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Mast Cell Activation Disorder
Mast cell activation disorder (MCAD), also called mast cell activation syndrome (MCAS), is a condition of aberrant mast cell activity in response to stimuli that normally do not activate mast cells or with excessive mast cell responses.
Mast Cell Biology
Mast cells are cells of the immune system that derive from bone marrow. Immature cells are released into the blood and travel to different locations throughout the body, directed by different chemicals produced by other immune cells. When they reach their destinations, they differentiate into their mature forms and remain local; they do not return to general circulation.
Mast cells are found in all tissues except the central nervous system and the retina of the eye, and can be divided into “mucosal” and “connective tissue” types. (1,2) Mucosal mast cells are found in the lining of the organs and tissues and the connective tissue types are found in high numbers in connective tissues, including tendons, ligaments, cartilage, and fat.
Mast cells store a huge number of different chemicals. The most well-known ones include histamine, interleukins, proteoglycans (e.g., heparin), tryptase, proteases, other enzymes, and cytokines, which are stored in sacs or granules. When the mast cell is stimulated by a trigger, they release the contents of their granules into the surrounding tissues, which produce local responses characteristic of mediator(s) released. (3) On stimulation, mast cells can also synthesize new chemicals in addition to the pre-formed ones in the granules. Mast cells can be triggered by allergens causing an IgE antibody reaction with receptors on the surface of the mast cell. However, mast cells can be affected by triggers other than IgE, and the amount, duration, and rate of the response will depend on the type of trigger. (4)
The chemicals released by mast cells have a wide range of effects. Histamine is most often associated with allergic responses, but it also causes the release of gastric acid in the stomach, acts as a neurotransmitter in the brain, and a communication chemical for many cells of the immune system. (5) Heparin prevents clot formation and tryptase plays an important role in inflammation. Proteases are enzymes that break down proteins, which can be important in destroying bacteria or tissue remodeling from wounds. Cytokines are communication chemicals of the immune system. Other mast cell chemicals may oppose inflammation or regulate the release of mediators from the granules and can enhance or suppress their actions once released.
Mast cells play an important role in immune function. They can exert a positive (enhancing) or negative (suppressing) effect on other cells of the immune system, changing the overall immune response. They serve as a first-line defense and are involved in the development and maturation of T cells. (6) They can help clear bacterial infections, and enhance immune reactions by modulating inflammatory responses to infections. (7) Mast cells also play a key role in clearing the chemicals produced by the immune system to kill infections, which is important because many of these chemicals can have adverse effects at high concentrations. (7) Mast cells can also have protective functions against different venoms and parasites and can help prevent sepsis-related mortality associated with infections. (8) Several of the chemicals released by mast cells can promote blood vessel formation, which is important in wound healing. (9)
Overall, mast cells can have a powerful effect on every system of the body. These effects can be protective or harmful, depending on the type and amount of the chemicals they release into the surrounding area.
Other Mast Cell Related Conditions
Most commonly, mast cells are associated with allergies because of the histamine release due to the IgE antibody trigger. With exposure to an allergen, people generally have symptoms in the system that contacted the allergen, i.e., respiratory symptoms from an inhaled allergen, or skin symptoms from a topical exposure. Exposure to food allergens also most commonly cause gastrointestinal symptoms but can cause more systemic symptoms if the allergen is absorbed into the body through the intestines.
Other conditions associated with mast cells are systemic mastocytosis (SM) and possibly histamine intolerance. SM differs from MCAD in that SM is a group of disorders characterized by increased actual numbers of mast cells and infiltration of mast cells into the skin, other organs, or both. (10) SM is caused by a gene (KIT-816V) mutation that allows for uncontrolled proliferation of mast cells. “This mutation isn’t seen consistently in MCAD but has supported theory that there may be mutations affecting mast cell biology. A genetic cause is a likely factor because the risk of MCAD in patients with a relative with MCAD is triple that of the general population.” (11) Dr. Lawrence Afrin, one of the main researchers into MCAD, theorizes that there are “one of more inheritable ‘genetic fragility factors’ which interact with different stressors…to cause additional non-inheritable mutations” (11) and that combination of mutations can lead to MCAD.
Histamine intolerance can cause many similar symptoms to MCAD but appears to be more limited to histamine, rather than the whole variety of mast cell chemicals, and may have more to do with an inability to breakdown histamine than a condition of mast cell instability. (12)
Symptoms of MCAD
Symptoms of MCAD can be extremely varied and can occur in every system of the body. Symptoms are often low-grade and chronic and can be episodic with periods of calm and flares. (13) One of the most important characteristics is that there are multiple symptoms in multiple systems of the body. (13)
Dr. Afrin and colleagues have developed an extensive list of symptoms they have observed with patients and includes the following:
- Constitutional: fatigue/malaise, weakness, “chronic fatigue syndrome”, subjective and/or objective increased or decreased temperature, “sense of feeling cold much of the time”, sweats (not always nocturnal), flushing, redness or paleness, increased or decreased appetite, early fullness when eating, weight gain or loss, chemical and/or physical environmental sensitivities (often odd)
- Skin: rashes , freckles, dry skin, warts, skin tags, inflammation of hair follicles, ulcers, eczema, itching, sometimes triggered by exposure to water, stretch marks, streaking on scratching the skin, hair thinning and loss, brittle nails, longitudinal ridges in nails, poor wound healing
- Lymph: swollen lymph nodes, often changing in size or location, sometimes no symptoms but may be tender, left upper quadrant discomfort in abdomen
- Lung: nasal inflammation, sinusitis, throat inflammation, bronchitis, lung inflammation or pneumonitis (often confused with infectious pneumonia), cough, difficulty breathing/dyspnea (often low-grade, “I just can’t catch a deep breath”), wheezing, obstructive sleep apnea, pulmonary hypertension
- Cardiovascular: lightheadedness, weakness, dizziness, vertigo, fainting, postural orthostatic tachycardia syndrome or neurocardiogenic fainting, high and/or low blood pressure, palpitations, abnormal heart rhythms, chest discomfort or pain, atherosclerosis/spasm, heart failure , aneurysms, hemorrhoids, varicose veins, aberrant angiogenesis (cherry angiomas, hemangiomas, arteriovenous malformations, spider veins) , migratory swelling (often non-dependent and with normal cardiac and renal function)
- Gastrointestinal: swallowing air, swelling (angioedema) in any segment of the GI, difficulty swallowing, bloating/gas, abdominal pain/inflammation (often migratory) , queasiness, nausea, vomiting (sometimes “cyclical”), diarrhea and/or constipation (often alternating), malabsorption (more often selective micronutrient than general protein-calorie malabsorption), abdominal edema/water retention, gastroesophageal reflux disease (often “treatment-refractory”) , inflammatory or irritable bowel syndrome, microscopic colitis
- Genito-urinary: inflammation of urethra, bladder, or kidney (often migratory), inflammation of vagina or prostate, chronic kidney disease, endometriosis, chronic low back pain or side pain, hydronephrosis , infertility, erectile dysfunction, decreased libido , miscarriages
- Musculo-skeletal: muscle pain, often diffusely migratory, fibromyalgia , arthritis (typically migratory), joint laxity/hypermobility, diagnosis of Ehlers-Danlos Syndrome Type III, osteoporosis/osteopenia, osteosclerosis, musculoskeletal pain poorly responsive to NSAIDs and narcotics, possible elevated creatine kinase
- Neurologic: headache (esp. migraine), peripheral sensory and/or motor issues including abnormal sensations, tics, tremors (typically resting) , chronic inflammatory demyelinating polyneuropathy, seizure disorders (can be “treatment-refractory”), pseudoseizures, dysautonomia
- Endocrine/Metabolic: abnormal electrolytes (including magnesium), abnormal liver function tests, delayed puberty, menstrual cramps, hypothyroidism or hyperthyroidism, abnormal cholesterol/lipids, elevated ferritin, selective vitamin and/or other micronutrient deficiencies
- Immune: hypersensitivity reactions, autoimmunity, increased susceptibility to infection, elevated or decreased levels of one or more types of immunoglobulin
- Blood: elevated red blood cell count (polycythemia), anemia (may be macrocytic, normocytic, or microcytic), high or low white blood cell counts, high monocytes, eosinophils or basophils, high or low platelets, clotting disease, easy bruising/bleeding
- Psychiatric: mood disturbances (g., anger, depression), bipolar affective disorder, attention deficit-hyperactivity disorder, post-traumatic stress disorder, anxiety and panic, psychoses, memory difficulties, word-finding difficulties, other cognitive dysfunction, sleep disruptions (13)
Research is being done into the potential causative role of mast cells in plaque build-up in arteries, because of the pro-inflammatory chemicals (14) as well as in cancer, both from the inflammatory and blood-vessel building effects. (15) However, the net role of mast cells in cancer development may benefit either the host or the tumor, depending on a variety of factors, including genetics, overall immune health, and the micro-environment of the tumor location. (15)
Because of the effects on the immune system, MCAD may also be associated with an increased risk of autoimmune disease and chronic infection. (11) There may also be quality of life issues and narcotics risk with chronic pain and malnutrition from intestinal inflammation. (11).
