida yeasts, which may then compete with the bacteria in the gut for survival and growth. This fungal overgrowth can make the host more susceptible to mold illness, paving the way for an immune response that may invoke chronic inflammation, autoimmunity, or IBD.

It appears also that certain components of the cell walls of fungi can trigger immune responses, which may add to the overall exposomeXI.

  1. Gut microbiome

Recent studies have highlighted the association between the gut microbiome and the pathogenesis of IBD. 

Reduced biodiversity of the gut microbiome is apparent even at the onset of diagnosis, before treatment is initiated. CD, especially ileal CD, has been associated with increased frequency of pathogenic bacteria such as enteroinvasive E. coli. There can also be a reduction in the frequency of anti-inflammatory bacterial subgroups, particularly Faecalibacterium prausnitzii. Giving strains of this specific bacteria has resulted in improved outcomes and amelioration of colitis in animal models.

By the time someone reaches adulthood, the immune system has matured and lifestyle factors become more apparent as choices are increased. Adult exposures seem to be involved in changing the already developed immune system. Several environmental factors have been identified as playing a role in IBD development independent of stage of life, previous development of acute bacterial gastroenteritis, geographical location, and vitamin D. 

Bacterial gastroenteritis as a result of Clostridium difficile, Campylobacter, and/or Salmonella infections can increase risk of IBD. The risk of developing IBD increases significantly after bacterial gastroenteritis, especially within the first year. The largest effect is seen with CD, for which there is a 2.9-fold increase, rather than the 2.1-fold for UC. This may be explained by the increase in interleukin-6 (IL6), blockage of T-reg cells, and the activation of self-reactive T-cells, leading to a chronic inflammatory response.

  1. Mycobacterium avium infection

M. avium subspecies paratuberculosis (MAP) infection rates are higher in CD, although a causative link hasn’t been established. Meta-analysis has shown a 7-fold increase in CD in MAP infections, but the timing of this infection couldn’t be ascertained to be a cause of CD and is perhaps merely a bystander. 

  1. Tap water

Drinking tap water lowers the risk of CD 2-fold. It’s been proposed that this might be due to harmless microorganisms triggering regulatory T-cells.  

  1. Flying

Individuals have an increased risk of disease flare following high-altitude flights or after travelling more than 2,000 metres above sea level. Mild hypoxia leads to an increase in IL6 and C-reactive protein (CRP), which are markers of inflammation.

  1. Obesity

An American cohort study showed a 2.5-fold increase in CD in obese women with a body mass index (BMI) greater than 30 kg/m2. 

  1. Smoking 

Smoking confers a 2-fold increase in risk of CD, which is somewhat lessened when stopping smoking, although the pathogenic mechanism remains unknown. 

Smoking is associated with a more aggressive form of CD, more surgery, and an earlier risk of recurrence and re-operation following a bowel resection. Stopping smoking prior to the diagnosis can result in a reduced likelihood of progressing to complicated disease behaviour or the need for surgery. Smoking cessation is also associated with a reduced rate of relapse regarding CD.

With UC, current but not former smokers appear to have some protection, with half the risk of UC in current smokers compared to individuals that have never smoked. Smoking confers a 1.7-fold reduction in risk for UC. 

For former smokers, the risk for both UC and for CD increases by the same amount.

For patients with UC, smoking leads to a more benign disease course with fewer flares, a reduced need for steroids, and lower colectomy rates. Smoking cessation increases the risk, with the effect lasting for up to ten years after quitting smoking. This suggests that smoking only defers the development of UC. Quitting smoking is also associated with flare-ups.

Passive, or second-hand, smoking has a weaker beneficial effect. The mechanism of this different effect between CD and UC is unknown, but is thought to be influenced by the constituents of cigarette smoke having different effects on oxidative stress in mononuclear cells.

Smoking is known to affect the immune system through both cellular and humeral pathways by transforming the synthesis of pro-inflammatory cytokines, altering gut permeability, reducing smooth muscle tone and contractility due to nitrous oxide, and effecting changes in the gut microflora. 

There’s also an interaction between smoking and genetic variants in the CYP2A6/EGLN 2 locus and glutathione transferase enzymes (GSTP1) and risk of CD and UC. Snips in these genes showed significantly different outcomes. 

  1. Appendectomy

There are divergent effects between UC and CD following appendectomy.

When performed before the age of twenty, there’s an increased risk of UC with no effect or only a slightly increased risk of CD. The mechanisms remain unclear, and appendectomy may result in intestinal microbiome alteration with a protective effect on UC. The microbiome composition in the appendix also appears to confer protective effects against UC

  1. Diet 

The role of diet has been problematic to determine. This is due to difficulty in tracking it through the course of a lifetime, different recall between controls and cases, and potential restrictions on diet choices pre-diagnosis based on the nature of the disease. 

Increased fibre of approximately 24 grams was associated with a significant reduction in risk of CD but not UC.   This was related to fruit fibre and not that of vegetables, including cruciferous ones. No association was found between fibre from cereals, whole grains, or legumes. 

Fibre may confer epithelial integrity and reduce translocation of potentially pathogenic bacteria such as enterovirus E. Coli, which may play a role in CD. Fibre activates the aryl hydrocarbon receptor (AhR) expressed in intestinal lymphocytes, which offers protection against environmental antigens.  

A diet high in long-chain n-3 polyunsaturated fatty acids (PUFA) was associated with a reduced risk of UC. CD had no modifiable fat intake risk factors for CD. One large study found omega-3 supplements had no beneficial effects, while a high intake of animal protein revealed a potential association with IBD. Sugar and a high-carbohydrate diet are associated with an increased risk of IBD, while fruits and vegetables seem to have a protective effect.

Alteration of diet can trigger flares in many different types of disease. High fat diets result in expansion of specific bacterial subpopulations that are associated with a pro-inflammatory response, particularly diets high in meats, as well as polyunsaturated omega-6 fats (like those found in industrial seed oils such as soybean oil, corn oil, and canola oil).XVI Elemental diets show improved outcomes in CD, whereas partial and complete enteral nutrition show effects superior to placebo but lower than steroids. 

Elimination diets, such as the specific carbohydrate diet, lectin-free diet, autoimmune paleo, and Whole30, are of particular interest as well, but there is still a lack of strong evidence regarding their efficacy for IBD treatment.

Childhood diet and antibiotic exposure is an important determinant of microbiome composition. Breastfeeding appears to reduce UC risk, but it doesn’t appear that formula-feeding necessarily increases UC risk. Researchers have found that the gut microbiome of both breastfed and formula-fed children changes significantly after the introduction of foods. Therefore, the first foods a child receives (other than breastmilk or formula), and the foods they eat throughout their early childhood, may profoundly affect their gut microbiota composition and affect their IBD risk level.

  1. Glyphosate

Glyphosate is the world’s most widely produced herbicide. It’s the primary toxic chemical in Roundup™ and many other herbicides. As a broad-spectrum herbicide, glyphosate is present in more than 700 different products and used in industries such as agriculture and forestry, and even in the home. 

Glyphosate was introduced in the 1970s to kill weeds by targeting the enzymes that produce the amino acids tyrosine, tryptophan, and phenylalanine. However, the enzymes of many bacteria are susceptible to inhibition by this chemical, so it can also alter the gut flora of many animals. 

Usage of glyphosate significantly increased after the introduction of genetically modified (GMO), glyphosate-resistant crops that grow well despite the presence of this chemical in the soil. In addition, the toxicity of the surfactant polyoxyethyleneamine (POEA), which is commonly mixed with glyphosate, is greater than the toxicity of glyphosate alone. 

In addition, Enlist Duo™, a herbicide product containing a 2,4-dichlorophenoxyacetic acid (2,4-D) salt and glyphosate, was approved for use in Canada and the United States in 2014. This was for use on GMO soybeans and maize, both of which were designed to be resistant to both 2,4-D and glyphosate. 2,4-D has many toxic effects of its own. 

Research has shown that glyphosate disrupts the microbiome in the intestine, causing a decrease in the ratio of beneficial to harmful bacteria. Highly pathogenic bacteria such as Salmonella entritidis, Salmonella gallinarum, Salmonella typhimurium, Clostridium perfringens, and Clostridium botulinum are highly resistant to glyphosate. Unfortunately, however, most beneficial bacteria such as Enterococcus faecalis, Enterococcus faecium, Bacillus badius, Bifidobacterium adolescentis, and Lactobacillus ssp. were found to be moderately to highly susceptible. 

The relationship between the microbiome of the intestine and overall human health is still unclear.

 However, current research indicates that disruption of the microbiome could lead to conditions such as metabolic disorder, diabetes, depression, autism, cardiovascular disease, and autoimmune diseases such as IBD. 

  1. Celiac disease, IBD, and the glyphosate connection

Researchers have found that people with Celiac disease are about 10 times as likely as a control group to have IBD. Conversely, the prevalence of Celiac disease in IBD appears to be comparable with that indicated in controls.

Celiac disease, and more generally, gluten intolerance, is a growing problem worldwide. It’s particularly serious in North America and Europe, where an estimated 5% of the population now suffers from this condition. It’s a multi-factorial disease associated with numerous nutritional deficiencies, as well as reproductive issues and an increased risk of thyroid disease, kidney failure, and cancer. 

It has been proposed by researchers Samsel and Seneff that glyphosate is the most important causal factor in this epidemic. Fish exposed to glyphosate develop digestive problems that are reminiscent of Celiac disease. The condition is associated with imbalances in gut bacteria that can be fully explained by the known effects of glyphosate on these particular types of bacteria. 

Characteristics of celiac disease point to impairment in many cytochrome P450 (CYP450) enzymes, which are involved with detoxifying environmental toxins, activating vitamin D3, catabolizing vitamin A, and maintaining bile acid production and sulfate supplies to the gut. Glyphosate is known to inhibit CYP450 enzymes. 

Deficiencies in iron, cobalt, molybdenum, copper, and other rare metals associated with Celiac disease can also be attributed to glyphosate’s strong ability to chelate these elements. Deficiencies in tryptophan, tyrosine, methionine, and selenomethionine associated with Celiac disease also match glyphosate’s known depletion of these amino acids. 

Celiac disease patients have an increased risk of developing non-Hodgkin’s lymphoma, which has also been implicated in glyphosate exposure. Reproductive issues associated with Celiac disease, such as infertility, miscarriages, and birth defects, can similarly be linked to glyphosate. 

Glyphosate residues in wheat and other crops have been increasing recently due to the growing practice of crop desiccation just prior to the harvest. The practice of ‘ripening’ sugar cane with glyphosate may also explain the recent surge in cases of kidney failure among agricultural workers in Central America. 

  1. Mast Cell Activation Syndrome (MCAS)

As early as 1980, Dvorak and colleagues reported that mast cells were markedly increased in the ileum of patients with CD. In 1990, Nolte et al. showed the same findings in patients with UC. There were increased numbers of mast cells with associated degranulation products of histamine and tryptase, along with associated increases in cytokines and leukotrienes IL-16. TNF-alpha and substance P have also been found in the mucosa of patients with IBD, particularly when stained with the CD 117 stain. 

According to the latest literature research conducted by Dr. Lawrence Afrin, one of the key researchers in MCAS, mast cells release at least 1,000 mediators of inflammation. This includes, but isn’t limited, to histamine, proteoglycans (heparin and chondroitin sulfate), proteases (tryptase, chymase and carboxypeptidase), eicosanoids, and platelet activating factor (PAF).

Activation of mast cells leads to the release of the eicosanoid arachidonic acid from the phospholipids on the cell membrane. This 20-carbon fatty acid is then rapidly oxidised, along either the cyclooxygenase pathway to form prostaglandin D2 (PGD2) or the lipoxygenase pathway to form leukotriene C4 (LTC4). Histamine triggers the histamine H1 receptor and tryptase, the protease-activated receptor 2 (PAR2).

Therapies aimed at down-regulation of mast cell activity may be important in the treatment of IBD. 

Mast cell cytokines constitute a third category in that they may be both preformed and newly synthesized. These include IL-4, IL-5, IL-6 and TNF-alpha in the nasal mucosa and bronchi, as well as IL-1B, IL-3, IL-8, IL-9, IL-10, IL-13, IL-16, IL-18, IL-25, granulocyte -macrophage colony stimulating factor (GM-CSF), and stem cell factor macrophage chemotactic peptide (MCP)-1, MCP-3, and MCP-4. 

Many factors are known to activate mast cells, and their activation is a crucial step involving pathophysiological changes. These factors include antigens, anti-IgE, substance P, VIP, C5a, C3a, somatostatin, morphine, very low-density lipoprotein, stem cell factor, tryptase, and eosinophil cationic protein, all of which are known to activate mast cells. 

It should be noted that mechanisms of mast cell activation differ with different classes of triggers.

  1. Nutrient deficiencies 

UC patients were found to have lower levels of vitamin A, vitamin E, and carotenoids than those in  controls. This implies that certain nutrient deficiencies may either play a role in the development of UC, or, conversely, are a complication of UC. 

  1. Vitamin D

Vitamin D intake is inversely associated with UC risk, meaning that higher vitamin D intake is linked to a lower UC risk.  Additionally, higher blood levels of vitamin D are associated with reduced risk of CD.

 Patients who increased their blood vitamin D levels had a 1.9-fold protective effect for CD, but not for UC. They also had a lower risk of surgery compared to those who remained vitamin D deficient. Low vitamin D levels are also associated with a higher rate of colon cancer and C. difficile infections.

Vitamin D administration may reduce the risk of IBD relapses. Vitamin D is also known to play a role in the regulation of the innate immune system by activating the TH1 lymphocytes and monocytes. This causes the inflammatory response to be down-regulated. 

  1. Weather and latitude

Incidence of IBD is higher in northern latitudes where people have reduced exposure to ultraviolet (UV) light. The Women’s Health Initiative (WHI) study noted a lower risk for both UC and CD in women in southern latitudes (1.6-fold for UC) compared to those at higher latitudes. Living in southern latitudes appears to be protective, likely due to increased UV light and subsequently higher vitamin D levels.

Warm summers have a protective effect for UC and possibly for CD as well. This is also the case for other inflammatory diseases such as multiple sclerosis (MS), rheumatoid arthritis (RA), and systemic lupus erythematosus (SLE). This is thought to be due to an increase in microbial diversity, which in turn confers benefit.

  1. Psychological behaviours

IBD has long been associated with neuroticism, dependency, anxiety, and perfectionism. Recent well-designed studies have confirmed that adverse life events, chronic stress, and depression increase the likelihood of relapse in patients with quiescent (dormant) IBD.

The evolving science of psychoneuroimmunology has outlined the mechanisms by which the nervous system can affect immune function at both the systemic and gut mucosal levels. These mechanisms are thought to be due to changes in the hypothalamic-pituitary-adrenal (HPA) axis and alterations in the bacterial mucosal barrier. These occur via mucosal mast cells and mediators, such as corticotrophin releasing factor (CRF). 

To maintain homeostasis, a living organism must constantly adapt at a mental, emotional, molecular, cellular, physiological, and environmental level. Stress is defined as a threat to an organism’s homeostasis. The function of the stress response is to maintain homeostasis through behavioural and biological or physiological adaptations. The stress response involves the complex integration between a series of interconnected regions within the brain. These are the hypothalamus, the amygdala, and the hippocampus. This hub receives inputs from viscera and somatic afferents and from higher cortical structures, including the internal dialogue and mental perceptions of the patient. This in turn, affects the neuroendocrine stress response via two interconnected effector pathways, namely the HPA axis and the autonomic nervous system (ANS).  

Stress stimulates the release of CRF from the hypothalamus, causing the release of adrenocorticotrophic hormone (ACTH) from the anterior pituitary. This in turn causes the release of cortisol from the adrenal cortex. Stress also activates the descending neural pathways from the hypothalamus to pontomedullary nuclei, which control the autonomic nervous system response. Stimulation of the sympathetic nervous system (fight/flight) causes the release of adrenaline and noradrenaline from the adrenal medulla. This is in addition to supplying the entire gut directly. The parasympathetic vagus nerve and sacral nerves provide parasympathetic input to the upper gut and to the distal colon and rectum. 

The gut has its own nervous supply called the enteric nervous system (ENS), which is innervated by both sympathetic and parasympathetic fibres. This network has been termed the gut-brain axis. The ENS contains 100 million neurons and regulates the motility, the exocrine and endocrine functions, and the microcirculation of the gut. These axes (HPA, ANS, ENS) can then interact directly with the immune system. Psychoneuroimmunology is the study of how behavioural factors and CNS function can influence the immune system, and hence inflammation, at both systemic and local tissue levels.

Nerve fibres of the ANS form close effector junctions with lymphocytes and macrophages in lymph glands, bone marrow, the thymus, the spleen, and mucosa associated lymph tissue. These nerve fibres also release a number of chemicals called neurotransmitters, such as catecholamines, vasoactive intestinal peptides, angiotensin II, neurotensin, somatostatin, and substance P. These are capable of affecting lymphocytes, macrophages, neutrophils, and other inflammatory cells at the neuro-immune cell junction. Lymphocytes and other inflammatory cells also carry receptors for the hormones and neuropeptides of the HPA axis, such as growth hormone, ACTH, corticosteroids, and CRF. 

At high concentrations, cortisol has an immunosuppressive effect, increasing the release of anti-inflammatory proteins and IL-10. Transcription of inflammatory signalling molecules such as IL-6, IL-1, and TNF-α are reduced through transcription factors AP-1 and nuclear factor kappa beta. At lower doses, cortisol has an immune stimulating effect.

Similarly, adrenaline and noradrenaline have mixed effects at different doses on immunity and inflammation. Adrenaline causes an increase in serum IL-6, an increase in lipopolysaccharide (LPS) induced IL-8 and IL-10, and an increase in cytotoxic (cell-killing) T-cells and natural killer (NK) cells.

Chronic sustained stress due to adverse life events, such as bereavement, divorce, and depression, have been shown to reduce the numbers of cluster of differentiation 8 (CD8, a glycoprotein) lymphocytes, NK cells, and macrophages in the blood. However, in addition to immunosuppression, chronic stress with reduced heart rate variability, which is a sign of increased sympathetic tone, has been shown to increase inflammation, showing raised CRP.  

Acute stress causes stimulation of the sympathetic nervous system with a rise in adrenaline and noradrenaline, followed a little later by a rise in cortisol. This leads to an acute episode of immune enhancement with an increase in inflammatory cytokines that are known to be associated with flares of IBD. This includes a rise in cytotoxic CD8 T lymphocytes and NK cells and an increase in their cytolytic activity, in addition to platelet activation and thrombin generation, producing effects of microcirculation ischemia causing thrombosis and microinfarction. This effect is lowered with beta blockers rather than aspirin, suggesting that a stress response or sympathetic activation is at the root of it. 

Psycho-social stressors have long been associated with triggers. Recent and remote stress is associated with an increased incidence of IBD, with recent stress being more significant. When questioned, patients indicated that stress was the trigger for 70% of their flares. Depression feelings were associated with a 2.4-fold increased risk of CD, but not UC. Depression, anxiety, and stress are also associated with increased rates of relapse and surgery for IBD.

The inflammatory response to stress through elevation of IL-6 levels can be changed in mice by administrating antibiotics, suggesting antibiotics exerts their effects through changes in the gut microbiota.

Using medications to treat these conditions appears to have variable effects. People referred for therapy following increased stress due to the diagnosis have reduced rates of relapse, outpatient attendance, and use of steroids or other medications for IBD. 

In summary, stress can play a significant role in immune system dysfunction leading to an inflammatory response, which may trigger new-onset IBD or a flare of existing disease.

  1. Sleep

Both increased and reduced amounts of sleep have been associated with negative health outcomes. Reduced sleep quality was associated with an increased risk of relapse at six months post-remission in CD, supporting an association between poor sleep and gut inflammation. Sleep disturbances in IBD may lead to a 2-fold increase of disease flare. Sleep deprivation also leads to activation of the immune cascade.

  1. Nonsteroidal anti-inflammatory drugs

The use of nonsteroidal anti-inflammatory drugs (NSAIDS) for fifteen days per month increases the risk of UC 1.9-fold and CD 1.6-fold. These figures are increased by greater weekly dosage, and a higher frequency or longer duration of use. NSAIDS lead to inhibition of cyclooxygenase (COX), resulting in a decrease in protective prostaglandins in the gut mucosa, increasing gut permeability. 

  1. Oral contraceptives

Current use of oral contraceptives (OCP) leads to 1.3-fold increased risk of UC. The risk of developing CD with current use of OCP is increased by 1.5-fold. 

  1. Post -menopausal HRT

Post menopausal HRT increases the risk of UC by 1.7-fold, but not CD. It’s been proposed that estrogen modulates gut inflammation by acting on estrogen receptors that are found on gastrointestinal epithelial and immune cells. 

UC is a Th2 mediated illness, and estrogen promotes Th2 cytokines. The same holds true for other Th2 mediated diseases, such as RA and SLE. However, this is not the case with CD, which is a Th1 mediated illness. 

A prospective cohort study (the Women’s Health Study) followed 108,844 postmenopausal American women, with a median age of 54, without a prior history of CD or UC in 1976. The risk of UC appeared to increase with longer duration of hormone use and decrease depending on the time since discontinuation. There was no difference in risk according to the type of hormone therapy used, such as estrogen as opposed to estrogen and progestin. No association was noted between the current use of hormones and the risk of CD. The effect of hormones on the risk of UC and CD was also not modified by age, BMI, or smoking.

  1. Ambient air pollution

On the whole, air pollution exposure wasn’t associated with the incidence of IBD. However, residential exposure to sulfur dioxide and nitrous dioxide gases found in industrialized regions may increase the risk of early-onset UC and CD respectively. 

Living in regions with high sulfur dioxide emissions before the age of 25 increases the chances of UC 2-fold. A high nitrogen dioxide exposure before the age of 23 increases the chance of CD 2.3-fold. Total pollutant emissions correlate significantly with an increased risk of hospitalization in established IBD. Pollutants may also be absorbed and incite the inflammatory process that’s characteristic of IBD.

  1. Physical activity

Researchers have found that women engaging in active physical activity have a 44% reduction in CD risk compared with sedentary women. Physical activity was not associated with risk of UC.

The absolute risk of UC and CD among women in the highest fifth of physical activity levels was at just 8 and 6 events per 100,000 person years. This compares to 11 and 16 events per 100,000 person years among women in the lowest fifth of physical activity. 

Age, smoking, BMI, and cohort didn’t significantly modify the association between physical activity and the risk of UC or CD in these findings. The pathway appears to be mediated through the autophagy (clearing out or recycling of damaged cells) pathway or cell senescence (cell aging).

Summary

There’s a rich body of research showing potential environmental risk factors for the development of IBD. However, there aren’t many high-quality studies showing that environmental changes may have a large effect on disease outcomes. For a large number of possible environmental factors, meta-analyses are not yet available.

Many novel factors are identified by large cohort or case-control studies, but are yet to be reproduced by and validated by independent research groups. Consequently, the level of evidence is somewhat low and caution should be exercised when drawing firm conclusions or making recommendations.