Diagnosis of MCAD
Diagnosis of MCAD is based on symptoms, history, lab testing, response to MCAD-based treatment, and ruling out other possible conditions. Symptoms and history can be identified by the patient interview and the checklist developed by Dr. Afrin and colleagues. (13) Lab testing can be difficult because of the challenges with many of the lab tests. First, many of the tests require very specific handling procedures because several of the tests are not heat-stable. If the samples are not kept chilled for the entire time between collection and analysis, false negative results are highly possible. Once the sample is provided to the lab, it may be difficult to know if the sample was kept chilled the entire time.
Second, some of the tests need to be run during a flare-up of symptoms which can be difficult for collection; results from samples collected outside a flare-up may show falsely low results. Third, the samples are collected from blood and/or urine, which reflect conditions throughout the body. A person could still have very significant local mast cell effects while these systemic test results could be negative. Additionally, many of the local labs I have contacted do not even run some of the tests recommended for MCAD diagnosis. Given these challenges, I discuss with each patient the advantages and disadvantages of running the different tests that could give us information about MCAD. Many patients also opt for a trial of MCAD-based therapy to see if symptoms improve.
Treatment of MCAD
MCAD is an extremely complex condition with a myriad of presentations. As such, I follow the treatment principles outlined by Dr. Afrin:
- “#1: get patients feeling better, not perfect and not all the time
- #2: be patient and persistent and use a methodical approach
- #3: change only one thing at a time
- #4: start with the cheapest medications and change only as necessary
- #5: if a patient destabilizes, review what changed over the weeks before to try to identify a cause
- #6: remember that active and inactive ingredients of medications can cause flare-ups
- #7: simpler is better
- #8: if one drug in one class doesn’t work, don’t give up on all the drugs within that class (check inactive ingredients)
- #9: identify and avoid triggers
- #10: remember all the other preventative screenings and general health measures” (11)
It is important to keep in mind that “with the exception of classic histamine-related symptoms, at present it is virtually impossible to predict effective therapy for the individual MCAS patient based on the presenting symptoms and findings.” (11)
Identifying and avoiding triggers is crucial to treatment. Avoiding a flare-up is much easier than trying to calm it once it has started. However, potential triggers can be extremely varied and the list I’ve compiled from a variety of sources may include:
- Stress, sympathetic activation, accidents, surgery
- Sleep deprivation
- Sun/heat, temperature changes (especially sudden), pressure/touch
- “caine” anesthetics, NSAIDs, narcotics, active or inactive ingredients in any medications
- Aspirin (especially for tryptase-driven issues)
- Alcohol, high sugar
- Oxidative stress
- Zinc or vitamin C deficiency
- Excess salt
- Chronic infection
- Exposure to allergens
- Hormone imbalances
Specific treatment for MCAD can include pharmaceuticals, naturopathic treatments, and other supportive therapies. Pharmaceutical treatments may include:
- steroids to reduce inflammation;
- mast cell stabilizers (ketotifen and cromolyn sodium);
- histamine blockers for histamine-related symptoms;
- leukotriene blockers; and
- medications to manage symptoms, such as pain or anxiety. (11)
There are some medications that have some anecdotal use, and some that theoretically could be helpful but there is no MCAD-specific data on their efficacy. (11) There are also some medications that are still in clinical trials and could become options in the future.
Naturopathic treatments include:
- evaluation of diet, especially for high histamine, high histidine, and high salicylate foods;
- evaluation of intestinal bacterial balance because certain types of bacteria produce histamine while others break it down (16);
- herbal and nutritional mast cell stabilizers;
- anti-inflammatory herbs and nutrients;
- treatment to support histamine breakdown, especially via methylation; and
- lactoferrin especially for tryptase and heparin.
Other therapies may be non-medication ideas for symptom support and/or stabilization. For example, for a patient with low blood pressure, maintaining consistently adequate water intake and electrolytes along with wearing compression garments might be helpful.
I also feel that part of naturopathic treatment is patient advocacy. The understanding of MCAD in the medical field is still emerging and many practitioners are not aware of the condition or diagnosis. Many patients are told their symptoms are “all in their heads”; while MCAD can cause many neurologic and psychiatric symptoms, there is a true physiological basis for what MCAD patients are experiencing.
Understanding and treating MCAD takes patience and perseverance, and with both, significant improvements can be made for people who never had answers before.
(11) Afrin, L. Never Bet Against Occam: Mast Cell Activation Disease and the Modern Epidemics of Chronic Illness and Medical Complexity. 2016
(13) Afrin LB, Molderings GJ. A concise, practical guide to diagnostic assessment for mast cell activation disease. World J Hematol2014; 3(1): 1-17
Epstein-Barr virus (EBV) is part of the Herpes family of viruses. There are eight separate viruses within this family: Herpes simplex 1 and 2 (HV 1, HV 2), Varicella (HV 3), EBV (HV 4), Cytomegalovirus (HV 5), Herpes virus 6 (HV 6), Herpes virus 7 (HV 7), and Kaposi sarcoma-associated virus (HV 8) (1). HV1 and 2 are most commonly associated with oral and genital herpes. Varicella causes chickenpox and shingles and CMV causes CMV mononucleosis, which is similar to EBV mononucleosis but is often less severe. HV6 and HV7 are most commonly associated with roseola infantum. HV8 is not a known cause of acute illness but may cause Kaposi sarcoma and AIDS-related non-Hodgkin lymphomas. (1)
Infection and Transmission
All herpes viruses can remain latent within the body and EBV infects the B cells of the immune system. EBV spreads primarily through body fluids, most commonly through saliva (3); it can also be transmitted through sexual contact, blood transfusions, and organ transplants (3). EBV does not survive on surfaces but it “can be spread by using objects, such as a toothbrush or drinking glass that an infected person recently used. The virus probably survives on an object at least as long as the object remains moist.” (3)
An infected person can shed the virus for weeks before symptoms appear and “if the virus reactivates, (a person) can potentially spread EBV to others no matter how much time has passed since the initial infection.” (3) People with reactivated infections may also be able to transmit EBV to other people even if they themselves do not have active symptoms. (1)
Symptoms of Acute Infection
Half of children are infected with EBV before the age of 5 (2) and “EBV infections in children usually do not cause symptoms, or the symptoms are not distinguishable from other mild, brief childhood illnesses.” (3)
Symptoms of infectious mononucleosis develop most often in older children and adults and include fever, sore throat (pharyngitis), and lymph node swelling (adenopathy). (2) The lymph node swelling is usually symmetrical, can include any group of lymph nodes, and may be the only symptom (2) Patients may also experience enlargement of the spleen and/or liver, swelling around the eyes, and rash.
The typical symptoms of acute infectious mononucleosis can be similar to those of other infections, and patients with this presentation should also be evaluated for primary HIV infection, cytomegalovirus infection, “toxoplasmosis, hepatitis B, rubella, or atypical lymphocytes associated with adverse drug reactions.” (2)
Complications of Acute Infection
Patients typically recover completely from EBV mononucleosis but fatigue can last for months after other symptoms resolve. (2, 3) Acute complications of the infection are rare but may be significant and can include:
- Neurologic complications:encephalitis, seizures, Guillain-Barré syndrome, peripheral neuropathy, viral meningitis, myelitis, cranial nerve palsies, and psychosis
- Hematologic complications: granulocytopenia, thrombocytopenia, hemolytic anemia
- Splenic rupture
- Respiratory complications: upper airway obstruction due to adenopathy
- Hepatic complications: elevated aminotransferase levels, jaundice (2)
Chronic Infection Concerns
In addition to causing infectious mononucleosis, EBV is known as a potential cause of hepatitis, encephalitis, nasopharyngeal carcinoma, Hodgkin lymphoma, and Burkitt lymphoma (1, 2). While EBV may remain latent for many people, significant research is being done into links between EBV and many autoimmune diseases. A search of the NIH website for research done in just the last 5 years showed studies linking EBV as a potential cause of the development and exacerbation of multiple sclerosis (4, 5, 6), lupus (5), rheumatoid arthritis (7, 8), oral lichen planus (8), Sjögren’s syndrome (7, 9), Hashimoto’s and Grave’s diseases (autoimmune thyroid diseases) as well as possibly primary thyroid lymphoma (10). “Autoimmune liver diseases (AiLDs), including autoimmune hepatitis (AIH), primary biliary cirrhosis (PBC), and primary sclerosing cholangitis (PSC), have a potential causative link with EBV” (11) as do “interstitial pneumonia, malignant lymphoma, and coronary aneurysm.” (12)
The findings of a 2015 study indicated that EBV infections can become life-threatening in rare cases, but in contrast, “a range of other EBV-positive malignancies of lymphoid or epithelial origin arise in individuals with seemingly intact immune systems through mechanisms that remain to be understood.” (13) This indicates that EBV may cause significant immune disruption, including cancers, in otherwise immune healthy patients, through routes and interactions with other factors that we have not yet identified. Given that the vast majority of the population has been infected with EBV but not everyone develops these conditions, we know that EBV infection alone is not the cause. However, we also do not know what the characteristics are that would cause any individual person to go on to develop one of these conditions with EBV as one of the causative factors.
Diagnosis of acute infectious mononucleosis is based on symptoms and signs and a positive heterophile antibody (monospot) test. Patients should know that “heterophile antibodies are present in only 50% of patients less than 5 years old and in about 80 to 90% of adolescents and adults with infectious mononucleosis.” (2) This test may also give a false-positive result in patients with acute HIV infection. (2) If there is high suspicion of mono but a negative monospot, it is worth repeating the test after 7 to 10 days, as the antibody levels rise in the 2nd and 3rd weeks of illness. (2) A complete blood count may also show atypical lymphocytes; it is important to know that “atypical lymphocytes may also be present in HIV or CMV infection, hepatitis B, influenza B, rubella, or other viral illnesses… however, very high atypical lymphocyte counts are typically seen only in primary EBV and CMV infection.” (2)
Laboratory testing may also include antibodies to EBV. There are four different types of EBV antibodies: IgG antibodies for Early Antigen (EA-IgG), IgM antibodies to the viral capsid (VCA-IgM), IgG antibodies to the viral capsid (VCA-IgG), and IgG antibodies to the nuclear antigen (EBNA-IgG). These represent different phases of the immune system’s response to different parts of the virus itself. Most labs provide a table to interpret the pattern of a patient’s results. The following is from Labcorp:
|EBV Interpretation Table (14)|
|Key — Antibody present: + Antibody absent: −|
|Acute primary infection||+||±||+||−|
If all these antibody tests are negative, then it means the patient has never been exposed to EBV. A positive titer for VCA-IgM indicates a primary EBV infection because the IgM antibodies are the first to appear and the first to disappear, typically within 3 months after infection. (2) VCA-IgM antibodies can also reappear in a reactivated infection, but are not always present. The EA-IgG and VCA-IgG antibodies develop after the IgM antibodies and there can be a time of overlap between the presences of these two types of antibodies. The EBNA-IgG antibodies are the last to appear and VCA-IgG and EBNA-IgG persist for life.
According to the Merck Manual, “over 90% of adults are seropositive for EBV.” (2) This means that 90% of adults in the general population have been exposed to EBV and will show positives for past infection. This is a very different pattern than that of patients with active infection. Additionally, while the lab table indicates that the EA-IgG is positive for a reactivated infection, Dr. Oethinger , the director of microbiology at Providence Laboratory, indicated in personal communication that “the EA doesn’t need to be positive again during reactivation.” (15) This means that the pattern between past and reactivated infections can be difficult to differentiate and individual patients must be evaluated based on symptoms as well as potential risks for future issues.
Treatment of EBV needs to be assessed based on a patient’s current symptoms, test results, and concerns for possible development of future conditions linked to EBV. Because I see many patients with autoimmune conditions, I am very concerned about the developing body of research linking EBV as a potential causative factor for many common autoimmune diseases.
Autoimmune diseases occur due to a combination of many different genetic and environmental factors. Some factors, such as our genes, we cannot change. There may be other factors medicine hasn’t identified yet. Since these are areas we cannot treat, I look to those known environmental factors that are significant risk factors. By reducing their impact, we can hopefully prevent future disease or reduce disease activity for those patients already diagnosed with autoimmune conditions.