However, individuals with a genetic susceptibility can be cognisant of environmental factors and do their best to lower or delay their genetic expression, as their exposure threshold may not be reached. Being aware of which environmental factors are involved in developmental phases as well as along the course of the disease to increase flares and development of complications, gives the treating physician and patient as advocate the opportunity to make the necessary adjustments along the patient’s timeline.

 This has the effect of lowering the risk of disease expression with a more personalized treatment plan.

In Part 2, I will be reviewing the lab tests that are used to diagnose CD and UC, along with lifestyle changes and treatment options that are often successfully employed in IBD care.

In the meantime, I encourage you to contact my office if you are seeking functional and integrative care for your IBD. 

Podcast: Looking at Lyme: Understanding Symptoms and Treating the Whole Person

Looking at Lyme

I was recently interviewed by Sarah Cormode for an episode of Looking at Lyme, an educational podcast created by the Canadian Lyme Disease Foundation, where I highlight the importance of taking an in-depth patient history to understand and document Lyme disease symptoms.

I also discuss several approaches to treating Lyme disease and explain why such a variety of symptoms amongst patients with Lyme disease exists.

Take a listen below.

I was recently interviewed by Sarah Cormode for an episode of Looking at Lyme, an educational podcast created by the Canadian Lyme Disease Foundation, where I highlight the importance of taking an in-depth patient history to understand and document symptoms.

I also discuss several approaches to treating Lyme disease and explain why such a variety of symptoms amongst patients with Lyme disease exists.

People with Lyme disease have a lot of different symptoms, the bacteria attacks the body in so many different ways. Sometimes it attacks the brain, the heart, the joints, you name it. Today I'm looking at Lyme, we're going to dive into functional medicine, we'll look at the body from a holistic perspective and meet a doctor who treats the whole body and the mind.

Getting treated early for acute Lyme disease is critical. Some people find the attach ticks and others might get a bull's eye rash. But that's not always the case. And without these telltale signs, people might not get diagnosed. The longer that you have the disease, the worse it gets, and the harder it is to treat. That's when we need to go to the doctor. So, let's do that. There are very few medical doctors with the expertise of Dr. Bruce Hoffman. He practices functional medicine, and we'll get him to tell us more about that. We reached him at his Calgary clinic. Good morning, Dr. Hoffman.

Good morning to you.

What's the first thing that you look for in a patient who potentially has Lyme disease?

Your patients present to a doctor's office with many symptoms and many complex, interlocking possible what we call in medicine, differential diagnosis. So, they present with a whole host of symptoms. And it's the task of the doctor taking the history to try and work out what may or may not be Lyme disease. And sometimes patients come in with some Lyme test and say they definitively have Lyme disease, or they have positive biomarkers for Lyme disease on some of the tests they've done. But when a closer history is taken, that may not be the case. So, there's quite a lot to really sift through when you're trying to differentiate whether somebody has Lyme disease or not. The most important thing is the symptomatology. You want to take a very definitive history. In my clinic, we use different types of questionnaires to try and determine whether or not Lyme may be a diagnosis. And we also then start to take a very specific history about whether they visited endemic areas, which is somewhat a moot point because Lyme disease is somewhat, you know, it's specific, it's everywhere. If they visit an endemic area, if they've been bitten by a tick, if they've had the rash, which is very uncommon, by the way. But we start to ask the history of exposure, history of tick bite, history of rashes and in a symptom history, looking over the variable symptoms that present with Lyme disease and/or co-infections that come along with Lyme disease. A lot of questions need to be asked, and you've got to sift through them and try and determine if Lyme disease is the primary presenting feature or are there any other coexisting disorders that interlock, like mold exposure, or heavy metal toxicity or food sensitivities? And there's many of them that may interlock with a symptom presentation. So, there's a lot to ask.

Yeah, it sounds like getting that patient history is just so critical. 

History is everything. You know, you've got to take a good history. You can’t have a patient walk in and say I've got Lyme disease, and I go, okay, let's treat you. No, no, you have to stop and really ask very specific questions.

And it also sounds like you mentioned that most of your patients don't ever remember having a tick attached or getting a rash.

You know, the majority don't. I do have a number of patients who went to college in northeast in the United States, and they were out in the fields and in the forests, have a history of tick bite and rash exposure. But I would say that's probably 5% of my population. My patient population, it's very low.

Guess when we spend time in the outdoors, if we check for ticks and do a tick check and actually found one attached, we have something to at least document or same with a rash. If you found one, it'd be a good idea to get a photo of that to share with your doctor.

Absolutely. It would be lovely if we had that cookie cutter you know, clear cut, walked in the woods, got a tick, notices for within three days a high fever, headache, and then the Lyme disease rash. That's so seldom.

It's never that that clear? Is it?

Never. I wish it was easier.

So how critical is it then for people to get diagnosed and treated early?

Oh, if they've been exposed and there's definitely a tick bite. And the symptomatology of high fever, sore neck, chills and joints. If that occurs, you get them on antibiotics while waiting for lab data or getting the tick, if it's discovered, sent off to the lab for analysis. Definitely, I’ll put them on treatment right away. And there's different standards of Lyme disease treatment, depending on which school of thought you belong to. Some schools of thought say, you just need like a brief dose of doxycycline. And others say at least four to six weeks of treatment. It depends on your approach.

Do you have a preference?

Longer term antibiotics, definitely not a short term

Yeah, that was certainly my experience, I had about 10 days of antibiotics, and then all of my symptoms came back afterwards.

Absolutely. If patients have an acute exposure, and they have symptomatology, we do have a baseline laboratory test. And then we repeat it four to eight weeks later to see if there's any rising titers. And we send the tick off for analysis. I usually cover them with antibiotics for at least six weeks. 

Wow. That's great to hear. And so, what is functional medicine?

Well, functional medicine is this emergent system of approaching a patient from a very different point of view. Like my medical training is what we, I don't mean to be derogatory, but it's called the N2D2 method of diagnosis and treatment; name the disease, name the drug. You know, that's how we learned in medical school, we just look at differential diagnoses, what disease or symptom cluster does this person have, and what drug can I pull out to help them. That's the specific training, highly relevant, nothing wrong with it. But now we have this emerging cohort of patients who have this chronic multi system, multi symptom disease profiles, with many interlocking issues. And that model doesn't work. And I tend to see and many people who are outside of the so-called traditional healthcare system tend to see that cohort of patients. Functional medicine attempts to take an upstream history back to what we call antecedents, mediators, and triggers. We go and look upstream to see, first of all, what's your symptom profile now? But, when did you start to feel unwell? One of the most relevant questions I ask a patient is; when did you last feel well, and then you want to take it from there, backwards and forwards. So functional medicine looks backwards as to the timeline, or the potential triggers and inherited factors which may play a role, the triggers what may have triggered the illness, and then what we call mediators, what may be keeping that symptom cluster alive. In conjunction with that we look at, not so much as pathology and disease laboratory tests, but we look at functional laboratory tests. How is the biochemistry and the metabolomics? How are they functioning? Are they optimized? Or are they deficient within a spectrum? Traditional Medicine has a reference range of, you know, negative or positive. Functional medicine optimizes function based on individual susceptibility and genetics. It's a very elegant form of practicing medicine within chemical principles. Just old school sort of, you know, when did you last feel well; what happened and what may have been playing a role. No longer looking at single factors, instead, looking at multiple causative factors as to what keeps this patient still symptomatic. And I can tell you, from my experience, that there is never one reason why a person is not feeling well. There's usually a whole myriad and host of issues from poor sleep, poor diet, early childhood trauma, dental issues, food and gut sensitivities. It is complex, long list of what made you unwell. 

Yeah, absolutely. Why do the symptoms vary so much from one patient to the other?

You mean with Lyme disease specifically?

Yes. with Lyme disease specifically?

Well, while it depends on a whole host of factors, it depends on the individual immune response of the person, the total toxic load, the infectious load, the expression of the Lyme disease spirochaete, with or without co infections, the metabolic and nutritional strength of the individual, the immune competencies, the presence of natural killer cell functions, whether they can suppress the immune response. The fact that Lyme disease goes from different forms; the cellular form to an intracellular form, to a cystic form to a biofilm form then it comes and goes depending on your immune surveillance. There's a lot of reasons why somebody has waxing and waning of symptoms and feels variations in their symptom profile.

Is it possible for someone to have Lyme but not have any symptoms?

You can have positive laboratory testing for Lyme and be asymptomatic. Absolutely, absolutely. But you don't see those people because they feel good.

Yeah, definitely. Do symptoms flare and go dormant normally for some of your patients?

They do. They wax and wane depending on stressors, diet, travel and multiple factors affect the expression of symptomatology. Treatment or no treatment. Some treatments exacerbate the symptomatology quite dramatically. They get what they call the Jarisch Herxheimer reaction (JHR) where you put in a treatment and the patient's symptoms just go through the roof. And so, there's all these variations as to why people wax and wane and get increased symptoms at times. But yeah, we certainly have people with, with no symptoms, who have positive laboratory tests as well.

Dr. Hoffman, are you seeing a larger increase in the number of patients that you suspect to have Lyme disease and other co infections?

Absolutely. Yeah. As you know that the Lyme disease diagnosis is highly controversial, depending on which school of thought you belong to. Whether you belong to the sort of infectious disease society, the infectious disease group of medicine, or whether you follow the ILADS criteria for the diagnosis and treatment. Those are these two different schools of thought. Now you know, even with that, there's been a tremendous uptake in the Lyme disease diagnosis and co-infections due to global warming. The migration of songbirds further north and the spread of ticks deeper into the north because of global warming. It's been estimated, one study showed that the songbird flight path from South America to North America brought up to 32 million tick species. In the yearly migration just northwards from South America. So, there's a there's a huge increase in the diagnosis. For sure.

Yeah, especially for anyone who's living along any kind of migratory bird path.

Absolutely. Yeah, absolutely. And there’s this great Canadian researcher, John Scott, showing us published papers on this issue.

Yes, hopefully, we'll get him on a future podcast as well. I'd love to hear more about his research

Absolutely. Yeah.

So I was fortunate to go to the ILADS conference last year in Boston, and I learned about mast cell activation. And I was just wondering if you could tell me a little bit about that disorder.

Well, Mast Cell Activation Syndrome (MCAS) is a relatively new diagnosis. It's been around for a while. Dr. Lawrence Afrin is one of the leaders in the diagnosis and treatment. He's just recently published, which I co-authored, a criteria for the diagnosis. And the reason why that has been important is because previously at medical school, we learned about systemic mastocytosis, which is an increase in the number of mast cells that create disease processes. But mast cell activation syndrome is an increase in activity without an increase in number. And there are different criteria for the diagnosis. Mast cell activation syndrome is a very, very important concept to keep in mind when seeing patients with chronic systemic illness because you'll see it a lot. I see it a lot. Mast cells or white cells act as vigilante cells to try and protect you from incoming stressors. Whatever they may be, whether it's mental, chemical, environmental, infections or food, they spew out at least 1000, not 200 as one's thought, but more than 1000 mediators of inflammation. One of them is histamines. Everybody knows the histamine is a sort of allergy hive reaction. There are many other mediators of inflammation. People with mast cell activation syndrome have this heightened inflammatory response to ongoing day to day environmental exposures and present with a multitude of symptoms in multiple organ systems. And they travel from doctor to doctor you know, they go to the allergist and the rheumatologist and to the neurologists, but nobody ties the systemic nature of this condition together. So, it's important again to take a thorough history and elicit whether somebody may be presenting with mast cell activation syndrome. Now, interestingly, mold exposures and Lyme disease trigger mast cell activation syndrome. So you often get a cross mapping of symptomatology.

Well, what would be your best advice for someone who suspects that they might have Lyme disease?

Well, it's a very tricky one. Because here's my experience. People often want to believe in a one diagnosis - one treatment approach when they present with complex illness. And it's really doesn't do them any favors to adopt that attitude. Yes, you may have a classic exposure and symptom profile, no question about that. But when you've got chronic illness, and chronic multi system, multi symptom exposures, and you go into a Lyme test with a naturopath or an MD, they send it to the states or even they send it to the Canadian Winnipeg group. And you come back with a positive test, it doesn't mean that the reason for your symptom profile is Lyme. Lyme may be the trigger, but you may have a whole host of underlying issues that are playing a role in your symptom profile. And one of the great tragedies that I see in my practice is people who come to see me, they've got a positive Lyme test and they've been treated for Lyme. But it's really not the key diagnosis, there are 70 other underlying factors that are far more relevant than that positive laboratory test. So, in response to your question is just be extremely discriminatory, when you jump to the diagnosis of Lyme disease as causing your symptoms, it may not be that. It may be there, you may have a positive test. But it doesn't mean that Lyme disease is at the root of it. It may be that it is. But you can't just take a positive test and treat it as if that's it. And I see that 90-95% of the time. They just go get treated for Lyme, but it's not really Lyme that's causing a symptom profile. Sometimes it is, of course it is, but you've got to discriminate.

So it's that combination of diagnostic testing and patient history,

History, history, history. If you're not taking a two-hour history with your patient, a timeline from conception to present, plus even intergenerational issues because we know that you inherit epigenetically family trauma. It is very well studied and well researched. Now, if you're not taking a thorough history, and following the timeline and symptom presentation of that patient, at least a two-hour history, you can't really discriminate on a history basis, whether this patient is suffering from one illness or 15 possible comorbid conditions. You have to take that history, then you back it up with laboratory data. The more laboratory data, the better, which unfortunately and again, with our healthcare system, that sort of privilege and that sort of luxury of a two-hour interview with extensive lab data. It doesn't exist. You have to go outside the healthcare system to get that service, you know, which is a tragedy, but it's the truth.

I couldn't agree more. Thank you so much for your time, Dr. Hoffman.

Thank you so much.

My key takeaway from that conversation was just how important it is that a doctor gets a full patient history. I know that in my case, I had a lot of symptoms and it was really confusing to understand what was going on in my body. That wraps up another podcast. Thank you so much for listening. Stay safe in the outdoors.

Diagnosis of Mast Cell Activation Syndrome – A Global Consensus 2

Diagnosis of Mast Cell Activation Syndrome - A Global Consensus

Please take a look at this newly published peer-reviewed article by Dr. Lawrence Afrin of which I was a co-author, on the revised criteria for the diagnosis of mast cell activation syndrome (MCAS):

Diagnosis of mast cell activation syndrome: a global “consensus-2”

One of the most common difficulties patients seem to face after they have been to our clinic and given a diagnosis of mast cell activation syndrome is when they return to their GP’s or specialists with a description of this syndrome. Traditional medicine is well-schooled in the diagnosis of systemic mastocytosis, a condition characterized by an increased number of mast cells as opposed to MCAS which is a diagnosis arrived at due to the increased activity of mast cells (and not an increase in the actual numbers).

Systemic mastocytosis is most often diagnosed by using a biomarker called tryptase, whereas the diagnosis of MCAS has much broader diagnostic criteria as this article will outline.

For a much more in-depth description of MCAS, please see my treatment page and the following articles:

  1. Treating Mast Cell Activation Syndrome (MCAS)
  2. Mast Cell Activation Syndrome: When You Immune System Runs Rampant
  3. Natural Treatments For Mast Cell Activation Syndrome
  4. Your Ultimate Guide to the Low-Histamine Diet

COVID-19 Testing: What You Need To Know

As I learn more about COVID-19 and share that information with you, my community, I’m increasingly asked about testing. Time is moving on and it’s clear that one of the limitations regarding the management of this global pandemic has been testing, or more specifically the lack of testing. There are still so many questions about how widespread SARS-CoV-2 (the virus that causes COVID-19 disease) is here in Alberta, Canada, and across the globe. We know that many people carry and spread the virus without showing any symptoms or just display very mild ones, but how many people are we talking about? 

As we enter the next phase of pandemic management, as people begin to enter communities again, testing will play a key role.1 It’s incredibly important to know who’s been exposed as well as who hasn’t and therefore may still be at risk. More widespread testing will help to keep those most vulnerable, including those with pre-existing conditions safe. 

While there’s undoubtedly still a lot to learn, in this article I’ll distill for you what I know and believe, as of now. I’ll cover:

  • Some background on testing, including understanding the timeline of COVID-19 infections
  • Types of testing, including viral RNA and antibody 
  • What test results mean
  • Test accuracy
  • Next steps for testing

Background on testing: The viral timeline 

To understand testing it’s helpful to understand the timeline of COVID-19 infection. This image was compiled by the Institute for Functional Medicine and provides a helpful visual.2 It’s important to note that this timeline is based on the data that has been collected so far, and some of it hasn’t been peer-reviewed and published yet. 

As you can see, the first thing that can be detected after exposure and with the onset of symptoms is the virus itself. This is depicted by the red and purple lines in the graph. 

After the initial infection, the body begins to mount an immune response and develop antibodies. This is depicted by the orange, blue, and green lines. 

Most of the testing that’s been done so far, mainly in hospitals, has been conducted when people are symptomatic. It’s also important to note that the time between when someone’s exposed to the virus and when they begin showing symptoms is widely variable. Some will show symptoms two days later and others may not show symptoms for three weeks. Others will show no symptoms at all, or only mild ones, yet still be spreading the virus during the first couple weeks of infection.

Time Course for testing after Exposure to SARS-CoV-2
Source:  https://p.widencdn.net/n3trkt/IFM_Sars_Graph_v3

Types of testing

There are two main types of testing, namely viral and antibody. Both have their place in the timeline of events. 

The Viral RNA tests look for an active viral infection. They test for the presence of RNA (ribonucleic acid) from SARS-CoV-2. The test will be positive for someone with a current or very recent infection.3 This test can be undertaken using several methods of collection.

  • Nasopharyngeal swab – This goes into the nose about three or four inches. 
  • Oropharyngeal swab – This down the throat and is similar to a test for strep throat. 
  • Sputum – This is the thick mucus produced by the lungs during an infection. If this can be collected from a person’s coughing, it can be tested. 
  • Saliva – Saliva collection for this test works best after a cough.
  • Stool – Viral RNA can be detected in the stool after an infection.4

A positive test result doesn’t necessarily mean that you’re contagious and are ‘shedding’ the virus. In order to verify that, we’d need to culture your sample in a laboratory. However, there are issues with safety and containing the virus in a laboratory setting, so this type of testing is mostly only done in a research environment at the moment. 

Therefore, we’ll assume that a positive test means you’re contagious and that you need to quarantine for two weeks in order to protect others. It also means that you should watch for symptoms and seek medical care if needed. You can read about treatment options, including herbs and nutrients, here. Tracking positive testing is also important from a public health perspective, in order to trace the spread of the virus.  

Viral RNA testing is going to be most accurate around four to six days after symptoms appear, since this is the peak of the viral RNA production.4 If you wait too long to be tested, you might get a negative Viral RNA test, even though you were infected. This is why this testing has a high false negative rate. You need to get the timing right. If you have a negative test, but a known exposure, you’ll still need to take precautions and may need to be tested again. 

The second type of test that’s helpful is an antibody test. This is a blood test that studies your immune response to the viral exposure. Essentially, it’s looking to determine if you were exposed to SARS-CoV-2 in the past and may be particularly helpful for mild or asymptomatic cases.5 The best time to take the test is about seven days after symptoms resolve or a minimum of fifteen to twenty-one days after exposure. 

There are two main antibodies that current testing is looking at.

  • IgM – This non-specific antibody is produced as the immune system is figuring out exactly what it’s dealing with. If you look at the chart above, you’ll see that IgM rises and then fades away as more specific antibodies (IgG) are produced. 
  • IgG – This more specific antibody takes a little time to develop and then stays high for a period of time.6

This pattern that we’re seeing with SARS-CoV-2 antibodies is typical of what we see with other viruses. 

A positive test suggests that you’ve been infected and that your body mounted an immune response to the infection, whether you had severe symptoms, mild ones, or no symptoms at all. Timing matters here as well. If you test IgG antibodies too early, you might miss them because they take some time, possibly around three weeks, to develop. False positive tests are also possible as some of the tests are detecting previous exposures to other coronaviruses, such as the ones that cause the common cold.4

A negative test might mean that you still need to take precautions to prevent exposure, especially if you’re at higher risk for severe COVID-19. Because of the timeline, it’s important to note that a negative antibody test does not rule out current infection. 

As you can see, the testing is quite nuanced, which is why connecting with your healthcare team for guidance is so important. 

Understanding test accuracy

Naturally, we want a test to be accurate, to be both sensitive and specific. This will limit false positive and false negative results. 

When it comes to accuracy, sensitivity refers to how likely a test is to pick up a positive result in those that have definitely been infected, known as true positives. It’s those that have been exposed to the virus that test positive. Specificity refers to individuals that haven’t been infected by the virus that test negative, which are referred to as true negatives.7. In a perfect world we always want a test to be 100 percent sensitive and 100 percent specific, but this isn’t the case when it comes to coronavirus testing. It can also be similar for many other antibody tests. The poor test results for Lyme disease detection are a good example of this.

We’ve already seen that there are cases of false positives and negatives based on timing and other factors. For example, with a viral RNA test, the nose swab can be really unpleasant so it’s possible that an error can occur as a result of not going deep enough to collect the appropriate sample. Alternatively, there might be low sensitivity because the test picks up antibodies to another coronavirus that are connected to a previous coronavirus infection.4

You might also hear the terms positive predictive value (PPV) and negative predictive value (NPV) in discussion regarding test accuracy. These take into account sensitivity and specificity in terms of the infection rates in a specific population.7 Of course, we need more testing to determine what rates are in each area. This article in Scientific American provides a useful guideline to the testing.

If I have the antibodies, am I immune? 

A conservative answer to this question is that we don’t know for sure. Because this virus is new, we don’t know if everyone that’s exposed develops antibodies, if those antibodies truly mean immunity, and if so for how long.4

However, it’s likely that this virus acts like other viruses that we know more about. For example, for a coronavirus that causes a common cold, you get the cold, develop antibodies, and those antibodies protect you for a while. For something more severe than a cold, such as chicken pox, you can develop immunity for a lifetime. 

You may have heard stories of those that tested positive, negative, and then tested positive again sometime later. However, this is more likely to be an issue with testing methods and timing more than a case of the immune system not creating immunity.  

That being said, I do think that having positive antibodies will be a tool that’s used to help open society up and allow individuals to return to daily life with more confidence.  

Should I get tested?

While I do think that widespread testing is important for both the individual and society, the availability of testing is still quite limited. 

There are many laboratories working to address the issues of access. These include functional testing laboratories, that are frequently used by myself and my colleagues, which are now coming to the market with tests. I have some colleagues that prefer one test over another and others that are waiting for the testing to become more accurate before widely applying it to their patient population. Another factor is that testing through private laboratories is quite expensive. At some point the cost will come down and testing will become more widely available. 

In Canada, we only have access to the provincial laboratory services, whereby they’ll perform PCR testing and antibody testing provided the correct criteria are met. If a private test is requested, we’re able to use certain US-based laboratories. Diagnostic Solutions Laboratory ships their COVID test kits to Canada. They have three test options, which are nasal swab, antibody and stool. 

A German laboratory called Euroimmun AG introduced a test with 100 percent specificity, thus eliminating the chance of a false positive. It’s been approved in the USA. A full list of all the tests approved for diagnostic purposes in all countries is included here at the Center for Health Security website. The Mayo Clinic has also launched an antibody assay with a specificity of 99.3 percent when tested against normal serum. Approximately three percent of serum is IgG positive less than seven days post-symptom onset, 35 percent are IgG positive in samples collected between eight and fourteen days after symptom onset, and 100 percent are IgG positive after fourteen days of symptom onset.