Western medicine has no options for treatment of EBV infections except supportive care and corticosteroids possibly for severe disease. (2) The anti-virals that are effective for other herpes family viruses (especially acyclovir) do not appear effective against EBV. Studies have shown that acyclovir reduces shedding of EBV in saliva, but it does not change any single symptom or course of disease and viral titers returned to pre-treatment levels one to three weeks after cessation of therapy. (16, 17, 18) These are older studies, but as of February 2016, the Merck Manual still states “there is no convincing evidence to warrant (acyclovir’s) clinical use” for EBV infection. (2) The Merck Manual does list two other medications as showing possible activity against EBV: cidofovir and foscarnet. However, both of these medications are only given IV and are limited by significant kidney toxicity. (2) Therefore, they would be reserved for the most severe cases.
Naturopathic medicine has many options for treating EBV both in terms of general anti-virals and options specifically designed for EBV. Levels of immune-essential nutrients, such as vitamin A, vitamin D and zinc, can be optimized. Monolaurin is a byproduct of coconut oil and is commonly used as a general anti-viral. Lysine, which is often used to treat herpes simplex outbreaks, can also be used for EBV, as can colostrum for patients who do not have issues with dairy. There are numerous herbs, including olive leaf, garlic, goldenseal, Echinacea, and grape seed, and mushrooms, including cordyceps, turkey tail, shiitake, and lion’s mane, that can be used individually or in combination formulas. Gemmotherapy preparations of several herbs are designed specifically to treat intra-cellular viruses, and essential oils can be added to herbal combinations. Treatments can also include supporting the T-regulatory cells of the immune system, including probiotics, fish oil, vitamin D, and glutathione.
When using any of these therapies, it is important to start with low doses and increase slowly to patient’s tolerance. Many people discuss “die-off” reactions with Lyme disease or candida overgrowth, and the same may be said for EBV infections. As such, a complete plan would also include supports for detoxification and elimination, and would balance and rotate any anti-viral therapies.
Because these anti-virals are generally safe and well-tolerated, and the impacts of autoimmune disease can be devastating, this is one situation where I personally err on the side of treatment, especially in cases where patients have very high antibody levels. My hope is that we can provide safe and relatively inexpensive treatment that could prevent a future autoimmune condition by treating a potential cause before symptoms arise.
(4) Epstein-Barr virus-specific adoptive immunotherapy for progressive multiple sclerosis (https://www.ncbi.nlm.nih.gov/pubmed/24493474)
(5) Epstein-Barr virus in multiple sclerosis. (https://www.ncbi.nlm.nih.gov/pubmed/25162741)
(6) Multiple sclerosis and environmental factors: the role of vitamin D, parasites, and Epstein-Barr virus infection. (https://www.ncbi.nlm.nih.gov/pubmed/26046559)
(7) Epstein-Barr virus in systemic autoimmune diseases (https://www.ncbi.nlm.nih.gov/pubmed/24062777)
(8) Epstein-Barr virus and its association with rheumatoid arthritis and oral lichen planus. (https://www.ncbi.nlm.nih.gov/pubmed/26980953)
(9) Connective tissue diseases: Epstein-Barr virus in Sjögren’s syndrome salivary glands drives local autoimmunity. (https://www.ncbi.nlm.nih.gov/pubmed/24934188)
(10) The role of Epstein-Barr virus infection in the development of autoimmune thyroid diseases. (https://www.ncbi.nlm.nih.gov/pubmed/25931043)
(11) Epstein-barr virus as a trigger of autoimmune liver diseases. (https://www.ncbi.nlm.nih.gov/pubmed/22693505)
(12) Possible autoimmune hepatitis induced after chronic active Epstein-Barr virus infection. ( https://www.ncbi.nlm.nih.gov/pubmed/26183510)
(13) The immunology of Epstein-Barr virus-induced disease. (https://www.ncbi.nlm.nih.gov/pubmed/25706097)
(15) personal communication, Dr. Kimberly Hindman and Dr. Oethinger
(16) Acyclovir treatment in primary Epstein-Barr virus infection. A double-blind placebo-controlled study. (https://www.ncbi.nlm.nih.gov/pubmed/3006226)
(17) Acyclovir and Epstein-Barr virus infection. (https://www.ncbi.nlm.nih.gov/pubmed/6313591)
(18) Acyclovir treatment in infectious mononucleosis: a clinical and virological study. (https://www.ncbi.nlm.nih.gov/pubmed/3036715)
What is pyroluria?
Pyroluria is a genetic disorder caused by abnormal hemoglobin synthesis. Hemoglobin is the protein in red blood cells that contains iron and carries oxygen throughout the body. During hemoglobin synthesis, by-product compounds called kryptopyrroles are formed. This is a normal process even though there is no known function of kryptopyrroles in the body. However, in people with pyroluria, these compounds are produced to excess, especially under stress, and create deficiencies of vitamin B6 (pyridoxine) and zinc. Because of this, most of the signs and symptoms associated with pyroluria are due to deficiencies of B6 and zinc.
Vitamin B6 and zinc are essential in the body. Vitamin B6 is required for more than 100 enzyme reactions in the body. It is specifically required for:
- Converting food into glucose for energy;
- Niacin production;
- lipid metabolism,
- carnitine synthesis,
- production of neurotransmitters serotonin, dopamine, norepinephrine, histamine, and GABA;
- functioning of the immune system;
- formation of red blood cells;
- control of homocysteine (along with B12 and folate); and
- hormone modulation.
Zinc is also essential for enzyme function and more than 50 enzymes in the body contain zinc. Zinc is important for:
- cell growth and replication;
- hormone activity and reproduction;
- vision, especially night vision;
- immune function;
- protein metabolism;
- wound healing and blood clot formation;
- breakdown of carbohydrates;
- thyroid function;
- resistance to stress;
- maintaining cognitive function, memory, and learning; and
- normal appetite, taste, and smell.
Moderate zinc deficiency is also associated with disorders of the intestine which interfere with food absorption (malabsorption syndromes), which can cause additional symptoms and health conditions. This may be why tendency to iron deficiency or low iron levels can be seen in patients with pyroluria.
Signs and symptoms of pyroluria
This condition is important to know about because a high incidence of pyrrole disorder is found in individuals with many conditions, including:
- Autism spectrum disorders
- obsessive-compulsive disorder
- bipolar disorder
- alcoholism and addictions
- Multiple sclerosis
- Lyme disease
“As many as 50% of those with autism, 40% of alcoholics, 70% of schizophrenics, 70% of persons with depression and 30% of persons struggling with ADD may have pyroluria underlying these conditions and make them very difficult to reach with traditional and even holistic therapies. –But pyroluria isn’t limited to these populations. As much as 10% of the population may have this metabolic condition and not know it…but may have lifelong symptoms associated with it that tend to worsen with age…and stress.” (http://www.primalbody-primalmind.com/do-you-have-pyroluria/)
In general, the symptoms of pyroluria can have a mysteriously intractable quality to them, and primarily relate to the B6 and/or zinc deficiencies. One source also indicated that accumulated pyrroles can also interfere with the conversion of B6 (pyridoxine) to its active form, pyridoxine-5-phosphate (P5P). The deficiency of P5P can then reduce hemoglobin synthesis, worsening many symptoms. Lower levels of P5P are also associated with lower glutathione levels, which will further increase oxidative stress and decrease detoxification in the body, causing additional symptoms.
I have listed symptoms gathered from a variety of sources and they may include:
- poor stress tolerance
- all symptoms worse with stress
- mood swings or instability
- inner tension
- irritability or emotional reactivity
- episodic anger or aggressiveness
- very sensitive to criticism
- difficulty concentrating
- poor short-term memory
- learning problems, especially with information in written format
- headaches, especially blinding or cluster type
- poor night vision
- poor dream recall
- restless leg syndrome, tingling or tremors
- motion sickness
- sensitivity to light, smell, sound, and/or touch
- frequent or chronic infections
- slow wound healing
- tendency to autoimmune disorders
- muscle weakness
- joint pain or stiffness, especially knee or leg
- hypermobile joints, muscle pain
- gets stitch in the side when running,
especially in children
- hair loss
- premature graying of hair
- white spots on nails
- rough and dry skin
- tendency to acne, eczema, or psoriasis
- being pale, having an inability to tan, or sun burning easily
- irritable bowel syndrome
- gluten intolerance
- difficulty digesting protein and fat
- fat distribution around abdomen
- diarrhea or constipation
- abdominal tenderness
- loss of appetite
- poor sense of taste or smell
- easy bruising/bleeding
- low blood pressure
- cold hands and feet, Raynaud’s syndrome
- spider veins, varicose veins
- heart disease
- higher clotting risk
- tendency to anemia, especially iron deficiency
- fatigue and low energy reserves
- slow growth
- sensitivity to medications
- wide variety of hormonal symptoms or imbalances- thyroid, adrenal, sex hormones
I have also found two slightly different pyroluria symptom questionnaires that may also be helpful at:
One important factor in pyroluria is that the doses of zinc and vitamin B6 required for treatment may be toxic for someone with a normal metabolism. Therefore, testing prior to initiating treatment is important. False negative results are possible and there is a higher incidence of false negative results in children because they have faster metabolisms than adults. Children can still be tested; the practitioner just needs to be aware of potential false negatives and a closely monitored trial of B6 and zinc may still be warranted with a negative result but strong clinical indications. Additionally, because pyroluria is a genetic disorder, other family members should also be tested.
Because pyrroles are excreted in the urine, testing for pyroluria is an easy urine test. Prior B6 and zinc supplements need to be avoided for 24 to 48 hours prior to testing. It is important to choose a lab that corrects for the concentration or dilution level of the sample. Additionally, kryptopyrroles are light sensitive, so the lab should include methods used to prevent the degradation prior to the sample analysis.
Fortunately, pyroluria is manageable with the use of regular supplements, typically high doses of zinc and B6, higher than what can be obtained from food. The type of supplement is important so they can be effectively absorbed; zinc picolinate or gluconate and pyridoxal-5-phsphate (P5P) tend to be the best forms of these nutrients. However, some patients may do best with a combination of P5P and standard B6. Supplementation may need to start at low levels and gradually increase. Supplementation does need to be monitored to avoid toxic levels, as well as ensuring patients are avoiding competing nutrients. For example, copper-rich foods and copper-containing supplements should be avoided because they are antagonistic to zinc.
People with pyroluria also have a higher than normal need for omega-6 fatty acids, particularly arachidonic acid and gamma linolenic acid (GLA). Arachidonic acid is found in eggs, butter, red meat and liver, and GLA is found in supplements like black currant seed oil and evening primrose oil. Other helpful nutrients may include high doses of probiotics; other B vitamins; antioxidants, including glutathione and vitamins A, C, and E; other minerals, including manganese and magnesium; and amino acids, including cysteine, 5-hydroxy tryptophan (5HTP), glutamine, taurine, or glycine. Proteolytic enzymes may be needed to break up accumulated pyrroles. Patients will also need digestive, liver, and brain support as well because the effects of zinc and B6 deficiencies can be wide spread through the body.
Ongoing treatment is required and symptom relapses will occur usually within several weeks of stopping supplementation. Because people with pyroluria have difficulty dealing with the effects of stress, relapses may also occur under different types of mental, emotional, and/or physical stress, including illness, lack of sleep, or injury. However, with proper, continued supplementation, patients with pyroluria can improve their health.
http://www.health-science-spirit.com/pyroluria.htm (Walter Last)
Dr. Renee Schwartz. Seminar: Nutritional Approaches to Treating Pyroluria and Other Depression Biotypes. November 2014.
Methylation is a process where a methyl group (a carbon and three hydrogens) is attached to another substance. Current research estimates that 30 to 40 percent of the population has abnormalities in one or two of the genes for the enzyme methyltetrahydrofolate reductase (MTHFR). This enzyme converts folic acid to 5-methylfolate, which is the active form of folate; abnormalities in this enzyme’s activity can lead to decreased methylfolate production, which can have profound biochemical effects in the body. However, methylation is an extremely complex process involving multiple enzymes and pathways, not just the MTHFR, and abnormalities can occur in other genes/enzymes as well. Abnormalities anywhere in the methylation cycle can result in overall under- or over-methylation, and as such, just testing for this one gene may not show the entire picture of methylation.
Functions of Methylation: Why Should We Care?
The methylation process can affect every cell and process in the human body.
Methylation and acetylation are the two major chemical gene regulators. Not all genes are active at all times and methylation appears to be one of the major methods by which cells lock genes in the “off” position. This is particularly important for turning off cancer genes, but all genes need to have a balance of activity; no gene should be active constantly. Because of this, proper DNA methylation is essential for cell growth and division, and research is indicating links between abnormal methylation with aging, cancer development and progression, and birth defects. Abnormal cell growth can affect any cell that naturally has a rapid turn-over-rate, such as skin, red and white blood cells, and the intestinal lining.
Methylation is required to activate vitamin B12 and folate; without the addition of that methyl group, those vitamins are inactive. If a person has abnormal methylation, the levels of B12 and folate measured in the blood could be normal, but the body could be functioning at a deficiency because those vitamins aren’t in the active form. Vitamin B12 and folate are cofactors in many processes and are essential in red blood cell production and therefore, energy metabolism.
Protein Metabolism and Homocysteine
Methylation is also essential for overall protein metabolism and specifically, the conversion of the amino acid homocysteine to methionine or cysteine. Homocysteine is highly inflammatory and a major and independent risk factor for coronary artery disease and heart disease. Homocysteine levels can be measured in the blood and can be used to evaluate both inflammation levels but also methylation status. Most labs use a reference range that has a normal level just below a cutoff value (e.g., < 15). I evaluate a patient’s result using both upper and lower values to provide a balanced range since either too much or too little methylation may be problematic.
Neurotransmitter Synthesis and BH4 Recycling
Synthesis of neurotransmitters, including serotonin, and dopamine, is dependent on methylfolate, which acts as an enzyme cofactor. If the methylation process is defective, a lower amount of methylfolate may be available, reducing the production of these neurotransmitters.
Methylfolate is also essential for the recycling of tetrahydrobiopterin (BH4), which is an essential cofactor for the production of the neurotransmitters serotonin, melatonin, dopamine, norepinephrine, and epinephrine. BH4 is also required for the production of nitric oxide, which is a strong vasodilator. There is some research that indicates a lack of BH4, and therefore, nitric oxide, may be responsible for circulation-related diseases.