We’ve learned a lot so far about SARS-CoV-2 and COVID-19, but still have plenty that we need to understand. I’ll be keeping a pulse on the new research as it becomes available and will continue these important discussions with my colleagues in order to keep you updated regarding the very latest information. My understanding of this virus is that it’s evolving day by day and although testing is relatively new, it’s still extremely important. 

As we navigate this next wave of outbreak management, testing will be key in order to understand who has active infections, who’s already been exposed, and who may still be at risk. Testing will help us to understand how the virus is spreading, answer important questions about immunity, and ultimately to save lives. My sense is that until the antibody testing can approach a specificity that’s close to 100 percent, it may be worthwhile to wait it out.  

Please don’t hesitate to reach out for support as needed. My team and I are always here for you during this challenging time. 

References: 

  1. Patel R, Babady E, Theel ES, et al. Report from the American Society for Microbiology COVID-19 International Summit, 23 March 2020: Value of Diagnostic Testing for SARS-CoV-2/COVID-19. mBio. 2020;11(2):e00722-20. Published 2020 Mar 26. Full text: https://mbio.asm.org/content/11/2/e00722-20 
  2. The Institute for Functional Medicine. The Functional Medicine Approach to COVID-19: Primer on SARS-CoV-2 Testing. https://www.ifm.org/news-insights/functional-medicine-approach-covid-19-primer-sars-cov-2-testing/ 
  3. Wölfel R, Corman VM, Guggemos W, et al. Virological assessment of hospitalized patients with COVID-2019 [published online ahead of print, 2020 Apr 1]. Nature. 2020;10.1038/s41586-020-2196-x. Abstract: https://pubmed.ncbi.nlm.nih.gov/32235945
  4. The Institute for Functional Medicine. The Functional Medicine Approach to COVID-19: Primer on SARS-CoV-2 Testing Webinar. Hosted by Dr. Patrick Hanaway with Dr. Helen Messier. April 28, 2020. 
  5. Guo L, Ren L, Yang S, et al. Profiling Early Humoral Response to Diagnose Novel Coronavirus Disease (COVID-19) [published online ahead of print, 2020 Mar 21]. Clin Infect Dis. 2020;ciaa310. Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7184472/ 
  6. He-wei Jiang, Yang Li, Hai-nan Zhang, Wei Wang, Dong Men, Xiao Yang, Huan Qi, Jie Zhou, Sheng-ce Tao. Global profiling of SARS-CoV-2 specific IgG/ IgM responses of convalescents using a proteome microarray. Preprint article: https://www.medrxiv.org/content/10.1101/2020.03.20.20039495v1 
  7. Abdul Ghaaliq Lalkhen, MB ChB FRCA, Anthony McCluskey, BSc MB ChB FRCA, Clinical tests: sensitivity and specificity, Continuing Education in Anaesthesia Critical Care & Pain, Volume 8, Issue 6, December 2008, Pages 221–223, Full text: https://academic.oup.com/bjaed/article/8/6/221/406440 

A Positive Outlook During the COVID-19 Outbreak

The vast majority of the world’s population that has access to any source of media outlets is currently under the collective fear-driven news cycles of an upcoming apocalypse due to the emergence and spread of the coronavirus, COVID-19.  As I write this, a CCN alert flashed across my screen stating that there were 3,000 cases of coronavirus in the United States with 62 deaths. This number was updated six hours later to 3,155 cases. No doubt by this evening, this number will be adjusted upwards, a trend that will probably increase for the foreseeable future, the exact end-point being entirely unknown.

While all due caution is absolutely imperative and all medical guidance should be strictly followed, as I stated in my other pieces regarding coronavirus, parts one and two, I couldn’t help but reflect on what appears to be an innate tendency of all living systems to trigger homeostatic mechanisms that force self-correction whenever one side of its expression become too polarized to either extreme. It appears that evolution itself has to adjust course in light of new information by self-correcting evolutionary realignments.

We know from history that disasters are often followed by tremendous gains and achievements. The extreme horrors of World War II were followed by an extraordinary period of increased economic, social, and political global growth and relatedness, rather than nationalism, which was unprecedented in history. It was the same with 9/11. Immediately following those events, murder rates plummeted, and kindness and appreciation were unleashed upon civil servants, hospitals, demolition crews, and emergency medical services. Out of control real estate, airline, and hotel prices were corrected, and there was increased dedication to global causes. The list is much more extensive but undoubtedly real, when previous issues and statistics were assessed through this lens. 

One of the greatest and most well remembered political speeches of all time was delivered at the first inauguration by Franklin D. Roosevelt as the 32nd President of the United States. At that time, the nation was at the peak of the Great Depression and the speech was heard by tens of millions of American citizens.  

“So, first of all, let me assert my firm belief that the only thing we have to fear is...fear itself — nameless, unreasoning, unjustified terror which paralyzes needed efforts to convert retreat into advance. In every dark hour of our national life a leadership of frankness and of vigor has met with that understanding and support of the people themselves, which is essential to victory. And I am convinced that you will again give that support to leadership in these critical days.”

He went on to say, “There is no unsolvable problem if we face it wisely and courageously. There are many ways in which it can be helped, but it can never be helped merely by talking about it. We must act and act quickly.”

So, while we’re currently in the grip of the downward, fear-driven spiral that’s mostly emphasizing the potential catastrophic consequences that may or may not result from CoVID-19, how can we best compensate for those fears and reflect on the potential upside of this situation? And most importantly, what can we do to mitigate this fear-driven spiral into ennui, inaction and a potential sense of hopelessness?

What follows are some compensatory ideas that are in no way meant to downplay or minimize the suffering that many people have gone through or are about to go through. However, if we’re to embrace the homeostatic principles that there are no crises without blessings and we don’t live in a one-sided world where there are only losses without gains. So, let’s examine a few potential consequences that might arise from this present situation. 

  1. Global warming. The global warming crisis seemed to be almost impossible to reign in, despite the most well-meaning attempts by a subset of global political and environmental leaders. With all kinds of global travel grinding to a halt, it’s inevitable that at least a pause to the upward tend of global warming, primarily due to the carbon footprint induced by travel, will be inevitable. When climate change experts examine this effect in months or years to come, maybe their statistics can be used to convince others of the need for a more sustained and ambitious action regarding this omnipresent threat.
  2. Exotic animal trade. China stopped the trade in wild animals for the purpose of consumption such as dogs, rodents, yaks, snakes, porcupines, and bats when the link between animals and the coronaviruses was discussed. Officials from the Chinese Center for Disease Control and Prevention said they isolated the virus taken from a seafood and wildlife market in Wuhan believed to be the source of the outbreak. The coronavirus that caused the 2003 SARS outbreak was traced to the civet cat, a wild animal considered a delicacy in parts of South China. The civet is used in the popular dragon tiger phoenix soup, which is believed by locals to help with arthritis, stimulate poor blood flow, and revive decreased libido. The movement of humans toward recognizing animals as sentient beings may be assisted, a movement initiated and kept alive by the PETA president and founder Ingrid Newkirk and written about in her best selling book, Animalkind.   
  3. Consumerism. Our western culture is an extroverted and consumer driven one. Perhaps by sitting at home for extended periods, with the stores, at least at present, bare of many types of consumer goods, we can reflect on our impulse to seek emotional consolation outside of ourselves by buying new items that we may not need. I do realize that the beast of online shopping may be unleashed but here’s hoping that the online stores may not be able transport unnecessary consumer goods due to the transport channels being slowed down. 
  4. Possibility of increased relatedness. A series of recent posts by Rebecca Arendell Franks, who along with her husband and child has now been on forced quarantine in China for over 50 days, is quite illuminating. She said that, “Our family life has never been better. Usually, one weekend is long enough before I’m ready to send each of us back to school or work. But for SEVEN weeks, we’ve been home together with very little outside influences or distraction, forced to reconnect with one another, learn how to communicate better, give each other space, slow down our pace, and be a stronger family than ever before. I encourage you to read the link regarding this at the end of this article. 
  5. Nature emerging from the technological and human encroachment upon its domain. It’s been observed in Wuhan that the sound of birds singing has been heard for the first time in a long time since the crisis began. In Wuhan, Rebecca Arendell Franks commented, “Right now, I hear birds outside my window (on the 25th floor). I used to think there weren’t really birds in Wuhan, because you rarely saw them and never heard them. I now know they were just muted and crowded out by the traffic and people. All day long now I hear birds singing. It stops me in my tracks to hear the sound of their wings.”
  6. Learning new technologies for virtual relatedness. How does ZOOM actually work and can I teach my grandfather to hook up? 
  7. Learning to cook. Maybe we can now, instead of ordering food in or going out to a restaurant, learn to cook for ourselves and make that tasty, healthy recipe that we’ve always been meaning to get around to. 
  8. Examination of our national leader’s skill set in crisis management. 
  9. Exercise. Finally, the Peloton bike or treadmill can be put to good use!
  10. Non-drug based medicine. Examination and renewed interest, along with a certain amount of respect given, of alternative methods for treating symptoms of coronavirus, and indeed other viral related illnesses such as the three studies currently underway in China on the use of IV vitamin C for the treatment of corona related pneumonia. See blog posts part one and two for further details. 
  11. Lifestyle factors. An awareness of how lifestyle factors such as diet, exercise, sleep, and stress play an extraordinary role in immune efficiency.
  12. Business awareness. Small business will become aware of cash flow issues, staffing needs, and unemployment issues.
  13. US Federal Reserve slashing interest rates. Maybe now is the time where one can afford the mortgage on a new home that seemed out of reach a few years before. Or maybe people with fixed student loan payments can borrow money at a lower rate to pay those off. 
  14. Learning to connect with others non-locally. There’s a common misconception that in order to benefit from the full experience of another human being we have to be in their physical presence. Yet if we truly love someone and see both sides, the dark and the light, of their being, we can sit quietly, hold them in our hearts, and send deep love and appreciation to them for being in our lives. It helps if we have an understanding of the Einstein-Podolsky- Rosenberg paradox (EPR paradox) in quantum physics that showed that if one particle had ever been in contact with another particle, if they were separated across the full expanse of the universe in space and time, they’d be eternally intertwined or entangled. Einstein called it “spooky action at a distance.”  

(Please note this is a very simplistic explanation for quite a complex issue.)  

A few more quick positive outlook possibilities:

  1. Increased revenues for the medical device industry.
  2. Increased revenues for the supplement industry.
  3. Increased connection to neighbours to assist with grocery runs.
  4. Appreciation for the media and their updates.
  5. Appreciation for our doctors, nurses, and miscellaneous healthcare workers and politicians for rising to the occasion and setting minute by minute guidelines
  6. Appreciation for mobile device apps, Google, Facebook, Instagram, and Twitter for keeping us informed.
  7. Appreciation and understanding of our own vulnerability.
  8.  Resetting of values and personal reflection on what is truly meaningful, including a reorganization of values and priorities.  

So, as we step back, reassessing our priorities both personally and collectively, these are a few thoughts I’ve had in these troubling and somewhat frightening times. If Nobel Prize winning chemist Ilya Prigogine is to be believed, even insentient material systems have an inherent drive to self-organization. When physical systems get pushed too “far from equilibrium” they escape this chaos by leaping into higher level states of organized order, referred to as “order out of chaos”. My challenge to all of you is, what inherent dynamic force may be at play in your life, driving you toward greater and greater wholeness, complexity, and consciousness in the midst of these very challenging times? What thoughts of this nature have come to your mind in these times?

While you contemplate having a positive outlook and these deeper thoughts, stay safe, follow your governmental and health directive guidelines, and do what you need to do to get through these times. We must attempt to move beyond the greatest fear, which is that of fear itself. 

See part one and two for specific coronavirus updates and treatment suggestions. 

Preventive and Treatment Strategies for COVID-19: Part 2

Part 1 of this series can be found here

Keep Fighting Fit

It’s only common sense to keep our bodies as healthy as we can to help us to fight off all kinds of illnesses. Obviously, we’re always going to encounter germs in our daily lives but keeping our immune systems in good condition is an excellent defense strategy. 

Follow these steps: 

  • Get enough sleep, ideally seven or eight hours each night. 
  • Try to reduce stress where you can in your life. 
  • Make sure you’re on a diet that contains plenty of plant-based antioxidants, minerals and vitamins and eat healthy food to keep your body and immune system in good shape. 
  • Make sure that you always get enough exercise whenever you can to keep everything in working order. 
  • Stop consuming all sugar
  • Stop smoking or vaping immediately. 

Wear Mask Protection

Get some N95 facemasks before supplies are gone. 

  • An N95 respirator is a respiratory protective device designed to achieve a very close facial fit and very efficient filtration of airborne particles.
  • The ‘N95’ designation means that when subjected to careful testing, the respirator blocks at least 95% of very small (0.3 micron) test particles. If properly fitted, the filtration capabilities of N95 respirators exceed those of facemasks. However, even a properly fitted N95 respirator doesn’t completely eliminate the risk of illness or death.

N95 respirators aren’t designed for children or people with facial hair. Because a proper fit cannot be achieved on children and people with facial hair, the N95 respirator may not provide full protection.

A full list of FDA approved respirators is provided below. These might already be out of stock everywhere but put orders in regardless of the backorder. 

  • 3M™ Particulate Respirator 8612F
  • Pasture Tm F550G Respirator
  • Pasture Tm A520G Respirator

Wear Eye Protection

Transmission through the eye is a common vector for the aerosolized virus. One of the common transmissions is touching public items then touching your face and transmitting it through the eye. Frequent hand washing and excellent hygiene are paramount.

Drug treatments

General

It’s important to be aware that there are at present no antiviral treatments that are effective for the treatment of Covid-19. There are currently no vaccines available for SARS-CoV-2. The present treatment approach is for supportive care and symptom management only. If people become severely ill, vital organ function support is necessary, usually in a hospital or ICU setting. 

Here’s a link to the number of drugs that as of February 2020 were being studied for the treatment of Covid 19.

The CDC also has a site discussing antiviral medications for the flu here

Chloroquine Phosphate

A Chinese multicenter collaboration group suggested this malaria drug might be useful for the treatment of Covid-19 pneumonia. In another recently published paper, the use of hydroxychloroquine, 400 mg twice daily followed by a maintenance dose of 200mg twice daily for four days, was found to be more potent than chloroquine to inhibit SARS-CoV2. Hydroxychloroquine was also shown to have fewer side effects than chloroquine while still addressing the inflammatory cytokine storm induced by the virus. 

The recommended dose of chloroquine phosphate was 500mg twice daily for ten days. 

Alinia (Nitazoxanide)

This drug is traditionally is used as an antiparasitic and has been studied for the treatment of Middle East Respiratory Syndrome (MERS) coronavirus. This drug has been shown, in test tube studies at least, to have activity against MERS-CoV and other coronaviruses. Further studies are being undertaken to determine its true efficacy. The recommended dose was 1000mg twice daily for 10 days.

HIV Drug - Kaletra (lopinavir-ritonavir)

A 62-year-old man who became Spain’s first coronavirus patient is believed to have made a full recovery after being treated with an HIV drug called Kaletra or lopinavir-ritonavir. Miguel Ángel Benítez was admitted to the Virgen del Rocio Hospital in Seville, where he received an antiretroviral drug, which has been used to treat HIV and AIDS for over ten years. The drug was combined with interferon beta, which is a protein that prevents cells from becoming infected and is administered to multiple sclerosis patients. Santiago Moreno, head of infectious diseases at the Ramón y Cajal hospital in Madrid, said that the “SARS-CoV-2 protease is very similar to that of HIV,” using a name that sometimes refers to the novel coronavirus.

Mast Cell Activation Syndrome (MCAS

In this February 2020 article it was discussed that “Coronavirus infection (regardless of the various types of corona virus) is primarily attacked by immune cells including mast cells (MCs), which are located in the submucosa of the respiratory tract and in the nasal cavity and represent a barrier of protection against microorganisms. Virus activate MCs which release early inflammatory chemical compounds including histamine and protease; while late activation provokes the generation of pro-inflammatory IL-1 family members including IL-1 and IL-33.” The article proposes for the first time that inflammation by coronavirus may be inhibited by anti-inflammatory cytokines belonging to the IL-1 family members. 

It may be that individuals with MCAS are at higher risk for developing the serious consequences of this infection and thus may benefit from much stricter control of the mast cell activation syndrome if infected. Nebulized cromolyn and/or glutathione or n-acetyl cysteine (NAC) and/or IV Benadryl may be extremely helpful in these conditions.

Alternative Remedies

In addition to the previous suggestions, there are a number of natural substances and supplements that can be of help in lowering your risk of becoming infected with the current coronavirus. Many of these approaches are not specific treatments for the coronavirus but have been studied and referenced in the literature as having antiviral effects.

Vitamin C

It’s common knowledge that vitamin C is good for us but there have been clinical trials in China regarding the intravenous use of vitamin C to help treat patients suffering from Covid-19. A dose of between 100 and 200 mg/kg body weight (this is equal to quite a low dose of between 7.5 and 15 grams for a 180 lb person) was given to patients intravenously for three consecutive days and was very effective. There are currently three clinical trials sponsored by the Chinese government studying vitamin C. Dr. Tom Levy and Dr. Jeanne Drisko from the integrative U.S. medical community are involved in the Chinese studies. Dr. Richard Cheng MD PhD, who has been studying IV vitamin C, is suggesting the use of oral vitamin C.  The one study can be found at the clinicaltrial.gov website. High dose vitamin C at 20 grams has been used in ICUs for some time in an attempt to reduce mortality from septic shock, in one study from 40% to 4%. However, most hospitals refuse to administer IV vitamin C for viral infections since it’s not considered standard of care. It’s quite likely that these Chinese studies will place high dose IV vitamin C therapy for viral infections a part of mainstream treatment in the future.   

In the United States, doctors who have pioneered vitamin and mineral therapies have also been studying the effects of intravenous vitamin C, with a February 2020 paper being published. “Early Large Dose Intravenous Vitamin C is the Treatment of Choice for 2019-nCov Infected Pneumonia” recommends this for the treatment for pneumonia resulting from the virus. 

A recommended minimum oral daily dose of vitamin C is 2,000mg. Twice daily dosing is recommended due to the water-soluble nature of vitamin C and the fact that it’s quickly metabolized. If one wants a liposomal formulation, certain brands do provide this option or you can make your own by adding https://klinghardtinstitute.com/one or two teaspoons of Body Bio PC (phosphatidyl choline) to 2 grams of powdered vitamin C and stirring it vigorously. Divide your dose and take twice daily. Watch for diarrhea if your dose is excessive.

Vitamin D

This is also very important. It’s recommended that we have a minimum of 2,000 IU and a maximum of 10,000 IU per day. The usual daily dosage for vitamin D is 1000 IU per 25 pounds of body weight. It’s best to get vitamin D levels measured and to have serum levels in Canada between 150 and 200 nmol/l. People tend to have lower vitamin D levels in the fall and winter months due to fewer hours of sunlight. However, our bodies need vitamin D to support our immune system so we need to make sure that we’re getting enough of this vital ingredient. All the cells in our bodies have receptor sites but only two types are in every cell. These are thyroid hormone receptor sites, which are responsible for metabolism, and vitamin D receptor sides. This gives you some idea of the importance of vitamin D in maintaining our overall health and wellbeing. Research indicates that vitamin D may even be more effective than the flu vaccine when it comes to flu prevention. Consequently, it’s a good idea to include vitamin D in the fight against Covid-19.

It has been reported by many clinicians that high doses vitamin D of 50,000 IU over three days is highly effective in treating acute viral infections. This dosing is contraindicated in any person with lymphoid malignancies and in any patient with granulomatous diseases such as sarcoidosis, where high calcium levels are an issue. Also, a relative contraindication is pregnancy. This is by no means an approved treatment for Covid 19.   

Zinc 

This has been shown to be effective in fighting infections and also supports the immune system. Zinc can help to prevent coronavirus and other viruses multiplying in the throat and nasopharynx, which is the space above the soft palate at the back of the nose connecting the nose to the mouth and allowing us to breathe through our nose. When you begin to exhibit symptoms of the illness zinc capsules can be taken several times a day. The recommended dose for zinc is between 40 and 50mg per day.

Silver 

This has also has some antibacterial and anti-viral properties. If you use an official product such as Argentyn 23 you have a clear idea of how much silver you are putting into your body and don’t run the risk of taking too much. If you have viral symptoms, the recommended dosage is one teaspoon seven times per day. However, this is only a short-term solution as there are side effects such as skin discoloration if silver is used for too long.

Andrographis 

This herb has been used in traditional Chinese medicine and Ayurveda for a long time. It’s been shown that the herb’s compounds have anti-inflammatory, antiviral, and antioxidant benefits. The herb boosts the immune system and is often employed to fight cold and flu symptoms. As a result it does have a role to play in treating the latest version of coronavirus, at least in the short term. One capsule twice a day is the recommended dose of the herbal supplement if you exhibit symptoms of the virus. There are a number of referenced articles that demonstrate its effectiveness against the influenza virus, particularly with regards to respiratory symptoms. Lyme patients with active disease may have a Herxheimer reaction as it increases lymphocyte proliferation and interleukin -2. 

Elderberry

Another natural short-term solution if you have typical flu symptoms, such as a cough, sneezing, and a runny nose, is elderberry extract taken up to six times a day. Elderberries come from the European elder tree, which is not the same as the American Elder, Elderflower, or Dwarf Elder. People believe the extract helps with the common cold, influenza, boosts the immune system, and reduces inflammation.

Calendula

Is also known as marigold and has been used as a medicinal herb for a very long time. The plant’s extracts have antiviral, antigenotoxic, and anti-inflammatory properties that can be used to treat some of the symptoms of Covid-19. 

Taraxasterol 

Also known as dandelion, this can also be used as an anti-inflammatory supplement. Dandelion also has antioxidant properties and some studies indicate that it has antiviral benefits and is good for our immune system. 

Propolis 

This is known to be a potent antiviral, particularly in animal models infected with corona virus. Dr. Ramzi Asfour, an infectious disease physician, suggests Beekeeper’s Natural propolis spray. Propolis increases cellular immune responses and has antiviral properties. Propolis can also be dispensed in a vaporizer (available from Ki Science) and has been shown to neutralize circulating mycotoxins in the air. 

CAUTION: Propolis is not to be taken if you have a Honey or Bee allergy.

Scutellaria

Most commonly known as skullcap, this is another flowering plant with medicinal qualities. It has been used to treat conditions such as respiratory infections and inflammation and have antibacterial, antiviral, and antioxidant properties. 

Artemisia annua

Also referred to as sweet wormwood this has been used in traditional medicine for some time and has been employed in medicines to treat malaria. There are some indications that the plant may also be used to treat some coronavirus symptoms, particularly the SARS related coronavirus.

Dr. Klinghardt, in his extremely informative PowerPoint presentation, has recommended placing calendula, licorice, scutalaria, andrographis, artemisia, and dandelion tinctures, calculated for their weekly dose, in a blender with 100mls of clean water and 14 grams of vitamin C powder. Add two tablespoons of liquid Body Bio PC phosphatidyl choline and blend for a few minutes. Put this mixture in a glass and keep in the fridge. Each day, drink one seventh of the dose.