One of the other major roles of methylation is detoxification, as it is one of the major Phase 2 detoxification pathways in the liver. Detoxification occurs in two phases; the first phase occurs by enzymes in the liver cells and it serves to break down a substance so that in Phase 2, another group can be added to it to make it easier for the body to eliminate. There are a number of different phase 2 pathways, and different substances, including hormones, neurotransmitters, and chemicals, are detoxified through different pathways. The challenge in this system lies in the fact that often the product of Phase 1 detoxification is more toxic than the original substance and if there are problems with its Phase 2 pathway, that more toxic substance will remain active in the body for a longer time period.
One particular issue with methylation as a detoxification route is that estrogen is one of the main substances that are detoxified by methylation. Estrogen gets converted to hydroxyl-estrogen via Phase 1, and this form of estrogen is highly toxic, causing DNA damage and contributing to breast cancer risk. Through Phase 2 methylation, that hydroxyl-estrogen is converted to the much less active and safer methyl-estrogen; this form of estrogen actually appears to have some beneficial cardiovascular effects. Understanding the role of methylation becomes exceptionally important in looking at a woman’s estrogen exposure and breast cancer risk, separate from her total estrogen level or her breast cancer genetic status.
Impaired methylation can also decrease glutathione production; glutathione is the primary antioxidant in the human body and one of the major detoxification routes, especially for heavy metals. Methylation is also the breakdown pathway for histamine, and elevated levels of histamine are associated with allergies and brain inflammation. Blood levels of histamine can be evaluated along with homocysteine to give a window into a person’s actual methylation status.
Methyl group donation is essential for the synthesis of carnitine and CoQ10. These two nutrients are required to produce cellular energy in the mitochondria. Without them, the mitochondria cannot produce energy (ATP), which is the biochemical energy source for every process in the body.
Symptoms of Methylation Abnormality
Many different symptoms can be associated with methylation abnormalities, and patients can be overmethylators or undermethylators. Not every patient with a methylation abnormality will have all of these symptoms and some of these symptoms can also be associated with other causes besides methylation. Additionally, there may be overlap between the two patterns.
Symptoms of those two patterns can include:
|Anxiety/ panic attacks||Low pain tolerance|
|ADHD, Hyperactivity, restless legs||Frequent headaches|
|Sleep disorders||Perfectionism, rumination about past|
|Food and chemical sensitivities||Fewer food allergies|
|Lack of respiratory allergies||Environmental/respiratory allergies|
|Dry eyes and mouth||Easy tears, saliva|
|Low libido||High libido|
|Depression but usually worse on SSRIs||Depression better with SSRIs, antihistamines|
Normal methylation and methylfolate levels in particular clearly profoundly affect our health. The question becomes, if a person has one or more of those genetic abnormalities, has evidence of abnormal homocysteine and/or blood histamine levels, and/or has symptoms associated with abnormal methylation, how can we support that process?
There are several supplements we can use to support methylation both directly and indirectly. These include:
- 5 MTHF and methylcobalamin (B12): these may act more directly as enzyme cofactors than methyl donors to the entire methylation cycle.
- Choline, TMG (trimethylglycine or betaine), and DMG (dimethylglycine): Choline is metabolized into TMG, which is involved in SAM(e) synthesis. DMG is formed when TMG loses one of its methyl groups. All three provide sources of methyl groups.
- S-adenosyl methionine [SAM(e)] and methionine: SAM(e) is produced in the liver from the amino acid methionine and is one the best methylating agents available. The challenge is that SAM(e) can be expensive to maintain appropriate dosing levels. Therefore, supplementing with methionine and supporting liver function may be an alternative solution.
Other nutrients that indirectly support methylation and may be considered include zinc, phosphatidylserine, inositol, calcium, magnesium, B complex, and Vitamins B2, B6, A, C, D and E. Glutathione or N-acetylcysteine supplementation may be needed because of the effect methylation has on glutathione production.
It is important to note that some patients who undermethylate do not tolerate methylfolate, especially in high doses. For those patients, other methyl donors may be a better way to support methylation. Additionally, the dose of methyl supports may need to be titrated up slowly to allow for other enzymes time to upregulate. For example, the COMT enzyme breaks down the catecholamine neurotransmitters (serotonin, dopamine, and norepinephrine). If a patient starts a high dose of methyl support and production of those neurotransmitters significantly increases, the COMT enzyme may not be able to keep up with the breakdown, leading to a state of catecholamine excess. Therefore, methylation support may need to be started slowly to reach a relatively high dose to replete deficiencies, and then decreased down to a maintenance level.
Methylation clearly plays a significant role in human health. However, this is definitely one situation where one size does not fit all. Patients need to be evaluated for their methylation status and different methylation supports may need to be used in different doses at different times to support optimal health.
All You Ever Wanted to Know About Thyroid
Thyroid anatomy and physiology
Thyroid gland is a butterfly shaped organ located in front of the throat. The follicular cells of the thyroid gland secrete tetraiodothyronine (T4) and triiodothyronine (T3), which are synthesized by attaching iodine atoms to the amino acid tyrosine. T3 and T4 combine with tyrosine-binding globulin (TBG), a transport protein in the blood, which carries the hormones throughout the body. Approximately 75 percent of the thyroid hormone is bound to TBG, and only the free/unbound portion of the hormone can act in the body.
More than 90 to 95 percent of the hormone the thyroid secretes directly is the inactive form of T4. Under normal circumstances, this T4 then gets converted into four different hormones:
- ~60 percent is converted into active T3 by the removal of one iodine atom by the 5’ deiodinase enzyme and 80 percent of this conversion occurs in the liver;
- ~20 percent is converted into reverse T3 (rT3), which is completely inactive and cannot be reactivated; and
- ~20 percent is converted into T3 sulfate (T3S) and triiodothroacetic acid (T3AC). These are inactive until an enzyme in the intestines converts them into active T3. This process requires healthy intestinal bacteria.
T3 is four times as potent as T4, but lasts a much shorter time. Therefore T4 acts as a reserve for thyroid activity because it can be converted to T3 as needed. There are also specialized cells within the thyroid that secrete calcitonin, which helps regulate calcium levels.
Thyroid hormone secretion is controlled by feedback systems with the pituitary and hypothalamus glands as well as the body’s iodine level. Low levels of T3 and T4 or a lower metabolic rate will trigger the hypothalamus to secrete thyrotropin releasing hormone (TRH). TRH then stimulates the pituitary to secrete thyroid stimulating hormone (TSH), which stimulates the production and release of T3 and T4 from the thyroid gland. So as T3/T4 levels begin to decrease in the body, TRH from the hypothalamus and TSH from the pituitary begin to increase, stimulating the thyroid gland to produce more T4. Production of thyroid hormone will also be stimulated by any situation that increases energy demand, including a cold environment, low blood sugar, pregnancy, and high altitude.