Beyond Balance Herb Tinctures- IMN-V-III

This product contains 19 different herbs with antiviral and immune modulating effects, including licorice, skullcap, dandelion, and rosemary.

Peptides

Some patients have access to peptides with immunomodulating effects. I recently returned from a peptide conference in Los Angeles and the following peptides were suggested for their antiviral and immune modulatory effects.         

  • Thymosin alpha 1 - This is the most recommended peptide for immune stimulation. This should be used as a treatment adjuvant and a prophylactic and can help with many conditions beyond viral illness. The recommended daily dose in 450mcg.
  • Thymosin beta 4 - Natural killer cells are essential for defense against tumors and virus-infected cells. The cells are activated in by ONF-Gamma. This is activated by IL-18, which TB4 upregulates. Therefore, TB4 has ben studied for many Immune related diseases. Caution is warranted with cancer patients as it can increase the growth of cancers.
  • LL 37 (cathelicidin) - This peptide has broad spectrum antiviral/microbial, fungal effects. Peptides such as LL 37 are key components of innate defenses against infection, with both microbial and host defense modulatory functions. In addition to their well documented bactericidal potential, CHDP have more recently been shown to have antiviral properties. LL 37 has ben shown to be highly effective in preventing viral attachment to cells. It’s been used in several virus studies and has been anecdotally reported to work well with respiratory tract viruses.
  • Pentosan polysulfate - Polysulfates are highly potent and selective inhibitors of the in vitro replication of HIV and other enveloped viruses such as coronavirus. The anti-viral activity of polysulfates is a result of their shielding of the positively charged sites in the V3 loop of the viral envelope glycoprotein gpl120, which inhibits viral entry into cells and allows for immune clearance. The usual dose is 2mg/kg.
  • Selank - This is a variant of the immune molecule tufstin and has potent antiviral properties in addition to its neurological effects. The antiviral characteristics of Selank were evaluated both in vitro and in vivo against the influenza virus strain H3N2 and H5N1 and the type 1 and 2 Herpes virus. It was revealed that Selank might have a prophylactic effect during influenza infection and a therapeutic effect during a herpes virus infection. It could also be helpful with Covid-19.

The Hoffman Centre Programs for cold and flu treatment

We have developed a number of potential programs for acute cold and flu treatment. While the details aren’t specific to coronavirus many of the recommendations are applicable to dealing with virus that commonly infect us in the winter months. These recommendations are in no way a substitute for quick and rapid communication with your healthcare providers and the guidelines as issued via websites (like this one), previously mentioned at the beginning of this article.

Any treatment that you decide to undertake should start at the first onset of symptoms. The following instructions are to be followed for the duration of symptoms unless otherwise stated. 

Immediately stop consuming any sugar, since this paralyzes your white blood cells, the body’s first defense against illness. Make sure you also get plenty of sleep, at least between 7.5 and 8.5 hours per night. Hot apple cider vinegar baths twice a day will help to speed up the progression of the cold and reduce your fever, potentially halving the amount of time you may have symptoms. Add two cups of apple cider vinegar to a full bath of hot water and soak for twenty minutes, remembering to fully submerge your body. If the illness has affected the chest, you can steam water over the stove, add eucalyptus drops, and breathe in the vapor for some relief from your symptoms.

Please note that this treatment program is not to be undertaken if you are pregnant or breastfeeding.

Adult Dosage (age 16 and up)

Oscillococcinum is the first supplement to take at the first sign of a cold or flu. This works better for flu like symptoms (not cold symptoms) and you simply need to follow the directions on the package.

  • Vitamin D - 50,000 IU for three days. Contraindication to use of high dose vitamin D is lymphoid malignancies, pregnancy, and granulomatous diseases such as sarcoidosis
  • Mycelized vitamin A - 100,000 IU for three days. Contraindicated in pregnancy. 
  • Vitamin C - 1 to 2g two to three times daily (titrate dose upward to bowel tolerance)
  • Astragalus Tincture - 1 dropper three times daily
  • Echinamide Anti-Cold tincture - 2ml three times daily
  • Probiomax probiotic - 1 capsule two times daily 
  • Saccharomyces Boulardii - 2 capsules twice daily
  • Garlic/allicin - 2 capsules three times daily after meals. Open the capsule in 6oz of water and let sit for two minutes before drinking.
  • Argentyn 23 colloidal silver  - 1 teaspoon three times daily in water
  • Andrographis - 2 dropperfuls twice daily in water
  • Transfer Factor Multi Immune - 2 capsules twice daily
  • DHEA - 50mg per day for two to three days will boost the immune system and fight infection. Note that this is for adults only.
  • For muscle aches take arnica and/or magnesium malate - 2 caps three times daily
  • Add anti-viral supplements such as olive leaf extract - 2 capsules three times daily, oil of oregano (brand name ADP) 2 capsules three times per day and lysine 500mg 2 capsules three times daily

IV Treatment for 3 days

  • IV vitamin C - 15 to 35g once per day. Check for G6PG enzyme deficiency first
  • Alternatively - IV Hydrogen Peroxide, once per day

Child Dosage (2 years and older)

    • Mycelized vitamin A – 10,000 IU for three days
    • Vitamin D - 10,000 IU for three days
    • Vitamin C - Between 250 and 500mg three times daily (to bowel tolerance)
    • Echinamide Anti-Cold - Between an third and a half a dropper three times daily 
    • Probiomax probiotic  - Half a capsule twice daily
    • Saccharomyces Boulardii - Half to a full capsule twice daily
    • Garlic - Half to a full capsule twice daily after meals. Open capsule in 6oz of water and let sit for two minutes before drinking. Note that it is difficult to get a child to take this.
    • Argentyn 23 colloidal silver - Half a teaspoon three times daily in water
    • Transfer Factor Multi Immune - 2 capsules daily

Maintenance and Prevention 

Remember to stop consuming any sugar immediately, since sugar paralyzes your white blood cells, which provide your body’s first defense against sickness. Make sure you get at least 7.5 to 8.5 hours of sleep each night as well. This treatment program is not for women that are pregnant or breastfeeding.

Throat Infection

  • Zinc - 30 to 50mg lozenges. The topical antimicrobial effect can be important in infections of the throat.
  • Biocidin throat spray - 2 sprays three to five times daily
  • Propolis throat spray – 5 sprays three times daily
  • Argentyn 23 throat spray- 3 sprays three times per day
  • See your doctor for a throat swab to exclude strep throat and/or mononucleosis

CAUTION: Propolis is not to be taken if you have a Honey or Bee allergy.

Nasal Irrigation

Use a Neti Pot, particular with upper respiratory infection, for three days. 

  • Place one dropper full of Nasya wash into your Neti Pot with warm water and a heaping quarter teaspoon of pure non-ionized Neti Pot Salt. 
  • Stir until salt is dissolved. 
  • Add three drops of Echinacea Anti Cold and Core Phyto Lavage to the solution. Use this to perform the nasal wash as directed by the Neti Pot instructions on the bottle.

Air Spray

  • Add a quarter teaspoon of salt to the bottom of an empty spray bottle. 
  • Add five drops of Thieves, an essential oil by Young Living, on top of the salt as this will help to dissipate it, 
  • Fill bottle with warm water. 

Now you now have an air spray that will assist in lowering counts of viruses, bacteria, and molds in the air. 

  • Spray your home, office, and other areas a couple of times a day. 
  • You can also put Thieves drops into your palms and cup your hands over your face then inhale five or six times. 
  • This will prevent you from contracting a sinus or lung infection, especially during long distance flights.

Dr. Alex Vasquez Recommendations

Dr. Alex Vasquez is an internationally recognized author, presenter, and teacher, particularly with regards to immune related disorders. He earned three doctorate degrees from fully accredited universities in the United States and has worked in various clinical facilities ranging from private boutique clinics to inpatient hospital settings. Dr. Vasquez has published 120 books, articles, letters and editorials in various magazines and peer-reviewed medical journals, including British Medical Journal, Journal of the American Medical Association, Nature Reviews Rheumatology, and Annals of the New York Academy of Sciences.

What follows are his recommendations for viral infections and are not meant to be specific treatments for any infections, particularly coronavirus. I’ve included these references for those curious patients who are always checking out protocols online.  

Antiviral

  • Powdered Glycyrrhiza Glabra - 1.5g BID for a maximum of four weeks. Works as a tea. This is a great expectorant but avoid in heart failure patients, monitor BP and potassium
  • Zinc - Between 20 and 50mg a day
  • Selenium – 400 to 600 ug per day
  • Iodoral Iodine/Iodide - 12.5mg a day for two weeks
  • Melissa officialis - Dose variable depending on formulation
  • Carica papaya leaf extract
  • Grape seed extract (see Biotics Research Bio-Cyanidins below)

Viral Anti-replication

  • SAMe - 400mg TID plus Betaine TMG 3g BID for one week
  • Methyl-Folate - 1.6mg od for one to two weeks
  • Alpha Lipoic Acid - 300 to 400mg TID plus Thiamine 100mg (or B Complex High Potency)
  • NAC - 600mg BID to TID between meals

Immunonutrition

  • Paleo-Mediterranean Diet with no refined carbohydrates 
  • Protectamin Whey Protein - 45g a day for immune dipeptides, if dairy tolerant
  • L-Glutamine powder - 9g TID between meals 
  • Vitamin A - 100,000 IU load for three to five days, then 25,000 to 50,000 IU for two weeks (not during pregnancy)
  • Vitamin D3 - 100,000 to 300,000 IU load for one dose, then 10,000 IU for ten days to increase endogenous antimicrobial peptides
  • Nordic Naturals Arctic Cod Liver Oil without vitamin D - One teaspoon TID with meals
  • Selenium - 600-800mcg/d plus 800 IU vitamin E per day
  • Melatonin - 20mg qHS
  • Ubiquinol CoQ10 - 300mg od to protect the mitochondria
  • Biotics Research KappArest - Three capsules BID as NFKB hijacked by viruses for replication
  • Biotics Research Bio-Cyanidins - One tablet BID (contains marine pine bark and grape seed extract)
  • Biotics Research UltraVir-X - One capsule TID (Red-rooted sage, Boneset, Actratylodes, Sweet Violet, Wheat Grass, Bupleurum, Astralagus, Bee Propolis, Maitake, Black Walnut, Hesperidin, Rutin)
  • Biotics Research POA-Phytolens (Cats’ Claw, Lens esculenta extract) - One capsule TID
  • Consider broad spectrum multi such as Metagenics PhytoMulti at two tablets per day (adjust dosage of Zinc and Selenium above)

CAUTION: Propolis is not to be taken if you have a Honey or Bee allergy.

Treatment and Vaccines

  • There is no vaccine currently available to combat the current coronavirus outbreak. 
  • The best advice is to protect yourself in some of the ways outlined above and avoid contact with infected individuals or locations where you might encounter potential carriers of the virus. 
  • There’s no specific antiviral treatment that’s recommended for patients with the Covid-19 virus. 
  • Those infected should receive the medical treatment required to deal with their symptoms, including care of vital organs in the most severe cases. 

In Conclusion

  • While we still don’t know everything about the current Covid-19 virus, common sense and taking precautions and preventative measures will be a great help. 
  • The feeling in the medical community is that the virus is likely to become less aggressive and less dangerous over time, as many viruses do, although this is far from certain. 
  • Many viruses adapt, mutate, and continue to live with us everyday. Time will tell if the latest threat will follow the same pattern in the coming weeks and months.

As a final note, in the current circumstances, if you’re suffering from what you’d describe as symptom similar to flu such as a cough, fever, chills, or an aching feeling in the body, please don’t visit the office. If you have an appointment we can do a phone consultation instead or even connect via zoom online. Staying at home will allow you the opportunity to recover and also reduce the likelihood that you’ll pass on the virus to others.

Resources

 https://www.cdc.gov/coronavirus/2019-ncov/about/prevention.html?CDC_AA_refVal=https%3A%2F%2Fwww.cdc.gov%2Fcoronavirus%2F2019-ncov%2Fabout%2Fprevention-treatment.html
 Courtesy of Tailor Made Pharmacy  
https://www.cdc.gov/coronavirus/2019-ncov/about/prevention-treatment.html 
 Expert consensus on chloroquine phosphate for the treatment of novel coronavirus pneumonia. Zhonghua Jie He He Hu Xi Za ZHi 2020 Feb 20. 43:E019
https://www.ncbi.nlm.nih.gov/pubmed/32150618
 https://www.sciencedirect.com/science/article/pii/S1876034116300181
https://nypost.com/2020/03/05/coronavirus-patient-in-spain-reportedly-recovers-after-being-treated-with-hiv-drug/
https://www.ncbi.nlm.nih.gov/pubmed/32013309/
https://clinicaltrials.gov/ct2/show/NCT04264533
 http://orthomolecular.org/resources/omns/v16n11.shtml
 Epidemic Influenza and Vit D. https://www.ncbi.nlm.nih.gov/pubmed/16959053
 https://www.argentyn23.com/
 https://link.springer.com/article/10.1007/s00705-016-3166-3
 Biol Pharm Bull. 2009 Aug; 32 (8) : 1385-91
https://www.webmd.com/vitamins/ai/ingredientmono-434/elderberry
 http://insajournal.in/insaojs/index.php/proceedings/article/view/305
https://www.ncbi.nlm.nih.gov/pubmed/28480383
 Ferreira L, Effect of the ethanolic extract from green propolis on production of antibodies after immunization against canine parvovirus (CPV) and canine coronavirus (CCOV). Brazilian Journal of Veterinary Research and Animal Science 49.2 (2012):116-121. http://www.revistas.usp.br/bjvras/article/view/40267
Dr Horowitz newsletter 
 https://kiscience.com/product/propolair-propolis-diffuser-therapy-model/
 https://www.sciencedirect.com/science/article/pii/S2211383520302999
http://www.hdbiosciences.com/Download/Identification%20of%20natural%20compounds%20with%20antiviral%20activities%20against%20SARS-associated%20coronavirus.pdf
 Antiviral Research 67, No 1 (2005): 18-23
 https://klinghardtinstitute.com/
 Courtesy of Tailor Made Pharmacy.
 https://www.inflammationmastery.com/

What You Need to Know About COVID-19: Part 1

Every day brings a new update about the spread of coronavirus. There are more cases all around the world every day and naturally people are very concerned. There’s certainly not a shortage of stories in the media but is the virus as dangerous as it’s being portrayed? And is the hysteria that’s being generated potentially more damaging than the threat posed by the virus?

In Canada, you can get the very latest updates courtesy of the federal government, including the current situation in different parts of the country, the risk to Canadians, how the government is monitoring the virus, travel advice, and the symptoms, treatment, and risk factors here.

A similar range of information is available for Alberta residents here. For those of you in the U.S. you can access pertinent information here

Mass panic is certainly not going to help the situation but neither will complacency. Despite the fear being whipped up on social media and in the traditional media reports, it’s perfectly natural to be anxious about this situation. This outbreak isn’t to be casually dismissed as it is very serious and everyone needs to accept that and not be in denial. We all need to work together to get through this. We may not know everything about the coronavirus yet and vaccines, treatment and indeed cures are still some way off, but we need to determine strategies that are going to work to protect ourselves and prevent the spread of the virus. So what exactly is coronavirus?

The Virus

Coronavirus is an illness that mostly affects our respiratory system. Doctors are still learning about the virus but it is thought to primarily be airborne, which means that it can be spread from one person to another. When a person coughs or sneezes they produce what are known as respiratory droplets. These can be breathed in by other people that are nearby or left on your hands if you touch your face after coughing or sneezing. In China, the fact that the illness seems to be mainly transmitted to family members, healthcare workers and others in close contact with an infected person strongly indicates the transfer of the virus is by respiratory droplets. The droplets can also remain on objects that have been touched, such as door handles, keyboard, elevator buttons, and many other everyday items. The virus can then spread if a person comes into contact with a surface that’s been contaminated. 

It has been suggested by recent studies that asymptomatic patients are also able to transmit the infection. This means that isolation might not be as effective a weapon against the virus as was previously thought. Researchers followed viral expression through infection through throat and nasal throat swabs in a small select group of patients. The researchers discovered that there were increases in viral loads at the point when the patients became asymptomatic. Doctors in Wuhan, China, studied 425 patients that had the virus. Many of the earliest cases were linked to direct exposure to live animal and seafood markets. However, later cases were unconnected to the animal markets, reinforcing the theory that the virus is transmitted between humans. 

There are believed to be many different types of coronavirus but only 7 of them can cause disease in humans. Some of the coronaviruses that usually affect animals are also able to infect people. The diseases Severe Acute Respiratory Syndrome (SARS) and Middle East Respiratory Syndrome (MERS) are also caused by coronaviruses that moved to people from animals. Like MERS and SARS, COVID-19 is believed to have originated in bats. Before the illness was brought under control in 2003, SARS infected more than 8,000 people and almost 800 died. 2,465 cases of MERS have been reported since 2012 and 850 people have died. The mortality rate for SARS was around 10%, whereas for MERS the mortality rate is around 34.5%.

The coronavirus that is currently in the news is called SARS-COV-2 (formerly called 2019-nCOV). The disease that it causes has been called Coronavirus disease 2019 (Covid-19). Once someone has the virus, the symptoms can be very mild but for some people they can be very serious and endanger life. Although we’re still learning about COVID-19 it does seem to be milder in its effects than SARS or MERS, with only a 2% mortality rate. Initially, the World Health Organization (WHO) reported that the worst severe cases in China were mostly in adults over 40 years old with significant comorbidities. This means that the patient has more than one chronic medical condition. The illness also seemed to affect more men than women, although this could change as the outbreak continues. As of March 12, 2020, COVID-19 had been confirmed in more than 128,343 people, mostly in China. To date 68,324 people have recovered from the infection. By this date, the virus had caused more than 4,720 deaths and has spread to more and more countries. These websites have information on the global situation that is updated regularly. Keep in mind that an estimated 291,000 to 646,000 people die worldwide from flu every year.

Symptoms of Coronavirus

A person that has Covid-19 might not show any symptoms at all for between 2 and 12.5 days, with the average time being 5.2 days. This one can easily pass it on to others without even knowing that they are infected in the early stages. The average time from infection to symptoms appears to be 12.5 days. The pandemic worldwide appears to be doubling every 7 days and every infected person appears to infect an average of 2.2 others.

Symptoms can include:

  • Fever
  • Cough
  • Breathing difficulties and shortness of breath.

While some of the symptoms are similar to colds and flu that people suffer from throughout the year, there are important differences. With the common cold we suffer from a runny nose and there is sputum or phlegm. This is the mixture of mucus and saliva that we cough up from our lungs when we get sick. With the coronavirus there’s a dry cough but no runny nose. This may occur in a small percentage of patients (4%) but it’s thought this is because they already have some form of flu or cold symptoms.

If nasal congestion does occur with this virus, it is usually very severe. If there is an associated sore throat, it can last for three or four days. The virus might then move to the trachea and lungs, resulting in pneumonia that can last for five or six days. Breathing difficulties and a high fever are also likely at this stage of the illness. People infected might have one or more other symptoms including headaches, muscle pain and stiffness, fatigue, loss of appetite, chills and sweats, a rash, dizziness, stomach upsets, or nausea. Numbers do vary but around 90-98% of people have a fever, 80% a dry cough, and 30% have trouble breathing and extreme fatigue. Acute respiratory distress syndrome developed in about 29 % of patients infected. Even though pneumonia is involved, 80% percent of these cases are mild and the person doesn’t need to go to a hospital. About 15 % had severe infection and 5 % were critical. The Chinese CDC analysis of 44,672 patients reported that the fatality rate on healthy people with no reported comorbid conditions was 0.9%.  

In general, children, younger people, and young adults seem to get mild versions of the illness. Those at the highest risk are people aged 70 to 75 or older that have existing medical conditions such as cardiac problems or pulmonary issues such as emphysema. The virus is also more likely to affect people with weakened immune systems, kidney disease, diabetes, hepatitis B, and cancer.

Protecting Yourself

There are a number of ways that you can protect yourself from being infected by the Covid-19 virus. Many of these are things should be part of our daily routines to prevent the spread of germs and keep our bodies healthy.

  • Washing your hands regularly throughout the day with soap and warm water for at least 20 seconds each time will help to keep infection at bay. 
  • All surfaces of the hands need to be cleaned, front and back, between the fingers and under the nails. You can use an alcohol-based non-toxic hand sanitizer (60% alcohol-based) if there’s no soap and water available. However, always use soap and water rather than hand sanitizer whenever possible. 
  • Always wash your hands before eating and touching your face. This is something you may have heard quite often recently, but infection can be spread via the nose, mouth, or eyes if your hands aren’t clean. Admittedly, the virus can only survive on your hands for between and ten minutes but although that may not seem long you could touch another part of your body in that time and spread the virus. 
  • Things that are frequently touched in the home, workplace or other locations must be regularly cleaned and disinfected with wipes or cleaning sprays. The virus can survive for up to twelve hours if it falls onto a metal surface. On fabric it lives for between six and twelve hours but regular laundry detergent will destroy the virus.
  • Gargling can work to protect your throat from the virus. You can use a standard solution from the drugstore but really one made from salt in warm water is all you really need. 
  • It’s also a good idea to drink plenty of warm liquids such as tea rather than cold drinks, either with or without ice. 
  • Some people have also found bee propolis mouth spray to work well. Propolis is a substance created by bees to protect their hives against bacteria. As a spray it helps to relieve a sore throat or other mouth issues and strengthens the immune systems. It also encourages antioxidants in our bodies. Antioxidants are molecules that neutralize free radicals, which are unstable molecules cause cell damage. CAUTION: Propolis is not to be taken if you have a Honey or Bee allergy.
  • If you’re showing no symptoms and remain healthy, avoid contact with others that are sick since the virus is considered to be airborne and spreads very quickly. It’s believed that the virus can travel between six and eight feet when it’s airborne. 
  • If you are sick with the virus, avoid contact with other so that you don’t help the virus to spread. Stay away from work or school and isolate yourself at home until you can recover. 
  • If you’re coughing and sneezing, try not to do this into your hands but into the crook of your arm or use a tissue to cover your nose and mouth and ensure that tissues are safely disposed of in the garbage. 
  • If you’re sick and have no choice but to go outside your home, wear a mask that covers your nose and mouth. This will stop you from infecting others while you’re out. However, bear in mind that if you don’t already have the virus a mask this will not protect you from catching the virus from an infected person that isn’t wearing a mask.