Thyroid functions in body
Thyroid hormones have a wide variety of functions in the body, including:
- regulating the basal metabolic rate to produce energy and heat;
- stimulating protein synthesis;
- enhancing triglyceride breakdown and cholesterol excretion;
- promoting normal growth and development of bone;
- affecting production and function of other hormones, including cortisol, testosterone, estrogen, progesterone, insulin, and growth hormone;
- supporting normal liver and gallbladder function, especially phase 2 detoxification;
- regulating brain inflammation and brain autoimmunity, especially through effects on microglial cells in the brain;
- influencing the actions of and receptors for neurotransmitters, including serotonin, dopamine, GABA, acetylcholine, adrenaline and noradrenaline;
- affecting methylation pathways, and therefore, estrogen metabolism and activity of B12 and folate; and
- accelerating body growth in children, especially in the nervous system.
Symptoms relating to thyroid disorders
Thyroid disorders can be generally divided into low (hypo-) or high (hyper-) thyroid, and in general, hypothyroid conditions are more common than hyperthyroid conditions. Patients with hypothyroid disorders may present with:
- weight gain even with reduced calories due to reduced overall metabolic rate;
- decreased mobilization of free fatty acids from fat tissue;
- slow degradation of lipids;
- delayed insulin response to glucose;
- slow glucose uptake by tissues and decreased glucose absorption in the intestines; and
- slower degradation of insulin, which may present clinically as hypoglycemia.
- morning headaches that wear off through the day;
- bone development delay; and
- muscle cramps and body pain.
- poor brain function;
- depression, and sometimes anxiety; and
- high need for sleep.
- sensitivity to cold/cold weather and poor circulation in extremities;
- low body temperature;
- facial swelling;
- loss of the outer third of the eyebrows;
- difficulty recovering from infections/ healing wounds;
- dry or brittle skin/hair/nails; and
- hair falling out.
- chronic low stomach acid/poor digestion;
- decreased intestinal transit time;
- altered intestinal absorption rates;
- reduced liver clearance with possible AST/ALT elevations on bloodwork;
- sluggish gallbladder contraction;
- abnormal phase II detoxification in the liver;
- decreased B12, folate, and iron absorption; and
- increased intestinal permeability to proteins.
- difficult menstrual periods and/or infertility;
- altered metabolism of androgens and estrogens;
- altered estrogen metabolism toward forms which increases risk for estrogen-related cell growth;
- reduced sensitivity at progesterone receptors (progesterone resistance); and
- increased sex-hormone binding globulin, which affects the free portions of sex hormones.
- atrial fibrillation
There may also be a painless swelling of the thyroid or a sensation of fullness in the throat. Low levels of thyroid hormone can also affect other hormones, such as estrogen or progesterone, which can then cause their own set of symptoms.
Patients with hyperthyroid disorders may present with hypermetabolism, rapid heart rate, and fatigue, weight loss despite normal to increased calories, excess heat, osteoporosis and bone demineralization, nervousness, and tremors.
Testing thyroid and what results mean
There are many tests of thyroid function and it is important to know the information that each of these tests does and does not provide.
- TSH is a direct measure of the amount of TSH produced by the pituitary. Many doctors feel this is best means of determining thyroid dysfunction because they feel normal results essentially rule out hyperthyroidism or hypothyroidism. However, using TSH to evaluate thyroid function doesn’t consider abnormal thyroid-pituitary feedback loops, peripheral thyroid metabolism/conversion issues, or autoimmune thyroid conditions.
- Total T4 (TT4) is a measure of bound and free T4 hormone. Changes in levels of TBG will produce corresponding changes in TT4.
- Free T4 (fT4) is a direct measure of the unbound T4 hormone. This can appear elevated if the TBG levels are decreased.
- Total T3 (TT3) is a measure of bound and free T3 hormone. It tightly bound to TBG (although 10 times less so than T4) and like TT4, TT3 levels are influenced by alterations in serum TBG level and by drugs that affect binding to TBG.
- Free T3 (fT3) is a direct measure of the unbound T3 hormone. This test is usually done to evaluate thyrotoxicosis or when a hyperthyroid patient has normal FT4 levels.
- Reverse T3 (rT3) is a direct measure of the reverse T3 levels. This will be higher primarily under conditions of elevated cortisol and an inability to clear rT3.
- T3 Uptake (T3U) is used to estimate protein binding and measures the number of sites for fT3 to bind with thyroxine binding proteins.
- Free Thyroxine Index (FTI) is a calculated value that corrects TT4 for the effects of varying amounts of thyroid hormone–binding serum proteins and thus gives an estimate of fT4 when TT4 is measured. While it is an older tests, the FTI is readily available and compares well with direct measurement of fT4.
- Thyroid antibodies are measurements of immune activity against different portions of the thyroid. The most common tests are thyroid peroxidase (TPO) and thyroglobulin (Tg) antibodies. These tests are used to identify cases where hypothyroidism (Hashimoto’s thyroiditis) or hyperthyroidism (Grave’s disease) is caused by autoimmune activity, and positive results indicate that treatment must be based on treating autoimmunity in addition to appropriate thyroid support.
TPO antibodies target the thyroid peroxidase enzyme, which is important in the synthesis of thyroid hormone inside the thyroid follicular cells. The TPO antibody test is the most sensitive test for detecting any autoimmune thyroid disease and are highest in patients with Hashimoto’s thyroiditis. Tg antibodies bind thyroglobulin, the major thyroid-specific protein that is crucial to thyroid hormone synthesis, storage, and release; these antibodies can interfere with thyroid hormone production. Tg is not released into circulation under normal conditions. However, inflammation, bleeding, or rapid growth of thyroid tumors can cause destruction of the thyroid follicular cells, causing Tg to leak into the blood. This process can cause the formation of Tg antibodies and the exposure of other thyroid proteins to the immune system, especially TPO.
TPO antibodies are positive in 90-100% of cases of Hashimoto’s thyroiditis and 50-80% of cases of Graves’ disease and Tg antibodies are positive in 80-90% of cases of Hashimoto’s thyroiditis and 50-70% of cases of Graves’ disease. TPO and/or Tg antiobdies may also be present in other autoimmune diseases (40% of cases), pregnancy (14% of cases) and sporadic multinodular goiter, isolated thyroid nodule, and thyroid cancer. Elevated levels of TPO or Tg antibodies may be present in 40-50% of relatives of patients with an autoimmune thyroid disorder.
TPO antibody tests are more sensitive than but equally specific to Tg antibody tests for diagnosing autoimmune thyroid conditions. However, for some patients, only the Tg antibodies are positive and anti-Tg levels should be evaluated if TPO antibodies are negative, but clinical suspicion of autoimmune thyroid disease is high. According to the Mayo Clinic, “in patients with subclinical hypothyroidism, the presence of TPO antibodies is associated with an increased risk of developing overt hypothyroidism. Many clinical endocrinologists use the TPO antibody test as a diagnostic tool in deciding whether to treat a patient with subclinical hypothyroidism.”
- Radioactive iodine uptake testing is used to help diagnose hyperthyroidism. A trace amount of radioiodine is given orally or IV and a scanner then detects the amount of radioiodine taken up by the thyroid.
It is important to know that there are medications that can affect both thyroid functioning as well as thyroid test results. Medications can:
- decrease TSH secretion;
- decrease or increase thyroid hormone production;
- decrease T4 absorption;
- increase or decrease TBG, thereby increasing or decreasing the free hormone levels;
- displace T3 and T4 from the transport proteins;
- increase liver metabolism; and
- decrease the 5’deiodinase activity.