To Follow: PREVENTIVE STRATEGIES AND TREATMENT SUGGESTIONS 

Resources

https://nas/content/live/hoffmancentre/medscape.com/viewarticle/924268.
https://www.nejm.org/doi/10.1056/NEJMc2001737
https://www.nejm.org/doi/full/10.1056/NEJMoa2001316
https://www.youtube.com/channel/UCMONnSecl445zOPy7-KXJKw?utm_source=Klinghardt+Institute+Newsletter&utm_campaign=72be1085f0-EMAIL_CAMPAIGN_2020_03_09_05_16_COPY_01&utm_medium=email&utm_term=0_e85a79fc40-72be1085f0-154835213&mc_cid=72be1085f0&mc_eid=980e013edf 
 https://www.medscape.com/viewarticle/924268.
https://www.arcgis.com/apps/opsdashboard/index.html#/bda7594740fd40299423467b48e9ecf6
 https://www.cdc.gov/coronavirus/2019-ncov/locations-confirmed-cases.html
http://cdc.gov/media/releases/2017p1213-flu-death-estimate.html
Li Q, Guan X, Wu P, et al. Early Transmission Dynamics in Wuhan, China of Novel Coronavirus-infected Pneumonia. N Engl. J Med. 2020 Jan 29 
 https://www.cdc.gov/coronavirus/2019-ncov/about/symptoms.html
 https://www.cdc.gov/coronavirus/2019-ncov/about/prevention.html?CDC_AA_refVal=https%3A%2F%2Fwww.cdc.gov%2Fcoronavirus%2F2019-ncov%2Fabout%2Fprevention-treatment.html

Podcast: Mast Cell Activation Syndrome With Dr Bruce Hoffman

I was recently interviewed for The Dr. Hedberg Show, where we spoke about mast cell activation syndrome and how exactly the condition is diagnosed. In this podcast, we reviewed the similarities that exist among certain conditions (fatigue, brain fog, and GERD to name a few) and how they may be indicative of mast cell activation syndrome.

 

Dr. Hedberg: Well, welcome everyone to “Functional Medicine Research.” I’m Dr. Hedberg. And I’m really looking forward to today’s conversation with Dr. Bruce Hoffman. He’s a board-certified physician, and he has a Fellowship in Anti-Aging Medicine, as well as a Master’s Degree in Clinical Nutrition. He’s a certified functional medicine practitioner. And, one of the really interesting things about him is that, in addition to his clinical training, he studied with many of the leading mind-body and spiritual healers of our time. People like Deepak Chopra, Paul Lowe, Osho, Ramesh Balsekar, and one of my favorites, Jon Kabat-Zinn.

So, Dr. Hoffman, you shared the stage with Dr. Deepak Chopra and Dr. John Demartini. And he continues to spread his inspiring vision of healing and wellness with audiences and patients around the world. So, Dr. Hoffman, welcome to the show.

Dr. Hoffman: Thanks very much, Nikolas. I’m glad to be here. Thank you.

Dr. Hedberg: Great. So I’m really looking forward to this discussion on mast cell activation syndrome. It’s something I haven’t seen a lot of in my practice. I have heard a number of lectures on this and read quite a bit about it. And it seems to be an area of your expertise. So why don’t we jump right in and just talk about what mast cell activation is, and how is this condition diagnosed?

Dr. Hoffman: Sure. I first got interested in mast cell activation syndrome when I started to work with a cancer patient advocate by the name of Dr. Mark Renneker out of San Francisco. And he alerted me to the connection between cancer and mast cell activation syndrome, particularly in gynecological cancers. And then put me in touch with Dr. Lawrence Afrin, who leads one of the major sort of advocacy groups for mast cell activation syndrome as opposed to systemic mastocytosis, which I’ll explain in a bit.

And so, I’ve been for the last three to four years working with Dr. Lawrence Afrin’s group and learning to understand the implications of mast cell activation syndrome in most of the patients that we see. Which are chronic multisystem, multisymptom patients who, as you know, have been everywhere and remain frustrated with the one disease, one drug paradigm that we learned at medical school. So, what I learned over time was how to separate between two specific conditions, one called systemic mastocytosis and the other called mast cell activation syndrome.

Mast CellBut before I begin with that, I’d like to say that mast cells are part of, they’re produced in our bone marrow, and they’re part of our immune system. And they make up a very small percentage of it. And they act as defense structures against incoming invading pathogens. So, anything that comes into our environment or into our biome, mast cells are often at the first line of defense. And they were actually discovered a long time ago, 1878, I believe, by Paul Ehrlich. And he called them mast cells because they were fat and puffy.

And the word mast in Greek means breast or the German means masticate. So, this is how the name mast cell got generated. Just for your North American readers, I say mast, and most people don’t know what I’m saying. So, it is mast in North America. People often don’t know mast cells, what I’m saying.

So, these were originally discovered by Paul Ehrlich when he developed specific staining for them. And since then, they sort of lingered on in the literature. They were linked early on to cancer, but that sort of faded out of the picture until it was resuscitated by some Italian researchers who now are doing massive amounts of work on mast cell activation syndrome and cancers. And then it really sort of resurfaced in the 1990s and didn’t really gather steam until about 2007, when two, you know, researchers and clinicians put together sort of a consensus statement on what constitutes MCAS.

There are two different schools of thought and they do tend to conflict with each other in terms of the diagnostic criteria. But basically, mast cells being part of the immune system, and regulating many of the incoming so-called antigens or toxins tend to be distributed in almost all tissues, but nowhere quite as much as on mucosal surfaces: so eyes, mouth, skin, GI tract, bladder, etc. They’re also found in other tissues, you know, lungs and heart tissues, and brain, many mast cells are activated in the brain.

And so, when they get triggered, they do tend to release many, many mediators of inflammation. And it was estimated that there were over 200 mediators of inflammation that get released by these mast cells. But Dr. Afrin in a very recent post, as of last night, said that he’s now changing his opinion that he believes there are over 1,000 mediators released by mast cells. All these inflammatory mediators like histamine, like proteases, prostaglandins, leukotrienes, all these inflammatory mediators that then set up this multisystem, inflammatory response, which can confuse diagnosticians particularly if you have been trained in single organ, you know, specialties.

So that leads to the sort of difficulty with the diagnosis as people present with many different symptoms. And unless you have an understanding of mast cell activation syndrome, and a method of sort of sifting through the multiple systems they can present, you can often get very confused and misled. So, the recent, you know, people speaking about mast cell activation syndrome is an attempt to bring some coherence to this somewhat disorganized field. And hence, establishing criteria for the diagnosis, lab tests, and then treatment protocols. So now it’s coming into its own and I think you’re going to hear a lot about it in the years to come.

Dr. Hedberg: Mm-hmm, so we’re talking about illnesses that may be so-called mystery illnesses, and multifactorial presentations like gut issues, skin, brain, and things like that. Can you just let everyone know some of the overlap that you see in various conditions in your practice that would specifically indicate mast cell activation syndrome?

Dr. Hoffman: Yeah. So, mast cells, when they release the inflammatory mediators, can present locally or systemically. So, a local condition would be something like hives, urticaria, or interstitial cystitis. Or it can be systemically like people can present with cognitive symptoms. So, they’ll have fatigue and brain fog, and associated GI symptoms, like GERD. GERD is a potentially very big diagnostic category for mast cell activation syndrome or, you know, the irritable bowel syndrome. Even the autoimmune diseases of Crohn’s disease and ulcerative colitis have been linked to mast cell activation syndrome.

Asthma is another one. Asthma, you know, if you analyze all the triggers of an asthma response, and you identify them, like, for instance, mold, allergy or mold inflammation, which are two different criteria, and you remove the trigger and downregulate the mast cell activation potential, I can’t tell you how many cases of asthma have been absolutely shut down when you treat the mast cell activation. It’s very rewarding. The same goes for GERD, the same goes for irritable bowel syndrome. The same goes for anxiety and cognitive decline. When you target the triggers and downregulate the mast cell activation, it’s very rewarding to treat these patients, and they’re very grateful. Angioedema, another one, canker sores another one, there’s many, many symptoms in all the organs that can present with this syndrome.

Afrin has written a chapter in a book. The book is called “Mast Cells,” the editor is David Murray. The chapter is chapter…I think it’s chapter 6, and it’s called Presentation, Diagnosis and Management of Mast Cell Activation Syndrome. And at the back, he gives a long, long list of every organ that can be affected from ophthalmic, to lymphatic, to pulmonary, to cardiovascular, and just goes through all the systems. Even fibromyalgia, even osteoporosis, headache, all the mood disorders, dysmenorrhea, endometriosis, many of the hematological conditions, the immunological conditions. There’s a huge long list of different organ systems that can be affected that present as isolated diagnoses to specialists, but often they miss the overriding pathophysiological basis to the condition.

And our training as MDs makes us very aware of what is called systemic mastocytosis, which is when the mast cell from a clonal perspective within the bone marrow becomes amplified. There’s actually a mutation of the KIT gene. And the mast cells become very high in numbers. So, there’s increased numbers of mast cells, which is systemic mastocytosis, which is very different from mast cell activation syndrome, which is an abnormal reaction of the mast cells, not an increased number.

So, I can’t tell you how many patients come back to me after having got the diagnosis of mast cell activation syndrome by myself with the criteria I use, go to the specialties, go to the hematologist, go to the gastroenterologist, or pulmonologist, who then does a serum tryptase and even sometimes go as far as do a bone marrow biopsy, and then come back and say, “Oh, that diagnosis is incorrect, he doesn’t or she doesn’t have systemic mastocytosis.” Systemic mastocytosis is a very rare condition, I’ve never seen one in my life. But I see almost twice a day, mast cell activation syndrome. Dr. Afrin believes that probably about 30% of the population gets affected to some degree or the other.

Dr. Hedberg: And are there any theories at this point about why mast cells become so overactive in an individual’s body. Any good research out there on that?

Dr. Hoffman: Well, there’s lots of speculation. And the most common hypothesis is that we do live in a much more sort of, you know…we’re inundated, so to speak, with multiple stressors far more than our capacity to withstand them. Our immune system, it just gets triggered because of multiple stressors. And there are many triggers for mast cell activation. Poor sleep. Stress is one of the biggest triggers. Food, I mean, food is incredible in its ability to trigger the mast cells that are in the mucosal surfaces of the mouth through to the anus.

So, we believe that our ability to…..we can no longer withstand the onslaught of our ongoing multiple stressors, whether they be environmental, emotional, nutritional. We just are in this constant state of over reactivity if you’re genetically predisposed. Now, Dr. Afrin doesn’t believe it’s necessarily a genetic condition that is transmitted through the germline. But he believes there are mutations in some of the mast cell production. And Dr. Molderings, who’s published a lot of papers with Dr. Afrin, has done a lot of research on the so-called KIT mutation, not in the bone marrow, but within the mast cells themselves, and has shown that they are these sporadic and spontaneous mutations that occur. Why those occur? I can’t say. I don’t know the answer to that. Yeah.

LAB TESTS

Lab Tests

Dr. Hedberg: So, there’s a number of functional medicine practitioners listening to this, so let’s just talk a little bit about lab tests, and some of the ones that you’re using and the ones that are beneficial. Obviously, CBC might be beneficial with elevated eosinophils, basophil, or possibly those are normal, histamine testing and things like that. What are some of the top tests you’re doing in your practice to identify this?

Dr. Hoffman: So yes, we do all the normal standard CBC and electrolytes, and liver function, etc., but those don’t usually yield what you’re looking for. And one of the challenges is that the lab testing positive results fluctuate depending on whether the symptoms are being expressed or not.

So, the first thing is you want to try and catch a person in a flare. Well, that’s difficult you know. So that’s the first challenge. And many of these tests need to be repeated over and over again until you get what Dr. Afrin likes to identify as two positive lab tests, which I’ll explain in a second. The second challenge is that you have to process a lot of these labs on ice. You have to have a refrigerated centrifuge to get accurate results. And it took me two years to get a refrigerated centrifuge. And as soon as I was able to, the positive rate of my lab has skyrocketed. Many of these lab specimens are very poorly handled. And, you know, they sit around for days and you’ll get these false positives for sure, false negatives, I mean. Sorry.

And also, a lot of the mast cell activation syndrome people or patients, they don’t always cause these abnormalities in the lab tests. Positive lab work is only obtained around 20% of the time. So, it’s quite frustrating, you know. But if you want to get lab work tests, I use sort of the minor and the major criteria. There are 10 major lab tests that we do. And then depending on the budget, we do the top 5 or 10, if we can.

And the tests that I recommend are plasma histamine, has to be chilled. And you should catch a person who’s in a flare. If they’re not in a flare, it will very often be negative. And you’ve also got to stop some of the inhibitors of histamine for five days prior to the test. Otherwise, you will get suppression of the histamine response. If people are on, you know, H1 or H2 blockers, you won’t get a positive test. And many people do take them intermittently you know.

Then we look for N-methylhistamine, which is a 24-hour urine also needs to be chilled. And then probably the one test that I get the most positives out of is the prostaglandin D2 plasma test, also must be chilled. And for that test, patients need to be off of all nonsteroidal anti-inflammatories, Motrin, Advil, or aspirin, or salicylate-containing foods. They can’t have a high salicylate diet. Anything containing aspirin for up to five days.

And then the one that is also done is the prostaglandin D2, 24-hour urine, also must be chilled with the same criteria of having to be off of all these medications. And then the last one is chromogranin A, and for that test you have to be off proton pump inhibitors and H2 blockers like famotidine. So, if you do go on proton pump inhibitors and so forth, they can falsely elevate chromogranin A.

And then after that, we’ve got prostaglandins 11 beta F2 alpha, a 24-hour urine, also must be chilled. And then the one that most MDs know about, which is serum tryptase. But this is rarely elevated in mast cell activation syndrome. It’s very important that every doctor who wishes to sort of work with mast cell patients knows this to be true. Because if the tryptase comes back normal, very often, the entire sort of clinical diagnostic differential gets thrown out, “Oh, they don’t have mast cell activation syndrome.” Big mistake, big, big, big mistake.

One of the criteria, one of the two different schools of the consensus criteria, they say that you have to have the serum tryptase elevated over 20% of baseline, or have a baseline greater than 15 nanograms per mil. But Dr. Afrin, who’s somewhat opposed to the consensus statement put out by Aiken and others, he highly disputes this finding and he doesn’t agree entirely that this is one of the main criteria to make the diagnosis. And I tend to agree with him.

Leukotriene E4, a 24-hour urine. Plasma heparin because heparin gets secreted by mast cells. And then a blood clotting profile, thrombin, PTT and INR is often done. And those are the top 10 and then after that, there’s many others; anti-IgE receptor antibodies, pheochromocytoma workup. We often do factor VIII deficiency workup, we do urinary metanephrines often. We almost always get an immunoglobulin profile IgG, IgA, IgE, and IgM. You might see IgE elevated or not. Often you won’t have an elevated IgE. So many people think “Oh, if a high IgE, then it can’t be this.” But that’s not true you can get a non-IgE-mediated mast cell activation. People then do bone marrow biopsies. People can do gastrin, serum gastrin levels. And then as you mentioned, the CBC with eosinophils and basophils can sometimes are elevated. Antiphospholipid antibodies are also often done.

And one test I like to do in the functional world is the Dunwoody Lab test for zonulin, histamine, and the DAO enzyme activity because that’s the diamine oxidase enzyme that sits on the villi that can be genetically compromised. Or because the villi are compromised, you cannot produce enough diamine oxidase. And that’s when you start to put people on low histamine diets and use the HistDAO enzyme to help break down any remaining histamine in food.

But I can tell you the one test that I tend to rely on more than any other right now, apart from the serum and urine test, is to get restaining of any gastric biopsies people have done. This has been overwhelmingly sort of helpful to some of my chronic GI tract patients in particular. So they would have gone, you know, to a GI specialist, they would have had the normal Giemsa tissue stain, and they comment on lymphocytosis. But they don’t actually comment on mast cell activation. And unless they get what’s called the CD117 stain, you won’t isolate the mast cells.

And almost 90% of people that I’ve clinically suspected of having mast cell activation syndrome turn up once they have their biopsies restained of having over 20 cells per high-power field being positive for mast cells. Which is the cut-off criteria that’s been agreed upon by numerous researchers, highly contested, by the way, by some pathologists and gastroenterologists. But we use a cut-off point of greater than 20 mast cells per high-power field to make a diagnosis of mast cell activation syndrome, particularly in the GI tract. The mast cells are very rich in the GI tract, particularly in the duodenum, not so much in the gastric tissue, but particularly in the duodenum.

So, if they ever had a biopsy in the duodenum, phone up the pathologist or write a letter and say, “Please will you restain for the CD117 stain.” And as I said, probably 9 out of 10 come back positive, very helpful. And then the patient sees that and the penny drops then they start reading up all the literature. And then they get on board for the treatment protocols which are, you know, quite…it can be onerous, and they can be extensive. But they’re very clearly delineated with multiple challenges along the way. Because people react to the medications and/or the supplements that you give them because that’s the nature of the condition.

EXCIPIENTS

pills

So, they’ll come back and say, “I can’t take the H1 blocker because I got worse.” Well, most of the time, it’s because it’s the excipient, the additive, the filler, or dye inside the medication that triggered the mast cell syndrome and it’s not the actual problem. You know, they’re not reactive to the supplement, they’re reactive to the excipient within the supplement or the drug. So those are some thoughts.

TREATMENTS

Doctors in meeting

Dr. Hedberg: Right. So once you’ve identified that someone has this syndrome, let’s talk about some of the natural treatments. You just mentioned that some of them are very difficult to follow. And some of these patients are…there’s probably a fair amount of trial and error with some of these patients figuring out what works for them. So, can you just talk a little bit about some of the treatments you’re using?

Dr. Hoffman: Sure. One of the hallmarks of this condition and one of the setups in my interaction with patients is a description of the complexity of the diagnosis and the challenges. And if you don’t have that conversation, you’ll often get a frustrated patient because they’ll come back with flare-ups and they understand it. So, I encourage that all your practitioners who wish to dive into this field really wont understand how patients can flare and how they

may have multiple triggers at any given time. And that the treatment may need to change, and that they mustn’t become frustrated, they must just stay for the long course. And they are sort of part of the team of trying to work out these multiple moving targets.

So the education is number one. I have two handouts, where I’ve described mast cell activation syndrome and mast cell activation syndrome treatment. I make sure they’ve read that. If they’re more interested, I give them Dr. Afrin’s book, “Never Bet Against Occam.” There are many patients who love to read because it’s filled with case histories. So once they get sort of an insight into other cases of complex presentation, they get encouraged to push on. So, education is first.

Second is to try and identify the triggers that trigger their mast cell activation. And this is one of the greatest challenges because there are many triggers from, you know, hot, too much heat, too much cold, stress, poor sleep, as mentioned. And then we get into the more obvious triggers, chemicals, heavy metals, dietary antigens, and then infections or inflammatory triggers like mold.

So, part of the process of working up mast cell patient is not just diagnosing the syndrome, but also trying to work up the triggers. So, in most patients, I do multiple food sensitivity profiles. I don’t just do IgG. I do IgG, IgG4, I do the so-called LEAP test. I do…am I allowed to mentioned lab names on your podcast?

Dr. Hedberg: Yes, definitely.

Dr. Hoffman: Okay. I do the lymphocyte sensitivity tests, the LEAP test. I do, as I said, IgE testing, IgG, IgG4. And I do Cyrex Lab food, I do the 10x, I think it is, with all three panels looking for dietary antigens. So, the Cyrex panel is different from the Meridian Valley food panel. Meridian Valley says it’s an IgG, IgE panel, but I disputed that once, and I’m not too sure there’s much IgE in the Meridian Valley panel. I think it’s more IgG. Whereas the Cyrex panel is more IgG and IgA. And you’ll often get contradictory findings. They’re very frustrating. That’s part of why allergists like to just throw them out, they say, “Don’t bring me this nonsense.”

But once you’ve been doing functional medicine for a long time and you have an understanding of the different complexities of dietary triggers, you can look at these profiles and you can sort of pull out the relevant data. And I encourage those of you who may be new practitioners is not to take each test literally. So, if they have a high say a banana on the one test and it’s not on the other, you want to look at the general profile of the dietary antigen testing. You don’t want to be too specific because if you get too specific, most people will have nothing left to eat. So, I’d look at the dietary antigens and most of the time, but not all the time, controversially or not, I tend to put people on the Paleo, autoimmune, low histamine diet for the first month or two. And I can’t tell you how many people immediately settle down just on that one intervention.

And I take out the high histaminic foods, and that is a very important part of it. And one of the great crazes right now is to use all these fermented foods to heal gut permeability, but it’s a disaster for the mast cell person. So, I’m always pulling people off sauerkraut, and kombuchas, and bone broth, it’s a huge trigger. So, all the fermented foods, and then all the leftover foods. As foods break down, then the proteins, the histamine gets broken down by bacteria that releases histamine. So, leftovers are no, no. We also ask people to, once they’ve cooked a meal, to put in the freezer and then to take it out and unfreeze it, but not to leave it sitting in the fridge for days.

And then things like tuna fish, huge triggers, the nightshades (tomato, potato, eggplant, peppers), huge triggers in many people. And even amongst, you know, some of the vegetable kingdom, you know, peas and beans can be triggers of mast cell activation. And so, you have to be careful when you look at the testing, you’re going to sort of see… when I look at particularly the Meridian Valley test, you can often see a mast cell patient, they’ll show up, all the legumes will be positive, all the histaminic fruits will be positive. Candida will often be positive.

And there’s like a trend you can see it and then immediately, you know this is a mast cell activation profile for food antigens. So, we remove the foods, we always treat gut dysbiosis as you know. I use two different labs for gut analysis. I use the Genova GI Effects, and I use the Diagnostic Laboratory Solution’s GI-MAPs. They contradict each other all the time, you know, one will have a zonulin of 700, the other one has zonulin as normal.

But then you just got to use your clinical acumen and your experience and correlate the labs against the symptom profile of the patient and do the best thing. I do tend to use Dunwoody Labs for the zonulin, the DAO, and histamine, as I mentioned. And then the second page of that test is all the LPS, the lipopolysaccharides, to see if there’s been any endotoxemia. And if there’s been any bacterial endotoxemia, you start entering into a whole new world of immune upregulation, which, you know, you have to down regulate in your treatment protocols and heal the leaky gut, etc. which I’m sure your listeners are very well aware of.

PHARMACEUTICALS

Stethescope sitting on open book

So A. is education, B. is testing, C. is removing the histaminic foods and downregulating inflammation in general. And then we get to specific treatments. And I differentiate between pharmaceuticals and botanicals. I tend to preferentially go to the pharmaceuticals to start with because they work quickly, if they’re going to work. And I tend to secondly, add botanicals. But I tend to be an MD, you know, it’s just my preference. I’m sure many naturopaths would go the other way. And many patients refuse to do pharmaceuticals and then I just have to use botanicals.

Pharmaceutical perspective, they must be compounded, you can’t get over-the-counter. Although paradoxically, some people do better on the over-the-counter than they do on the compounded. This is one of the challenges is what you think is going to work doesn’t work. This is why try, try, and try again, you know.

So, first thing, H1 blockers. Histamine 1 blockers, and I tend to use levocetirizine in a dose of 5 milligrams going up to 7.5, even 10 milligrams. And I think the trick to using H1 blockers is you have to dose it round the clock. You know on the box it will say “24-hour relief” that’s not true. You need to dose it at least 12 hourly and sometimes 8 hourly to create full round the clock mast cell blockade. And you’ve got your H1 blockers, you’ve got your first-generation and your second-generation. The first-generation H1 blockers like Benadryl, or ketotifen, cross the blood-brain barrier and have a sedating effect so those are often given at night.

I love to use ketotifen, I use lots of it on a dose ranging from 0.25mg, which is a homeopathic dose almost, right up 2 to 3 milligrams at night. And if there’s any issues with insomnia, it works like a dream. It’s absolutely spectacular for sedation. The problem is sometimes they over sedate when you have to lower the dose. But it also downregulates mast cell activity at night. So first-generation H1 blockers, I prefer ketotifen over Benadryl. Second-generation H1 blockers, I use levocetirizine as my preferred go-to H1 blocker.

And then I use H2 blockers, and I use famotidine in a dose of 20 milligrams twice a day, sometimes going up to three times a day. And this tends to downregulate all the mast cell activation activity in the GI tract.

One of the little tricks of the trade I’ve picked up over time is if you do the Genova GI Effects, you’ll often see that eosinophil protein X marker a little high, that’s almost a slam dunk for mast cell activation…not always because there’s other things that trigger that. But if you see that with a constellation of other positives, you follow that marker closely because when that starts to downregulate, you know, you’ve got your mast cell activity under control. So those are my first two go-to medications H1 and H2 blockers.

Probably my next is cromolyn. Cromolyn is a mast cell stabilizer particularly for people who are very food sensitive. You take it before meals. I give it along with the HistDAO enzyme. And that dose you can take it from 100 to 300 milligrams, and that can also be a major game-changer in many people’s lives. You have to play with the dose, you have to play with the different companies that make it. It’s a bit of a tricky thing, but it can really have a huge effect on downregulation of mast cell activation.

And then the fourth drug that I use, and many patients have come back to me with this fourth drug, Singulair, montelukast. This downregulates leukotrienes, which are one of the thousand mediators of inflammation. One of the things that we’ve noticed in mast cell syndrome is that when you think a patient has an upregulated leukotriene pathway, which is typical for asthma, you give the montelukast or the Singulair and the asthma is managed.

Well, it so happens that one can’t predict which class of drugs is going to work on which mediator. So, if you give a mast cell stabilizer for food sensitivities, guess what? The asthma may go away. Or if you give Singulair for asthma symptoms, the hives go away. So, thereis crosstalk amongst many of the mediators. And it’s a great mystery as to why that occurs, nobody’s worked it out yet. Dr. Afrin said he doesn’t know. He doesn’t know why this happens and he’s going to keep researching till he works it out. So those are the four drugs I use, probably the top four drugs I use over and over again.

SUPPLEMENTS

supplements

Nutraceuticals, of course, Quercetin, tops the list, no question about it. There’s a product called Natural D-Hist made by Ortho Molecular, that’s my go-to supplement over and over again. Two, three times a day seems to be the magic dose. And then using HistDAO one to two before each meal that seems to be the number one nutraceutical.

Number two would be vitamin C, either orally or intravenously, sometimes can have a huge benefit as well. Green tea has an effect. Turmeric or curcumin can have an effect but some people react to it. If you see on the food sensitivity profile, if you see that it’s positive in at least one or two tests, you can use it, but you want to be cautious because it can sometimes activate mast cell activation. You got to be careful with turmeric. Resveratrol is another one. And chamomile tea has some calming effects. So those are my sort of…they’re called the A team of my nutraceutical approach.

And the B team is sort of…there are many others like luteolin, Ginkgo biloba, Pycnogenol. Pycnogenol is a great one too I use quite a lot of Pycnogenol. Feverfew works. There are many things that can work. So, I pick and choose and go through them and change them. I ask everybody to first identify the triggers, if they can, and then to start rotating the pharmaceuticals and/or nutraceuticals and see which has the biggest blockade effect. And people soon work it out, you know. You’ve got to get a good compounding pharmacist on your side. And you got to make sure that they don’t fill the compounded pharmaceuticals with lots of fillers and dyes because some people react to that.

And then one of the other challenges…I just had a very seriously ill patient present to a hospital with anaphylaxis and she was on polypharmacy. She was on 10 different drugs. And many of the drugs she was on were triggers for her mast cell activation. And those were never identified as triggers by her medical team. And so, we asked the pharmacist to go through each drug and look for the additives. Many of them had iodine in them, many of them, there was soy extract base, and those had to be changed accordingly. And she settled down. So those are some of the challenges I have.

Dr. Hedberg: And one of the drugs that wasn’t mentioned was LDN, low-dose naltrexone, I know some practitioners are using that for this. Have you tried that or used it?

Dr. Hoffman: I do use low-dose naltrexone. It’s part of the many other…there’s many other alpha-lipoic, and so forth. And LDN is definitely part of it. And LDN has an effect particularly on autoimmune responses and downregulation of an inflammatory response. It’s not my first drug though, I don’t go to LDN as my first line. I use it if there’s autoimmunity and lots of gut permeability then I bring in LDN. And LDN is challenging because people give it at night but it can be very activating. Just yesterday, I saw a patient who since she started LDN hasn’t slept a wink. We changed it to morning.

Dr. Hedberg: Right. So how do you deal with the psychoneuroimmunology aspects of this condition? You know, some people, they develop a deep identification with their illness, and then they develop a lot of beliefs about things that they’re sensitive to. And we’re not saying that it’s all in their head, but we do know from the PNI research that what we believe, and what we emphasize, and think about, and focus on can affect the immune system and our biochemistry. So, are you using any kind of cognitive behavioral therapy or things like that, that could help some of these patients who are so focused on their condition and their hypersensitivities?

Dr. Hoffman: Yeah, because this opens up a huge area of the work that I’ve been forced to look at over time and for which I use quite a complex algorithm to sort of diagnose and treat. I’ve studied Ayurveda for years and I use the Ayurvedic model of layers and levels of healing. And when a person presents with specific belief systems around their condition, I have to sort of look through the layers and levels of what may be playing a role in that belief system.

Just very briefly, I tend to look at these diagnostic criteria. I look at the family system to see what family system they were born into and what beliefs the family system carried. Because I can’t tell you how many cases get resolved when we do what’s called family constellation therapy and look at the entanglements of the forefathers and ancestors, and how those epigenetically got transferred down to the offspring. Very profound piece of work, I cannot emphasize it enough. And I encourage all functional medicine practitioners to get a very sound footing on the epigenetic transfer of family system trauma and the entanglements that can be inherited, completely silently, unknown consciously to the patient, only uncovered through work in family constellation therapy whereby certain methodology is employed to determine what these factors may be. So that’s number one.

Number two, I look at early developmental trauma patterns, and ego strength, and defense systems of a patient. And I employ a number of ways to identify that. The number one system that I look at is looking at defense structures of the patient and the ego strength. And you can tell after, you know, half an hour, is this person…do they have good ego strength? Are they resilient or they do have a fragile ego structure? And I send people for quite a lot of psychometric testing to establish some of these criteria.

I have a psychologist I work with who is able to help me with some of the psychometrics. And we even do, you know, some of the simple psychometrics testing, and even the Burns Inventory, the ACE Questionnaire. When we do qEEGs, we do the in-depth psychological assessment that’s provided by the CNS Vital Signs software to look at which of their psychological profiles are most dominant. Is it anxiety, OCD, is it depression, etc.?

So we look at that level of their development, the ego strength and their defenses. And then we look at early developmental trauma. And as you know from literature, people who have early developmental trauma have very different brain structures. They have, you know, very often this hugely enlarged anterior cingulate gyrus. They have in their beta, their fast brainwaves, there’s two to three standard deviations above normal. Their capacity to inhibit the sort of reptilian, limbic brain is diminished. And those are challenging patients, very challenging, and you have to address that level of healing.

This is not a biological intervention. There’s not much you can do biologically unless you identify what the core ego strength resilience of the patient is. How much projection of will the patient has? Many patients will sit in front of you, project the will to heal on you. And that’s a slippery slope. If they are not invested in sort of figuring it out on their own with you, you have a problem on your hands, you know. And patients will often project their early developmental trauma of parents on to you, whether it’s positive or negative. Best to have a positive projection in the beginning. But if you are the evil father that you get projected onto you, you’re in trouble.

So it behooves all of us as functional medicine practitioners to kind of try and identify, who is this person sitting in front of me, what did they inherit, how was the early developmental life? And then what defenses are they employing to keep away feelings they don’t want to feel? And I use a psychological technique called ISTDP. And I refer that out to somebody who’s specialized in it. That person I use is also very well versed in CBT. But CBT, without the underpinnings of the complexity of the presentation, can sometimes not stick. It can be very helpful to some, but for those who are fragile with projection of will, CBT will not hold. You can’t use CBT, it washes off them, you know, they won’t be able to hold that.

The next thing I do, I do NeuroQuant MRIs on everybody as well as a qEEG. And I look at the brain patterns and I can’t tell you how helpful that is. If you’ve got this high beta brainwave, and you’ve got maybe high theta brainwaves with not enough alpha, you’ve got work to do. And then you correlate that with the NeuroQuant MRI, and we look particularly for the amygdala upregulation. Many of these people with anxiety, OCD, and belief systems around the illness, who are multiple chemically sensitive and environmentally sensitive and are triggered by everything, will have a very…..the amygdala will be 2 standard deviations above normal, being like in the 97th percentile. The thalamus will be in the 97th percentile.

Hand holding image of brain

And the thalamus is rich in mast cells. So, when the thalamus is high, the amygdala is high, you want to ask about mast cell activation, and you want to ask about early developmental trauma. Because the amygdala gets increased in size when there’s repeated stresses on the fear-based part of the limbic brain. And if I see that, I often start inquiring about other techniques to downregulate the amygdala. And that we use DNRS, as you’re probably aware of the Dynamic Neural Retraining System.

We do refer people to that, we do neurofeedback, we do biofeedback, we do vagal tone stimulation. And we start to bring in the Porges polyvagal theory of, you know, sympathetic, parasympathetic dorsal vagal shutdown. And we try to work out where in this constellation of symptoms is this patient presenting? Are they in dorsal vagal shutdown with a rigid defense and sort of no will to get better? Are they getting secondary gain? That’s a very different patient from the one who’s, you know, loved by the parents, no developmental trauma, is loved and seen by a mother, develop appropriate right prefrontal cortex to self-regulate, has financial resources, is loved by the husband, the kids are doing well, they have a home to go to. This is how it works.

And we have to work out who are we sitting in front of when it comes to addressing some of these complex beliefs about, you know, is this a biological overreactive reactive mast cell syndrome, or is this a psychologically overreactive amygdala? Or is this person highly defended? Do they have the ego structure to take on what I’m about to tell them? It’s complex, as you know. I think that…

Dr. Hedberg: Right. And it’s a difficult situation for everyone because, you know, we don’t really get a lot of training, if at all, in all these things you just mentioned. So, we have to learn these things on our own, learn how to incorporate them. And then at the same time, present these to the patient in a way that isn’t telling them that you know, “This is just all in your head” or helping them understand that some of this could be due to your childhood and the way that your parents treated you, and all these kinds of things that happen. And I have done a few podcasts with some experts on adverse childhood experiences and things like that.

So, it’s refreshing to hear you talk about all these things, and it just creates a very complex picture on how to put it all together. And you know, like you said, they come to see you and they put all the burden on you for the healing. And then, you know, you come back with recommendations that, “Well, we need to work on your childhood trauma or your relationships,” and things like that. So, this is a very difficult, you know, condition to take on as a practitioner. I mean its massive amount of mental and emotional output that you have to take on.

Dr. Hoffman: Yes, one of the commonest words I see in the referrals back from specialists is this so-called, awful term, somatization disorder. And it’s just not true 90% of one of the most stressful diagnoses for one of these patients to get is the so-called somatization disorder but it’s often handed out. You know, and, “Yeah, it’s all in your head,” this is so awful. There may be a component that is filtered through the neurological pathways and then synapses. And they may tend to have an upregulated sensory system that processes things somatically. But it doesn’t mean to say that we have to discard this as all psychological, which is very often the insurance companies like to do things like that and some of the specialties too.

I recently referred a patient to a psychiatrist for insurance purposes and I sent five articles plus a written response. “Please do not diagnose this patient as being psychiatric, he has the following conditions.” And then we listed the mast cell activation, the mold sensitivities, electromagnetic sensitivities, etc. And I sent him five papers in support of the validity of this diagnosis. I haven’t heard back yet; I’m waiting to see what the response is. We often have to advocate for our patients in this way because they do present with neuropsychiatric manifestations, but it’s as a consequence, it’s not the cause. Although there may be some issues which provoked, you know, an expression of a mast cell disorder, but you can’t separate you know, mind-body, you’ve got to work with the whole continuum.

Dr. Hedberg: Exactly. Well, this has been really excellent. How would you like people to find you online, what’s your website and contact information?

Dr. Hoffman: The website is hoffmancentre.com. And the phone number here is 403-206-2333. That’s the phone number for my clinic. I do have a number of blogs on my website, and I post to Facebook and Instagram. But my website has a lot of the histaminic articles as blogs, so they can access them on there.

Dr. Hedberg: Excellent. So, to all the listeners, I have created a transcript of this conversation, which will be on drhedberg.com. So just search for Dr. Hoffman and you’ll be able to get the entire transcript there in case you missed anything. Well, thanks for tuning in, everyone. Talk to you next time. This is Dr. Hedberg, and take care.

Functional Medicine Podcast: Healing Wisdom With Dr Bruce Hoffman

Dr. Bruce Hoffman joins Pandora Peoples on WOMR and WFMR radio to discuss the origins of The Hoffman Centre and the benefits of the integrative approach to functional medicine. Dr. Bruce Hoffman utilizes the ayurvedic model through a program he developed called, The Seven Stages of Health & Transformation™ that brings to light the hidden causes of what may be making you sick, and what you can do to heal yourself.

Full Transcript

00:12

You’re tuned in to 92.1 WOMAR, FM Provincetown and 91.3 WOMAR, FM Orleans, the voice and spirit of Cape Cod. I bid you welcome to another episode of Healing Wisdom. I’m your host Pandora people’s chartered herbalist and psychic medium healing wisdom explores Mind Body soul connections as we discussed the healing effects of the arts, metaphysical concepts, intuition and the spiritual aspects of everyday living. Healing wisdom begins in the heart. Our theme music is provided by mystic Pete

01:00

Hello, hello, hello, hello, Cape Cod and beyond. My guest today is functional medicine Dr. Bruce Hoffman, founder of the Hoffman Center for Integrative and Functional Medicine. His center encourages people to become involved with the process of health, restoration, self-master their health issues and make health a primary value. Dr. Hoffman has dedicated himself to research and education in cutting edge health care wellbeing and living a meaningful life. Welcome, Bruce, thank you so much for being with us.

01:28

Excellent. Thanks Pandora

01:29

So first off, what inspired you to go from an allopathic practice or a traditional practice to an integrative approach to functional medicine,

01:39

Curiosity more than anything and frustration at the drug-based model, you know, when you go to med school, you learn this is called n squared d squared, medicine = name of symptom name of drug. Although it’s interesting, it really limits your diagnostic and therapeutic options. So, when a patient presents say with complex illness, where there’s a mind -associated issue, and or environmental issue, nothing you can do with a drug based model, you know, you just diagnose a disease find a drug or refer to a specialist. And that’s it. It’s over. Whereas in an integrative model, you look far and wide for what they call in functional medicine, antecedents, mediators and triggers. So, you look upstream, you know, and in a functional model that I use functional medicine workup that I use, I’ve expanded beyond pure functional medicine into what I call the seven stages to health transformation. And I use an Ayurvedic model to explain the different layers and levels that come to the table when you’re trying to diagnose and treat somebody. Anywhere from the family systems into which they originated into the early emotional experiences and ego development and defenses, through to unresolved emotional traumas through the brain states and brain functions and then into biochemistry and toxicology. So, it’s a much broader diagnostic roadmap that we use ana a therapeutic roadmap, and I just found the drug-based model limiting. I enjoyed being a traditional MD. But now that I practice a much more expanded paradigm, it’s much more exciting and your results are tremendous when you apply this sort of wider model, you know.

03:17

Yes, indeed. So, after studying traditional Ayurvedic medicine, traditional Chinese medicine, homeopathy and looking at health care, from a mind, body, spirit perspective, I’m wondering what fundamental conclusions you’ve drawn about wellness that led you to your inspiration and the creation of the Hoffman Centre.

03:37

Wellness is a strange term because it denotes what I really try and help people with, which is to try and live in a state of maximum wellness, maximum potential. And that moves everybody from a disease-based paradigm into what we you know, what is called a wellness paradigm, but is somebody living at their maximum potential, are they fulfilling the desires of their most innate, instinctual talents and abilities, and illnesses and symptoms often sort of create a, what would the word be, they create a block in that person’s trajectory towards optimal performance of their destiny? And so, we use symptoms and diagnosis to, to sort of ask a lot more deeper questions and dive right into the potential reasons why a person may not be fulfilling their ordained destiny. And that’s what I love to do. And so that’s why I created the center to try and explore those possibilities with people and it’s very rewarding, and not everybody, somebody may just have something that’s physically based but many people with chronic illness have led many layers and levels of stressors on their systems, and the detective game of trying to diagnose and treat is what inspires me to keep doing what I love to do. 10 Center.

05:00

Very cool. I’m wondering what some of your fundamental theories that you’ve developed are as a result of your work that you could share with us or what some of your underlying ideas are, that are part of your mission.

05:18

Certain things that stand out, when I have somebody sitting in front of me with a complex illness, a) you’ve got to take into account all the basic lifestyle factors, diet, sleep, exercise, stress, if you don’t look at those in great detail and sort of dissect them into the multiple subsets, you know, like a diet, for example, there’s many different diets that you can therapeutically apply and what may fit one person may not work for the other. You have to really know your nutrition and dietary issues in great, great detail. A high histamine diet versus a ketogenic diet versus a paleo autoimmune diet versus the Ayurvedic Vata pacifying, that there’s many, many permutations, you got to know those things thoroughly. So that’s huge. And as you know, diet affects the gut microbiome. And the gut microbiome affects the vagus nerve and the vagus nerve runs into the brain. So, your brain-gut microbiome is huge. If you’re not looking at the gut-brain microbiome you can’t really work out what’s going on. So, diet is big. The gut microbiome is big.

Dentistry, I use a lot of dental insights in order to try and ascertain what may be going on particularly with people’s brains, because the inferior alveolar nerve in the lower part of the jaw runs back into the brainstem as well. So, you get a lot of toxic buildup in root canals, cavitation sites, etc, etc. So, dentistry, a lot of respect for dentistry. Everybody to get a panorex X ray and a 3D Cone Beam CT scan of the jaw, and then I send them to a biological dentist to do a complex workup and treat accordingly. So, dentistry is big. Diet is big.

Sleep, sleep, almost everybody I see has a sleep study, not one of those sleep apnea tests they take home. Do a full in-house sleep study. And I rely on that tremendous extensive can’t tell you how many people suffer ill health from sleep issues, sleep is huge. Which brings me to the whole thing of emf, electromagnetic field exposures, radio frequencies and electrical fields, magnetic fields. That has become a very dominant part of my intake history taking to see what people are doing, how much screen time, are they using blue light blocking glasses, are they turning off their routers at night? So, I take that all of that into account? Huge, huge, huge.

And then another piece that is huge in my work is I really don’t start to work with somebody unless I understand the family system into which they originated. The ancestral lineage not from a genetic but from an epigenetic perspective, what are the experiences of their mothers and fathers and grandparents? I find that is where I really begin my curiosity through taking a history. Are you in relationship with your mother or in your relationship with your father, if people say I can’t stand my mother, I can’t stand my father, I don’t want anything to do with them’ I know right then my task of healing is being brought to a halt. You can’t heal somebody who isn’t aligned with their family system in a flow of love, can’t do it. It doesn’t work. You can treat a symptom but you’re not going to help that person reach their maximum potential if they’ve shut down the influences of their parents or their ancestors, because people are half their mother, half their father, if you say no to your mother or say no to your father you are saying no to half of your life force. And that needs to be worked through. And I use family constellation therapy for that. And things like that, you know?

08:45

Yes, I was going to ask what you do for that for that situation? Because that, you know, there are a number of folks who are.  Is it family therapy?

08:57

No, it’s not family therapy, its family constellation therapy. Its different form family therapy

09:01

Can you explain that?

09:02

Well, you take a history or you ask people certain questions about their family of origin. What do you blame your mother for? What do you blame your father for? Those are the first question. And if they have a whole string of complaints that begins the diagnostic and therapeutic process. It was developed by Bert Hellinger, called family constellation therapy. He just died a few weeks ago, actually. And it’s a method of working people up through understanding the entanglement of the family system. We try to understand the laws that operate in family systems and those things that lead to good outcomes and those things that blocked the flow of energy in a family. You have to sort of study it and learn it.

09:46

Yes, it’s very, very intriguing. I’m wondering if you could just mention briefly, you described turning off your routers at night. So, these electromagnetic fields that we’re constantly in relation to in this digital age. They are really, truly bad for us.

10:03

Depends, yeah, there’s certain subtypes of people are more susceptible than others. And some work is  being done on basic detox for liver cytochrome p 450 enzymes. Liver enzyme pathways, detox pathways, people with certain liver detox enzyme susceptibilities do much worse, in terms of the electromagnetic hypersensitivities. So, when you sleep at night, you should be in a very deep parasympathetic healing state. Most people you see, particularly say in inner cities, have about two volts running through their body from the electrical fields around them. And then they have these electromagnetic radio frequency fields. This is from the cell phone towers and routers, like if you live in a condo, you’ve got everybody’s router beaming into your bed at night. And when you’re sleeping at night, you are meant to be in this very deep, relaxed state. But if you are surrounded by radio frequencies and electric fields and magnetic fields, you’re in a stress state. And that opens up the blood brain barrier, opens up the gut barrier, leads to suppression of melatonin, the whole glymphatic system or brain detox system doesn’t work, you’re in big trouble. And it’s not being emphasized enough, you know. And then with dentistry, if bite problems and grinding, you don’t detoxify through the glymphatic system and down through the, you know, through the lymphatics that go down through your internal jugular vein and other parts of your neck and thoracic region. So, you want to know these things. I send in Baubiologists or building biologists into homes to measure all of these things before I start treating people with cognitive difficulties or sleep difficulties. They go turn off routers, they help people with sleep, you know, screen time, they use blue light blocking glasses, they do all of these things. So, it’s an integral part of the work I do?

11:41

Well, that’s very exciting. I’m just wondering, I used to erase floppy disks by just touching them. So, I obviously have some sort of electromagnetic thing going on. would that mean that I would be more susceptible to energy from digital influences or to electromagnetic? Well,

12:01

I don’t know. I used to feel tingly and confused when you arrived cell phone towers. They go crazy. They can’t handle it.

12:10

Well, I used to be affected by Bluetooth. So yeah, perhaps perhaps. So environmental and lifestyle factors are considered by functional medicine doctors to be as you’ve been speaking about it very important, especially in complex situations with patients with chronic illness. So have certain input environments or lifestyle factors been linked to chronic Lyme disease.

12:31

Well, lyme disease is an immune disease, right? So, the bug gets entry if your immune system is compromised. So, you need to have reduced natural killer cells for Lyme disease to take hold. And so, to treat Lyme disease, you know, there is a whole emphasis on using whole rotating antibiotics and, and using herbs and/or pharmaceuticals to treat it. But really, it’s an immune incompetency disease. So often when you have a compromised immune system, you’ve got to look at factors that may have led to that and one of them, apart from the genetic imbalances in immune competency is stress. Stress is the greatest suppressor of the immune system. We know, people with stress they get viruses, they get colds and things; that’s the same principle, your surveillance system of our immune system gets compromised under chronic stress. And what causes chronic stress. Well take your pick, hundreds of factors cause chronic stress, it doesn’t just have to be a boss that gives you a hard time, it can be poor sleep, it can be poor diet, there’s many things that cause chronic stress. That dental infection that hasn’t been treated; they all can cause chronic stress in the body. So, for Lyme disease, the thing you got to look for is immune competency and that’s why one of the tests we do is called natural killer cell function, or CD 57. And we look at that to see if that’s suppressed. If that’s suppressed, your ability to fight Lyme disease is compromised and Lyme disease and co infections can run rampant. So, it’s just one of the things we look. There are genetic components to this as well. One researcher has done work on the genetics of people with Lyme disease, and specific markers that are upregulated. And then anything that compromises your overall resilience and homeostasis and mitochondrial resilience, anything, diet, any other factors, lack of exercise, obesity, any of them.

14:23

And if you’re tuning in just now, you’re listening to healing wisdom on WOMR 92.1 FM in Provincetown and WFM are 91.3 FM in New Orleans and streaming at Womar.org. We are speaking with Dr. Bruce Hoffman, functional medicine doctor, founder of the Hoffman Center for Integrative and Functional Medicine.

What are risk factors in Alzheimer’s? Have you seen significant improvements in patients with Alzheimer’s using integrative approaches?

14:53

Yeah, Alzheimer’s is very fascinating. I don’t know if you’re aware of the recent work that’s put out by Dale Bredesen and his group. He wrote a book called The End of Alzheimer’s. And I wrote a summary of that book on my website, there is a blog on it. Alzheimer’s is fascinating. He’s worked out that there’s six subtypes of Alzheimer’s disease and 36 biochemical pathways that need to be addressed. And he basically says that Alzheimer’s has six subtypes. The first can be anything that’s inflammatory, then anything that’s deficient is number two, anything that’s blood sugar, glucose, insulin related is number three, anything that’s toxic, like mold and heavy metals is number four, anything that’s cardiovascular related is number five, and anything that is head injury related is number six.  Those are the six subtypes of Alzheimer’s disease. And there’s many biochemical pathways that you look at when treating Alzheimer’s. So, for instance, all the deficiency issues, one of the main deficiencies in Alzheimer’s is all the hormones: growth hormone, testosterone, estrogen, progesterone, DHEA. So, we look at all of those pathways and try and repeat them, when we are treating Alzheimer’s:  inflammatory, all inflammatory chronic conditions, you know, eating an inflammatory diet, mold, illness, heavy metals, look and treat all of those issues. People with high blood sugar, high insulin, insulin resistance, treat that, that has a huge effect on people’s brains. And then a key underlying factor that seems to be very problematic if anybody has what’s called the Apoe 4/3 or 4/4 gene, that predisposes to a much higher risk later on in life of Alzheimer’s disease. We test for that gene, hopefully, you know, if you have a 3/4 or 4/4 gene, you should really increase everything you can in terms of lifestyle factors to make sure that gene doesn’t get expressed later on in life. There’s a whole website devoted to people with the Apoe4 gene, what they need to do in order to down regulate the risk? Well,

17:08

Yes, it’s interesting, because I know with my own grandmother who suffers from Alzheimer’s and my mother-in-law, and also one of my clients, it’s amazing how quickly an anti-inflammatory diet can help heal the brain. I mean, it seems like overnight, a person can have access to memories that they didn’t have before.

17:31

The other thing we do is, down regulating the gut microbiome and neuroinflammation through the vagus nerve. But we also assess all the fats. I test with the Kennedy Krieger fatty acid analysis and we look at all the Omega 3/6/9 and saturated fats and we treat very aggressively with the ketogenic diet and high fat intake, particularly something called phosphatidyl choline. Choline is one of our key nutrients to help restore brain function back to normal. In fact, the patient I saw just now had a huge deficiency in phosphatidyl choline with cognitive deficits.

18:11

Wow, can you dispel the mold myth mold illness is not an allergy, correct?

18:21

You do get IgE mold allergies, but we do not worry about that. That’s the least of one’s worries. Mold is a huge trigger of the innate immune system causing a condition called CIRS; chronic inflammatory response syndrome. And that plays havoc with your inflammatory cytokines, which then down-regulate areas in the brain, particularly the melanocyte stimulating hormone, MSH. And MSH controls many things; sleep, pain, gut function, and all the sex hormones and the diuretic hormones. So, when you get exposed to mold and you get inflamed from mold, and it appears that only 25 to 35% of people have a susceptibility to mold illness. They don’t downregulate the mycotoxins that are expressed. And they get very inflamed with consequences to their brain, consequences to their hormone’s, consequences to  mitochondrial and to oxygen delivery, sleep, gut function. Amazing. So moldy allergies is the least of our worries.  I don’t see people with mold allrgies, I see people for mold toxicity, mold inflammation. It’s a whole different subset, not taught, not understood. Respirology don’t know about it. The insurance companies certainly don’t want to know about it. It’s a huge problem. And I treat mold illness all day. Huge. Most homes are moldy.

19:46

Yes, many, many homes on Cape Cod, for example, are moldy. There’s just a ton of dampness and can you talk a little bit about mold illness?

19:55

Yeah, well, I work like as much as I work with a dentist and I work with building biologists for EMF’s, I work with mold, remediating indoor air specialists, we send people into homes to do a visual inspection. Anybody that I suspect, with mold illness, we have a questionnaire. And if people score very high on the questionnaire, we immediately suspect mold. And then we ask questions. Do you have any water damage? Do you have any damp areas? Do you have any condensation on your windows? Do you have any visible mold downstairs, or air conditioning? Have your ducts been cleaned lately, a whole bunch of questions. Then we send in the mold inspectors to go and do a good visual inspection, which takes hours. If somebody walks in with an air sample and waves it around and says you don’t have any mold in the air, run for the hills, because that’s was not a proper mold assessment. We also send people home with ERMI kits where they actually take swabs for DNA particles of mold, they take a swiffer cloth, mold samples from dust collected, or they vacuum the carpets and they collect the DNA spores and send it off to a lab to measure it. And then if they’ve got mold in their home, we assess the degree of the mold. And then we send in a remediation crew, and then we start to treat the mold illness. And there’s about 12 steps in how to treat mold illness. First step is to get out of the moldy home. Second step, bind the mold with binders like cholestyramine or charcoal or whatever. And then there’s a whole series of other steps that you do.

21:29

What are your thoughts on ozone for killing, mildew and mold?

21:33

Doesn’t work?

21:35

Oh, no.

21:38

It affects our immune system. Yes.

21:42

Mold exposure causes inflammation upregulation of the innate immune system which causes inflammation.

21:51

Yes. So I’m wondering about andropause. And why is it worth talking about? It’s not something that you know, people talk a lot about menopause, but not so much about andropause.  And I noticed that was on your website. I’d love to hear

22:06

Andropause. Yeah, it’s grumpy old men. Yeah. Men age slower than woman so they’re not as you know, andropause, it takes a year or two.   Women and perimenopause take about a year, but they notice when they start getting hot flashes and night sweats, it’s pretty quick. Men, their testosterone levels fall slower. And they don’t go into like an acute sort of jump off a cliff so to speak, it’s a slow, gradual decline, they put on weight, they get grumpy, they get depressed and they ache.  Their libido goes down, erections go down. And when you start measuring all the sex hormones, you find that they are deficient or you know, low normal. And that you know, usually in the age 50 onwards, and we measure all those hormones and treat accordingly and it can have tremendous effect when you start treating, particularly testosterone, dhea, sometimes growth hormone very seldom, melatonin, and then using thyroid hormone and adrenal support, some can make a tremendous difference to people’s wellbeing. So andropause is a real and undiagnosed, under treated condition. It is very rewarding once diagnosed and treated appropriately, you know.

23:28

Yes. Now this might seem like a strange thought. But I’m wondering if there is an evolutionary reason that people as you know, over a certain age tend to get up earlier. And earlier. And you know, if the oldest troubled sleep, maybe has, you know, if that’s really how people were living, organically naturally. I mean, I know, overall, people are dying, at much older ages, and so on and so forth. But I always wonder about this early rising business that seems to happen and be so much a part of our hormonal evolution over our lives.

24:06

You mean why older people sleep less.

24:08

Yes.

24:11

So succinctly said,

24:15

Multiple factors for that, you know, I mean, it’s definitely based on diminishing hormones, particularly, melatonin, melatonin levels go down as we age, too.  Melatonin is a major brain antioxidant. It’s also what turns on the suprachiasmic nucleus, which tells you that it’s nighttime. So, melatonin deficiency, as we age, affects the suprachiasmic nucleus and affects the ability of somebody to stay asleep for longer periods of time. There are many, many factors, but that’s just one of them.

24:53

As we go into colder months, it’s very important that we use preventative measures and make sure that we’re as healthy as we can in the fall so that going into winter, our immune systems are as strong as possible. I’m just wondering what your thoughts are on just simple things, people can start doing better to take care of themselves in the colder months?

25:14

Well, the thing that I always worried about the colder months is when people go indoors, and they shut themselves in. And so I always want you to worry about the indoor air quality, and these tightly sealed homes. So, when we not exposed to the outside sunlight, when we get sealed into our homes for six months of the year, the question is, what is the quality of your home? What is the quality of the indoor air? Are you being exposed to mold spores and mold toxins, volatile organic compounds, off gassing? That’s the thing I’m most concerned about in winter months, and many, many patients will tell you “ in October when winter comes, I get sick, I get worse, I get depressed”, or I get this or that”  a lot of it’s to do with the fact that they get sealed into their homes, and they don’t spend any time outside, you know. So that’s what I started to think about – quality of indoor and environmental indoor homes.

26:16

Okay, so we have one more minute left. So, my final, final question is just, if you could, if you could tell everyone, one or two things that would help improve most people’s lives, you know, mind body spirit, what would that thing be?

26:34

If you’re not connected with your mother and your father, if they are alive or dead, go do some work and try and reconnect yourself to their life spirit and to their love. If you’ve got a complaint about your parents,  go do your work. I really mean that.

26:57

If you cannot say yes to your mother and father for giving you life, your work is incomplete. If you are in complaint about your mother and father, you have got work to do. They gave you life, be grateful. All the rest was just an excess. It’s just the fact they gave you life that was enough. That if you’re not aligned with them, and the flow of love isn’t from you, to them to your children, you need to do your internal work to try and correct that. That’s what I say is the principle, the cardinal aspect of healing.

27:29

Thank you so much, Dr. Bruce Hoffman for joining us today on healing wisdom.

27:34

Okay, thank you very much. Thank you so much. Bye.

You’ve been listening to healing wisdom. I’m your host Pandora people’s certified chartered herbalist and psychic medium. You can find healing wisdom podcasts at Womar.org. Contact me with any feedback questions or show ideas at peachy pandora@yahoo.com. A big thanks to the Wizard of operations Matthew Dunn. Join me again next week.

The Ketogenic Diet – The Secret to Neuroprotection

Ever taken a trip to the grocery store only to forget why you went there in the first place? Or perhaps you have difficulty concentrating on something you usually enjoy, like reading a book. In either of these cases, you usually don’t feel as if your brain is working normally.

  • Maybe you’ve lost confidence in your mental abilities.mol
  • Maybe your doctor has dismissed your brain fog as a consequence of aging.
  • Maybe you’ve struggled with chronic migraines or cluster headaches for what feels like forever.
  • Maybe you’re apprehensive regarding a future that involves living with neurodegenerative disease.

Sound familiar?

Well, I’m here to tell you not to lose hope. There are ways in which conventional Western medicine is letting us all down. The idea of losing cognitive functions, your memory becoming poorer, or even not being able to recognize the faces of your family, is all pretty scary. Every 65 seconds a patient in the US develops Alzheimer’s disease and there’s no magic pill that cures it.

Fortunately, there’s another way.

As a functional and integrative doctor, I find the issue of cognitive decline to be on my mind regularly. My patients are concerned that they won’t be able to work, socialize, or enjoy hobbies for much longer. They even worry that they’ll have to give up on life.

However, I’m able to help them treat their neurodegenerative progression from the inside. By adopting the ketogenic diet for neurodegenerative diseases, you can change your life and turn back the clock. Dr. Dale Bredesen’s extensive research and treatments have shown that the effects of Alzheimer’s disease can be reversed with simple lifestyle changes. A modified version of the ketogenic diet is the backbone of Dr. Bredesen’s protocol and the science behind this is truly incredible.

The History of the Ketogenic Diet

While the ketogenic diet is currently very popular due to its fast and effective results related to weight loss, the diet actually started out as a medical therapy in the 1920s. Doctors saw that fasting was beneficial regarding controlling seizures in epileptic children, but restricting food was not a sustainable solution in the long term.

The doctors reasoned that when you fast, your levels of glucose and insulin drop and ketone bodies appear in your blood and urine. Ketone bodies indicate fat breakdown, so the doctors realized that a high-fat diet could build up levels of ketones that were sufficient enough to mimic the benefits of fasting, thus reducing their young patients’ seizures. Epileptic children who were prescribed the ketogenic diet did indeed stop seizing. However, the ketogenic diet never became a popularized form of therapy for epilepsy once anticonvulsant drugs were fully researched and then put into production.

The therapeutic effects of the ketogenic diet were only really rediscovered towards the end of the twentieth century. Many parents of epileptic children that were frustrated with the severe side effects of anticonvulsant drugs, and worried about the impact of seizures on their child’s cognitive abilities, did their research and decided that inducing ketosis was something that they’d like to try.

While the ketogenic diet isn’t the first option that medical practitioners explore when treating children with epilepsy, it has garnered more interest in the medical community as new and exciting applications have been discovered and research is increasingly being undertaken into the neuroprotective characteristics of the diet.

It’s important to realize that ketosis isn’t an unusual state for human beings. Infants are naturally in ketosis much of the time, since breast milk is high in medium chain triglycerides or MCT. We are naturally in ketosis during sleep, fasting and exercise as the body and brain have become accustomed to metabolic flexibility, shifting between glucose and ketones as fuel sources when the need arises. As human beings become more sedentary and accustomed to eating three meals a day with snacks, often well into the night, these diurnal and seasonal changes became a thing of the past.

What Neurological Disorders Does the Keto Diet Help Treat?

Following the ketogenic diet is often a game changer for patients suffering from:

  • Parkinson’s disease – Keto improved the condition of patients in a small study.
  • Traumatic brain injury – There has been success in an animal study, with potential for human application.
  • Epilepsy, Stroke, Migraine – All three conditions share similar characteristics, migraine patients are at an additional risk for stroke, and patients often deal with epilepsy and migraine together. Migraines and epilepsy share similar symptoms and often epilepsy medications are used to treat chronic migraines off-label. As the ketogenic diet has reduced the number of seizures for epileptics, chronic migraine patients have also experienced longer gaps between migraine attacks.
  • Chronic cluster headaches (CCH) – There has also been success for chronic cluster headache sufferers, suggesting that the anti-inflammatory nature of the ketogenic diet is particularly healing for CCH patients.
  • Autism – A ketogenic diet has had some success in reducing some symptoms of autism. One of the leading contributors of autism may be mitochondrial dysfunction and the ketogenic diet improves mitochondrial function.
  • Brain tumors – Many cancer patients have seen success with the ketogenic diet slowing down their tumor growth as several types of tumors require glucose and a very high carbohydrate diet. However, the ketogenic diet is not a one-size-fits-all remedy for cancer. Studies are ongoing.
  • Trigeminal Neuralgia – A study shows promise of relief for sufferers of this severe form of facial pain after adopting the keto diet.
  • Multiple Sclerosis – Research is ongoing, but there does seem to be potential for the keto diet to protect neurons from further damage.
  • Alzheimer’s disease – The ketogenic diet benefits Alzheimer’s disease patients because it combats insulin resistance, inflammation, gluten sensitivity, obesity, and leaky gut.

You’ll learn more about each of these subjects below.

The ketogenic lifestyle is also a fantastic solution for healthy individuals who wish to avoid neurodegenerative disease or cognitive dysfunction. The only good way to ensure better health when you’re older is to take action today. Even if you have the APOE4 gene, meaning that you’re more susceptible to developing Alzheimer’s, or have a formal diagnosis, you can benefit from the ketogenic diet. It’s never too late to start.

Neuroprotective and Disease-Modifying Effects of the Ketogenic Diet

There are a number of ways in which following a ketogenic diet can protect your brain and even reverse neurodegenerative disease. By severely restricting your carbohydrate intake, reducing protein, exercising regularly, and increasing your consumption of good fats, you encourage your body to look for an alternative energy source to sugars and carbohydrates. If you eat to a calorie deficit, your body begins breaking down fat stores and inducing a state known as ketosis. The brain prefers ketones to glucose as they cross the blood-brain barrier much easier since they don’t rely on transport proteins. They also produce less in the way of free radicals or oxidative damage, the key biochemical process underlying most forms of chronic disease including neuroinflammation and neurodegeneration. However, if you’re eating to maintain your existing weight, the fat is supplied purely through your diet.

The Power of the Humble Ketone

Most of your body can use the fat stores or dietary fat to power your cells. However, your brain and the central nervous system can’t access this energy in the same way. As a result, your liver breaks down the fatty acids and a by-product of this chemical process are ketones. These are your body’s alternative energy source.

Ketones are made up of acetone, acetoacetate, and beta-hydroxybutyrate.

Ketone bodies are capable of crossing the blood-brain barrier and are the only source of energy the brain can use that can replace glucose made from carbohydrates. As such, ketones can fuel up to 75% of the energy needed by your brain. The other 25% or more of your energy continues to be fueled by glucose, but it’s glucose that’s made by your body from the few carbs that you do eat and also by your protein sources.

Ketones are an amazing form of energy for your body and have a host of benefits for your metabolism and health.

Concentrating on neuroprotection, here’s a list of ketosis brain benefits:

  • Ketones are water-soluble and cross the blood-brain barrier in proportion to your blood levels. Consequently, they can compensate for an existing neurological disorder where there’s a regional brain glucose deficiency. It’s been observed that studies show reduction in glucose utilization in the Alzheimer regions of the brain in the temporal and frontal lobes long before cognition declines. This is due to insulin resistance, a concept that’s well described a little later.
  • When the cells of your body, and specifically those of your brain, convert ketones into adenosine triphosphate (ATP) via the mitochondria, ATP generation is markedly improved in mitochondria that are fed ketones. The keto diet improves the efficiency of your brain cells.
  • Ketones inhibit reproduction of the HDAC enzymes, which protect and repair the neurons that make up your double-stranded DNA. Ketones therefore have a powerful role to play in epigenetics and future research may potentially shed light on how they protect your brain.
  • The beta-hydroxybutyrate in ketones suppresses your NLRP3 inflammasome, reducing inflammation in your body. The mechanism is pivotal in the development of Alzheimer’s disease and related brain tissue damage. In animal studies, beta-hydroxybutyrate was found to suppress oxidative stress, protecting the integrity of the DNA and overall health.

What Is Insulin Resistance and Why Is It a Problem?

Normally, the insulin hormone is produced by the pancreas. Insulin joins your bloodstream to regulate the amount of glucose in your blood. In a healthy individual, when the insulin detects too much glucose in your blood, it signals muscles, tissues, and your liver to absorb the glucose.

The glucose is then converted into ATP, ready to be used as cellular energy or broken down by your liver. The levels of glucose in your bloodstream need to be controlled because they can be toxic at high levels.

When you have insulin resistance, which is often a precursor to diabetes, your body ignores or resists the insulin signal to absorb glucose. The levels of glucose build up and your pancreas creates more and more insulin in order to trigger glucose regulation.

Obviously, any condition that may lead to diabetes is a concern, but insulin resistance also has an impact on your neurological health. Sugar is a known inflammatory and inflammation can disrupt the careful balance of your blood-brain barrier.

More crucially, insulin is a signaller that aids neural cell survival. If there are high levels of insulin in your bloodstream, the amount of insulin should be reduced and your body needs several enzymes to break it down.

One enzyme called insulin-degrading enzyme (IDE) can break down insulin. However, if it’s responsible for working on an overabundance of insulin, the enzyme can’t be used to degrade amyloid beta. Amyloid beta in the brain contributes to Alzheimer’s disease.

However, if you increase your insulin sensitivity, it’s possible to reduce your chances of developing Alzheimer’s disease. Ketones also modulate your neurons by reducing glutamate toxicity and inhibiting gamma-aminobutyric acidergic (GABAergic) effects, limiting seizures if you’re epileptic.

The Mind-Gut Connection

In integrative and functional medicine approaches, it’s understood just how important the health of the gut is in relation to achieving optimal overall health. Understanding the connection between your brain and your gut microbiome is crucial to maximizing the neuroprotective conditions of the ketogenic diet. Sugar causes inflammation and can trigger conditions such as leaky gut. Eating whole foods and reducing your carbohydrates and processed food intake helps to heal your gut. Improving your gut microbiome actually improves your cognitive abilities as well

Keto Helps You Sleep Deeply

A lower-carb diet, such as the ketogenic diet, may help reduce your symptoms of sleep apnea or other sleep airway disorders. Quality of sleep and deep REM sleep are crucial for keeping your brain healthy.

An airway sleeping disorder usually results in your brain not receiving enough oxygen at night. The effect of a lack of oxygen is that your brain can’t fall into a deeper sleep and your brain is unable to perform certain neuroprotective tasks, such as autophagy where old cell components are recycled.

The recent discovery of the glymphatic system in the brain is of great interest to researchers examining neurodegenerative diseases. The glymphatic system only works while you’re asleep and removes excess fluid and waste products from the brain and spinal column tissues. Amyloid beta proteins are a form of waste in the brain that the glymphatic system deals with. Links have been established between these proteins, your cholesterol levels, and the lymphatic system in regard to neurodegenerative diseases.

The glymphatic system also delivers central building block nutrients, some of which are used in improving your cognitive functions. Unfortunately, with sleep apnoea your body is unable to undertake these functions, leading to neurodegeneration.

Ketogenic Basics: Macronutrients and Keeping Track

Macronutrients are another term for the basic food groups:

  • Protein
  • Fat
  • Carbohydrates

Both the standard American diet and calorie restrictive low-fat diet are heavily slanted toward the consumption of carbohydrates. In the ketogenic diet, the values are flipped on their head. On the keto diet, you aim for a high-fat intake, medium to low amounts of protein, and low levels of carbohydrates. A good rule of thumb is to not eat foods with a glycemic index of more than 35. Here is a link to a food glycemic index database that should be useful.

The original ketogenic diet for epileptic children focused on a 4:1 ratio, or four parts fat to one part carbohydrates and protein. However, this is at the extreme end of the ketogenic diet and is usually too difficult to attempt at home.

Generally, you should aim for your intake to be:

  • 60-75% fat
  • 15-35% protein
  • 5-10% of carbohydrates, although the lower the carbohydrates, the better.

Use a quality online ketogenic calculator to adjust your macros. This one has options for eating to maintain weight, lose weight, or gain weight.

To track whether your body is in the state of ketosis that’s creating ketones and using them as your body’s main source of energy, it’s advisable that you invest in a good ketone and glucose meter. By using it, you can keep an eye on what foods your body responds to after a meal. Tracking your ketones through beta-hydroxybutyrate levels in your blood is the most accurate way to keep tabs on whether you’re in ketosis. Unfortunately, ketone breathalyzers or keto sticks aren’t accurate enough to be reliable.

Ketogenic Neuroprotective Basics: The Diet

PLENTY OF VEGGIES AND FRUIT

Although an outsider may think the mainstream version of the ketogenic diet is mostly made up of bacon, the focus is actually on plant-based foods to promote the diet’s neuroprotective benefits. While it’s true that many vegetables contain high amounts of carbohydrates, these are usually tempered by fiber and the resistant starches that are found in complex carbohydrates.

Your body has a harder time breaking down complex carbohydrates, so they don’t raise your glycemic index so sharply. Simple carbohydrates, on the other hand, are sugars or carbohydrates that break down easily into glucose.

Here’s a guide to vegetables and fruit on a neuroprotective ketogenic food plan:

Eat frequently:

The majority of the diet should consist of organic, non-GMO, seasonal, local, colorful, deeply pigmented non-starchy vegetables with a limited amount of starchy vegetables.

Cruciferous vegetables – These contain sulfur, an important building block for production of amino acids, especially glutathione, which is the main brain antioxidant. These types of vegetables are ideally consumed after being lightly sautéed at medium heat or lightly steamed.

  • Alliums (onion family -shallots, garlic, leeks)
  • Brassicas (cabbage, broccoli, Brussel sprouts, bok choy, cauliflower)

Leafy green vegetables – These are at the top of the list for the ketogenic diet. They contain high levels of nutrients beneficial to your brain health, such as vitamins, minerals, polyphenols, carotenoids.

  • Spinach (caution if histaminic and high oxalates)
  • Kale (caution if high oxalates
  • Lettuce

Mushrooms – These contain sulfur and beta-D-glucan, which may help the reversal of cognitive decline through immune enhancing effects. There are many varieties, including Portobello, shitake, reishi, oyster, and white button mushrooms. Add them to sauces, stews, and for flavour when cooking other vegetables.

Resistant starches – The good bacteria in your gut microbiome can feast on resistant starches and fibre and they excrete short-chain fatty acids crucial for your wellbeing.

  • Rutabagas
  • Parsnips
  • Sweet potatoes
  • Green bananas

Herbs and spices – These contain antiviral and antimicrobial properties and are an essential part of a ketogenic diet. This extensive list includes ginger, turmeric, basil, bay leave, chives, cilantro cinnamon, coriander, cumin, lavender, marjoram, mint, oregano, parsley, rosemary, saffron, sage, thyme and more. Herbs and spices have been widely studied to determine their medicinal properties.

Nuts and Seeds – These are rich in vital brain protective nutrients and contain excellent sources of fat, protein, vitamins, minerals, and fibre. These should be raw, fresh, organic, and soaked if possible, thus reducing lectins and phytates. Use dry, roasted nuts where possible if you’re unable to roast them yourself. Roast at low temperatures (77-104 degrees C) while frequently turning the nuts during the process. Nuts that have already been roasted in added oils are usually rancid and oxidized, increasing the risk of inflammation. All nuts and seeds should be stored in the freezer or refrigerator to retain maximum freshness.

Eat sometimes:

Starchy vegetables

  • White potatoes (caution if high histaminic and sensitive to nightshades and not usually advised)
  • Corn (not the best food due to it being high glycemic, moldy, or GMO, amongst other issues)
  • Squash

Nightshades – These inflammatory vegetables contain solanine, a toxin that plants produce to deter animals from eating them. Solanine can stimulate the acetylcholine neurotransmitter in your brain and nervous system. For most people, this is of no concern, but for a patient facing early-onset Alzheimer’s disease, an imbalance in neurotransmitters can complicate matters.

  • Peppers (caution if high histaminic and pain syndromes)
  • Tomatoes (caution if high histaminic and pain syndromes)
  • Eggplant (caution if high histaminic and pain syndromes)

Legumes – Eat these with caution as legumes can raise glucose levels in the blood and shouldn’t be eaten in the early weeks of adopting the ketogenic diet. Depending on the severity of your insulin resistance, you may not be able to eat them.

  • Peas
  • Beans

Fruits – Small berries contain polyphenol compounds that can play a role in reducing cognitive decline:

  • Wild berries such as blueberries have been extensively studied for their antioxidant effects on brain health
  • Avocado is high in fibre, nutrients and beneficial fats
  • Olives
  • Lemons and limes (caution if high histaminic)

CONTROL YOUR PROTEIN

You may find it easy to go overboard with animal-based protein when beginning the ketogenic diet, but it’s crucial to calculate your daily allowance of protein. It’s advisable to employ the one gram of protein for each kg of your weight equation. For example, if you weigh 80kg you can consume up to 80g of protein per day.

Eating protein to excess ensures that some protein is converted to glucose, increasing the levels of insulin in your bloodstream. Think of your controlled amount of protein in the same way as when your ancestors would share a part of the communal hunting kill, only eating a small part of the animal. The rest of the time it was possible to get enough protein through plant-based food sources and this remains true today.

As much as possible, ensure that the protein you eat is organic, grass fed, grass finished, hormone and antibiotic free, and that the animals are not subjected to the stresses and toxins of concentrated feeding operations. To prevent muscle wasting, ensure weight training and weight bearing exercises are incorporated into your routine.

On a neuroprotective ketogenic diet, vegetarians need to get their protein from vegetables, nuts, seeds, tempeh, and beans. However, these are often incomplete proteins and vegetarians will need to supplement with omega-3’s, vitamin B’s, Vitamin D, and choline.

Eat frequently:

Oily fish – These are rich in Omega-3 and Omega-6 and both are excellent for brain health. Farmed fish or shrimp should be avoided. The least contaminated fish, which are smaller and don’t live as long, are known as the SMASH fish.

  • Salmon – The least contaminated are wild Alaskan and sock-eye
  • Mackerel – Fish from the United States and Canada is low in mercury, whereas King and Spanish mackerel are high in mercury
  • Anchovies
  • Sardines – Canned sardines are high in histamine and Pacific sardines are the best.
  • Herring

Free range eggs – These are full of protein and good fats, especially choline, which is a key nutrient for acetylcholine, the main neurotransmitter for memory. However, eggs can trigger a histamine response so caution may be warranted. A list of foods high in histamine and possible substitutes may be found here.

Eat sometimes:

  • Grass-fed beef – This is an acceptable occasional treat, but it’s incredibly easy to go over your protein allowance with a good steak.
  • Free-range chicken – While fantastic as part of a salad this shouldn’t be the main focus of the meal.
  • Meats are generally considered as a condiment, not as a main course.

Avoid eating:

Processed meats often contain hidden sugars, histamine, wheat, gluten, and other inflammatory ingredients.

  • Salami
  • Chorizo
  • Shaped ham
  • Bologna

Fish containing high levels of mercury, since this is known to cause cognitive decline.

  • Tuna
  • Shark
  • Swordfish

Dairy can be highly inflammatory as the lectin in dairy can irritate the gut, so dairy should be avoided as much as possible.

  • Milk
  • Cheese
  • Cream
  • Yoghurt

Alcohol is a known neurotoxicant and solvent and should be avoided, especially if you have the APOE4 gene. Alcohol will slow down fat loss in those patients that use the ketogenic diet for weight loss reasons. Many alcohol drinks such as beer, wine, cocktails, mixers, and flavoured liquors contain carbohydrates. Alcohol is ethanol, which is easily broken down into sugar.

Peanuts are a legume known to be moldy and inflammatory. If you’ve been exposed to mold, download my mold exposure guide here.

GOOD FATS VERSUS. BAD

Although the ketogenic diet is high in fat, not all fats are created equally. Developing an awareness of the different varieties of fat and what foods are good sources of fat ensures that you’ll find it easier to maintain the neuroprotective ketogenic diet in the long term.

Eat frequently:

Monounsaturated fatty acids (MFUA)

  • Avocados, avocado oil
  • Olives, extra virgin olive oil
  • Nuts and seeds, although be careful of walnuts, pecans and peanuts if high histaminic. Many nuts are also moldy
  • Walnuts have been associated with brain health but must be eaten raw. Macadamias are similarly highly desirable for maintaining brain health

Polyunsaturated fatty acids (PUFA) that include Omega-3 and Omega-6.

  • Seed oils such as walnut oil, macadamia oil, or sesame oil
  • Cod liver oil
  • Algae
  • Chia seeds
  • Fish, nuts, and seeds

Saturated fatty acids (SFA)

  • Animal fats are great for this but can be highly reactive in histaminic patients
  • Butter from grass-fed goats, sheep, or A2 cows, although in small amounts as dairy this is an inflammatory
  • Coconut oil
  • MCT oil
  • Free range eggs

Cocoa butter and nuts

  • The fat in chocolate comes from cocoa butter and is made up of equal amounts of oleic acid, a heart-healthy monounsaturated fat also found in olive oil, stearic and palmitic acids, which are forms of saturated fat.
  • They also contain flavanols and have four times the antioxidant properties of dark chocolate.
  • Dark chocolate (over 86%), also has brain health properties.

Avoid eating:

Trans fats and synthetic hydrogenated fats result in raised low-density lipoprotein (LDL) cholesterol levels. High levels of LDL cholesterol can occur at the onset of Alzheimer’s disease in middle age.

  • Avoid all seed, grain, bean and partially hydrogenated oils such as soy, corn, canola, peanut, sunflower oil, safflower (usually adulterated with oleic acid mix), cottonseed, and palm kernel.
  • Avoid all foods processed with trans fats such as crackers, cookies, cakes, chips, microwave popcorn, frozen dinners, pizza, creamers, margarine, cool whip, and fast food.

Testing for fats

With regards to fatty acid intake, it’s best not to engage in a guessing game regarding which fats you need in what ratios. It’s advisable to conduct the Kennedy Krieger fatty acids analysis through a company called Body Bio. In this way, your exact fatty acid dietary deficiencies and excesses can be measured and managed effectively through the correct ratios of biologically active fats, either through food, cooking, or supplementation. Phosphatidyl choline is an essential fat for cardiovascular, mitochondrial, and cognitive health and the levels are best measured before embarking on an extensive therapeutic fatty acid regime.

Saturated fats and cardiovascular risk

People with the ApoE4 gene need to be cautious when using increased amounts of saturated fats, as these are known to raise LDL particle number and APOB, a lipoprotein associated with increased cardiovascular disease. Although the increased saturated fats may increase cognitive health, in the long term it may lead to increased cardiovascular risk factors that are not beneficial. Therefore, it is advised that one monitors one’s cardiovascular risk factors including but not limited to APOB, oxidised LDL, LDL particle number and size, and HDL particle number and size. Increased saturated fats are known to lower triglycerides, increase HDL, and shift LDL particle size from the smaller dangerous particle size to the more advantageous larger ‘fluffy’ type, which is known to be cardioprotective.

Cooking Methods

The way you cook your food is almost as important as the food you choose to eat. Many everyday methods of cooking food can result in advanced glycation end products (AGE). These glycotoxins are produced when there’s a reaction between protein or fat and sugars, so AGEs can instigate inflammation and are bad news for brain health.

Methods to use:

  • Vegetables prepared raw
  • Steaming
  • Boiling
  • Marinating in lemon, lime, or vinegar (caution if histaminic)

 Methods to avoid:

  • Roasting
  • Broiling
  • Frying
  • Grilling

Fats to cook with:

  • Choose oils with a high smoking point, such as avocado, coconut, ghee, and animal fat

Foods to Avoid and Why

GRAINS AND GLUTEN

Grains are dense in carbohydrates, contain lectins that are known to be associated with ‘leaky gut’, phytates, and enzyme inhibitors. Gluten is a known inflammatory agent, especially when it provokes an autoimmune inflammatory response to brain proteins such as myelin and tubulin. Foods to avoid include:

  • Wheat
  • Barley
  • Oats
  • Corn
  • Rye
  • Soy
  • Flour
  • Bread
  • Polenta
  • Pasta
  • Tortilla wraps
  • Noodles
  • Rice
  • Nachos
  • Popcorn
  • Crackers

DAIRY 

Dairy foods are inflammatory particularly as the dairy cows in the United States are A1 cows that produce a protein similar to lectin. A2 cows do not contain these lectins. Furthermore, casein and whey, the two milk proteins, are frequently cross-reactive with gluten.

SUGARY OR CARBOHYDRATE LADEN FOOD

The glycemic index is too high with these types of foods:

  • Agave
  • Alcohol
  • Cane sugar
  • Candy
  • Cookies
  • Cake
  • Dessert
  • Fries
  • Fruit juices
  • High fructose corn syrup
  • Honey
  • Ice cream
  • Maple syrup
  • Pastries
  • Pizza
  • Potato chips
  • Soda
  • Anything containing sugar
PROCESSED FOODS 

  • Microwave dinners
  • Convenience food
  • Anything out of a packet

FRUIT WITH HIGH GLYCEMIC INDEX

  • Melon
  • Pineapple
  • Yellow bananas
  • Grapes
  • Cherries
  • Apricots
  • Mango

Food Intolerances and allergies – All patients that are using the ketogenic diet for cognitive health should be extensively tested for food sensitivities, gut ecology and permeability, leaky blood brain, and antibodies to brain proteins (detected using Cyrex labs 2, 10x, 12 and 20).

Different Ketogenic Diets 

STANDARD KETOGENIC DIET (SKD)

This diet is typically recommended for most people and is very effective. The diet focuses on high consumption of:

  • Healthy fats (70% of your diet)
  • Moderate protein (25% of your diet)
  • Very little carbohydrates (5% of your diet)

Keep in mind that there’s no set limit to the fat because energy requirements vary from person to person, depending on their daily physical activities. The majority of your calories still need to come from fats and you still need to limit your consumption of carbohydrates and protein for your diet to become a standard ketogenic one.

TARGETED KETOGENIC DIET (TKD)

This is generally geared towards fitness enthusiasts. In this approach, you eat the entirety of your allocated carbohydrates for the day in one meal, around 30 to 60 minutes before engaging in exercise.

With this diet the idea is to use the energy provided by the carbohydrates effectively before it disrupts ketosis. You eat carbs that are easily digestible with a high glycemic index to avoid upsetting your stomach. When you’re done exercising, increase your intake of protein to help with muscle recovery then continue consuming your fats afterward.

CYCLIC KETOGENIC DIET (CKD)

This one is generally focused more on athletes and body builders

Cycling between a normal ketogenic diet, followed by a set number of days of high carbohydrate consumption, also known as “carbo-loading”

The diet takes advantage of the carbohydrates to replenish the glycogen lost from your muscles during athletic activity or working out. This usually consists of five days of SKD, followed by two days of carb-loading. During the ketogenic cycle, carbohydrate consumption is around 50 grams, but when you reach the carb-loading cycle, the amount jumps to 450-600 grams.

This method isn’t recommended for people that don’t have a high rate of physical activity.

HIGH-PROTEIN KETOGENIC DIET

This method is a variant of SKD, in which you increase the ratio of protein consumption to 10% and reduce your healthy fat consumption by 10%. In a study involving obese men that tried this method, researchers noted that it helped reduce their hunger and lowered their food intake significantly, resulting in weight loss.

If you’re overweight or obese, this diet may help you initially, before you can transition to SKD after you normalize your weight.

RESTRICTED KETOGENIC DIET

As mentioned earlier, ketogenic diet can be an effective weapon against cancer. For this method to be effective, you need to be on a restricted ketogenic diet. By restricting your carbohydrate and calorie intake, your body loses glycogen and starts producing the ketones that your healthy cells can use as energy. Cancer cells are unable to use these ketones and starve to death.

Meal Examples

1st Meal

  • 4 to 5 cups of organic vegetables
  • Some limited starchy vegetables, such as sweet potato
  • One or two pasteurized eggs, lightly cooked or poached
  • Olive oil, MCT oil, or ghee as a dip for the vegetables
  • Use of spices, herbs, and sea salt for flavouring

2nd Meal

  • Organic, seasonal vegetables, either as a salad or lightly steamed
  • Small serving of fish or chicken
  • Healthy fats such as avocado, olives, nuts or seeds, and/or olive oil
  • Seasonings such as herbs, spices, and sea salt

Snack example

  • Coconut yoghurt or coconut milk kefir
  • Blueberries
  • Walnuts, almonds, or macadamias
  • Cocoa nibs
  • Coconut flakes
  • Stevia

Shake example

  • 2 tablespoons of Body Bio phosphatidyl choline
  • 1 tablespoon of Body Bio balanced oil
  • 1 tablespoon of MCT oil
  • 1 scoop of amino acid powder
  • Lions mane, turmeric, and /or mushroom powder
  • Stevia and vanilla to add flavour

Please note that the above ratios would be determined based on a fatty acid test

Neuroprotective Keto: Fasting and Exercising

Fasting and exercising aren’t optional when undergoing the ketogenic diet for neuroprotection. The good news is that neither has to be conducted to the extreme on order to get results.

Fasting is an effective way to stimulate ketogenesis, the process that produces ketones. Fasting also enables autophagy, as discussed above in the section about sleeping. Autophagy is an advantageous function that removes damaged proteins from the brain, protecting it from a dangerous build-up. Fasting has also been shown to have a number of other health benefits, including improved cardiovascular health, reduced cancer risk, increasing longevity (by increasing the sirtuin gene) and repairing damaged DNA.

Here are the easiest ways to incorporate fasting into your daily routine, without feeling like you’re missing out or that you’re going to be hungry:

  • Fast between the end of your dinner and your breakfast the next day. Aim for twelve hours without snacking. Individuals with the APOE4 gene may need to increase the fasting state for sixteen hours.
  • Make sure you eat your evening meal early so that you have a minimum of three to four hours between your evening meal and going to sleep.
  • Your body’s calorie burning clock is most effective in the morning and least effective at night. You don’t need food for energy at night so by eating less at that time you induce a fat burning state that helps prepare your body for detoxification and repair.
  • Water, black tea, or coffee are all allowed during the fast, particularly in the early morning. Stevia may be used as a sweetener

Remember that once you are fully in ketosis you won’t experience hunger pangs in the same way. In fact, you may be able to go even longer between meals.

Exercise is crucial for neuroprotection as it helps reduce insulin resistance, aids ketosis, and reduces stress. A combination of aerobic exercise and weight training can improve your sleep at night via vascular function in your brain and protect the hippocampus, which can often shrink in those suffering with Alzheimer’s disease. Start slowly and build your way up to a full program of activity.

Individuals with insulin resistance may have a harder time inducing ketosis and may suffer from carbohydrate cravings. Ask your doctor to measure your insulin, fasting glucose, and hemoglobin A1c levels. HbA1c is a measurement of your average glucose levels over three months. Using high dose medium chain triglyceride fats (MCT) or coconut fats assists in helping you overcome sugar cravings and glycotoxicity. One has to increase these fats slowly and use fat digesting enzymes containing lipase and emulsification aids such as ox-bile to initially assist in the increased fat load. Another way to combat the initial sugar cravings is to increase fats in your diet such as nuts and seeds, avocado, or non-starchy vegetables cooked in ghee, coconut, or avocado oil.

Neuroprotective Keto: Supplementation

As mentioned above in the section about the mind-gut connection, your brain and gut have a special relationship. In order to achieve neuroprotection, it’s necessary to heal your gut by encouraging your good bacteria to take charge. The best way to improve your gut microbiome is to take probiotics and prebiotics.

Probiotics contain the good bacteria that are able to take carbohydrates and convert them into lactic acid, which suppresses your bad bacteria. Probiotic should be used with caution if histaminic but include:

  • Kombucha
  • Miso
  • Pickled vegetables
  • Yogurt (unsweetened)
  • Kefir from coconut
  • Kimchi
  • Sauerkraut
  • Tempeh

Prebiotics comprise food that’s indigestible for you, but it can be digested in your colon by your good bacteria. The bacteria break probiotics down into materials that aid the maintenance of your gut. Many of the resistant starches and fibrous plants listed above count as prebiotics.

Here are a few further examples of prebiotic supplements:

  • Organic psyllium seed husks
  • Plantain
  • Green banana starch
  • Inulin
  • Acacia fibre

When you begin the ketogenic diet it takes a few days to achieve ketosis. In the meantime, you may experience some side effects, often referred to as ‘keto-flu’ by some people. With this condition, patients often experience:

  • Feeling run down
  • Brain fog
  • Headaches
  • Fatigue
  • Abdominal pain
  • Constipation
  • Diarrhea
  • Poor mood
  • Muscle cramps

All of these symptoms are perfectly normal, considering that you’re detoxing from sugar, training your body to run off ketones, and often experiencing the loss of electrolytes and dehydration. However, there are ways to combat this as follows:

  • Caffeine dehydrates you so you need to drink plenty of water to reduce dehydration symptoms, such as fatigue or headaches.
  • While iodized table salt is usually considered something that’s best avoided, increasing your intake of high mineral sea salt improves your water retention and replenishes your salt levels.
  • Supplement with magnesium in liquid form and foods rich in potassium, such as avocado, nuts, mushrooms, leafy salads, and bone broth.

You’ll discover that following the ketogenic diet is extremely rewarding because you’ll begin to feel some benefits within weeks. However, it may take at least six months to begin to feel the full advantages when attempting to reverse cognitive decline. The ketogenic diet tweaked to improve neuroprotection is a powerful tool in your quest for optimal health. Too often we treat the symptoms of disease when we could have headed off the condition years or decades earlier. Your body is amazing and can reverse the impact of poor diet, stress, and sometimes even genetics if you make the necessary changes.

What do you have to lose? Schedule an appointment at the Hoffman Centre For Integrative and Functional Medicine and get started with the ketogenic diet today.

Resources:

  1. https://www.alz.org/alzheimers-dementia/facts-figures
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  35. Mercola A Beginner’s Guide to the Ketogenic Diet: An Effective Way of Optimizing Your Health
  36. https://www.apollohealthco.com/dr-bredesen/ Dr Bredesen’s ReCODE Report Nutritional Guidelines Ketoflex 12/3
  37. https://bodybio.com/
  38. Organic Creamed Coconut – www.earthschoice.ca
  39. Quality Nuts and Seeds  – www.ranchovignola.com and https://nuts.com/nuts/pili
  40. Quality Olive Oil – www.rawelements.ca
  41. Nut pods unsweetened coffee creamer – www.naturamarket.ca
  42. MCT emulsified coffee creamer – www.onnit.com
  43. Exogenous ketone powder – www.perfectketo.com (salted chocolate caramel flavor is best)
  44. Ketone and glucose meter – www.keto-mojo.com
  45. Humanly raised Certified organic beef, pork, turkey, chicken, and eggs https://www.sunworksfarm.com/certified-organic-beef/     (Bush Lane Organics/ Community Natural Foods/ Amaranth Whole Foods/ Planet Organics-chicken & eggs mainly, other meats can be ordered). Also TK Ranch meats at https://tkranch.com/