Lab Findings with Thyroid Disorders
Lab test results will vary with different types of thyroid disorders.
With hypothyroidism, there will be a high TSH; low-normal TT4, FT4, TT3, FT3, FTI, and T3U; and normal rT3. Antibodies may be negative or positive depending if the cause is autoimmune. If hypothyroidism is caused by low pituitary functioning, the labs will be the same except that the TSH will be low instead of high. In that case, the thyroid itself may be able to function normally, but it is not getting the correct stimulation (TSH) from the pituitary. Other things to consider then include adrenal dysregulation, post-partum, thyroid receptor site resistance, and heavy metal toxicity, all of which will affect pituitary functioning.
Subclinical hypothyroidism occurs when the patient has hypothyroid symptoms and the TSH is mildly elevated but FT4 is within lab reference range; over 80% of patients have a TSH of less than 10 mIU/L. This condition is fairly common and the diagnosis can be supported by positive TPO antibodies. It may be considered a very early stage of an autoimmune condition because the majority of patients diagnosed do go on to develop full hypothyroidism, especially if those patients have positive TPO antibodies.
With hyperthyroidism, there will be a low TSH; high-normal TT4, FT4, TT3, FT3, and FTI; and normal T3U and rT3. Antibodies are almost always positive for hyperthyroidism because almost all cases are due to autoimmunity (Grave’s disease).
Thyroid underconversion is a very common pattern and occurs when the thyroid is producing T4 normally, but the T4 is not being converted to T3 correctly in the body. In this case, labs will show a normal TSH; high-normal TT4, FT4, and FTI; and low t3U, TT3, FT3, and rT3. In this case, current or past causes of downregulation of the 5’deiodinase enzyme need be investigated.
Thyroid overconversion occurs when too much T4 is converted to T3, and the chronic high T3 can lead to thyroid resistance. This is typically caused by elevated testosterone and insulin. In this case, TSH is normal with low-normal TT4, FT4, FTI; high-normal T3U, TT3 and FT3; and normal rT3.
Excess estrogen (e.g., oral contraceptives, hormone replacement therapy, pregnancy) can cause elevations of TBG. In this case, labs will show normal TSH, TT4, TT3, and rT3; low FT4, FT3, and T3U; and low-normal FTI. In this case, patients often do not respond to nutritional thyroid support or thyroid replacement and eliminating exposure to outside estrogens and balancing estrogen levels needs to be considered.
In thyroid resistance, all labs may be within normal ranges or FT4 and FT3 may be elevated. Patients may have no symptoms, or symptoms of either low or high thyroid function. This is may be caused by a fairly rare genetic condition or by functional issues, typically high cortisol, which down-regulates some of the thyroid receptor sites, making them unable to respond to thyroid hormone. For these non-genetic cases, there may also be issues with methylation (high homocysteine), vitamin A deficiency, or insulin resistance.
In Wilson’s syndrome, all lab tests are normal except a persistently elevated rT3 and the patient has hypothyroid symptoms. This is most commonly due to chronically elevated cortisol.
Euthyroid Sick Syndrome most commonly occurs when a patient has another chronic illness that begins to affect the thyroid function test results. The actual results may vary depending on the underlying condition, and for most of these patients, treatment focuses on the underlying illness and thyroid replacement is not recommended.
Autoimmune thyroid conditions can be difficult to assess because antibody levels and their resultant impact on thyroid function can fluctuate depending on factors affecting immune activity. Early cases of Hashimoto’s thyroiditis, patients may present with a high or even normal TSH, hypothyroid and/or hyperthyroid symptoms but no thyroid Abs; in this case there is an autoimmune reaction, but the thyroid tissue has not been attacked enough to cause a change in thyroid test levels. Without intervention, this patient would very likely continue on to develop Hashimoto’s thyroiditis with hypothyroid lab results. For a patient with a low TSH, hyperthyroid symptoms and positive antibodies, it could be Grave’s disease or Hashimoto’s thyroiditis in a hyperthyroid state.
Treatments for Thyroid Disorders
Treatments for thyroid disorders vary greatly and depend on the specific type of imbalance. Thyroid hormone replacement can include synthetic T4 (levothyroxine or synthroid), synthetic T3 (cytomel), synthetic combination (thyrolar) and natural thyroid sources, which include both T4 and T3 (e.g., Armour thyroid, Nature-throid, Westhyroid). Dosing goals should include both achieving optimum lab test results and resolution of patient symptoms.
Thyroid supports include nutrients, herbs, and remedies that support normal thyroid function. These may be helpful in addition to thyroid replacement or in cases where a patient’s lab values are not at optimum, but are still within the laboratory reference ranges. Supports need to be tailored to each patient, and there are some cautions in using thyroid supports. For example, while tyrosine and iodine are necessary to produce T3 and T4, excess levels can be suppressive to thyroid function. If thyroid support is needed, functioning of other hormones should also be addressed.
Autoimmune thyroid conditions require broader treatment to include both support for thyroid function as well as addressing the immune dysfunction, the underlying causes for that dysfunction, and other concurrent health issues. For example, some patients with Hashimoto’s thyroiditis have a defect in the vitamin D receptor which means these patients will require more vitamin D than a “normal” patient. Additionally, patients with Hashimoto’s thyroiditis may also have other concurrent autoimmune conditions, especially celiac disease, and have a higher risk of developing thyroid cancer or pernicious anemia, type I diabetes, or rheumatoid arthritis. It is also important to remember that patients with Hashimoto’s thyroiditis can have periods of episodes of hyperthyroidism if there are periods of greater immune activity and thus increased destruction of thyroid tissue and release of stored thyroid hormone. Autoimmune hyperthyroidism often requires surgical removal or irradiation of the thyroid or pharmaceuticals to significantly suppress thyroid function.
There can also be many other influences on thyroid function, and in some cases, abnormal thyroid labs or thyroid-related symptoms are due to a non-thyroid cause. Thyroid underconversion is most often caused by one or more of the following:
- High cortisol (due to chronic stress, low blood sugar, insulin resistance, anemia, acute or chronic infections, toxicity, surgery, accidents, chronic pain);
- Hepatic dysfunction;
- Imbalances in normal intestinal bacteria;
- Viral infections;
- Low selenium, zinc, and/or iodine;
- Heavy metals;
- Inflammation; and
- Low glutathione.
All of these factors can affect thyroid functioning in general, and any treatment plan needs to investigate these other factors, and provide thyroid support while addressing the underlying cause(s). This will also be true for the hormone imbalances that lead to thyroid overconversion or elevations of TBG. Gluten sensitivity, celiac disease, and gut inflammation can also have a negative effect on thyroid function, as can overconsumption of soy, especially the more highly processed forms. Many of the factors leading to thyroid underconversion may also result in thyroid resistance, and should be investigated when that condition is suspected.
The Merck Manual
Kharrazian, Datis. Functional Blood Chemistry Analysis Seminar.
Thom, Dick. Practical Endocrinology Seminar.
T-helper (Th) cells are classified in a variety of classes, the main ones being designated Th1 and Th2. The balance between these two types of T-helper cells can determine the state of your immune system functions in and impact your overall health.
Th1 cells correlate to the idea of Wei qi, or defensive energy, in Chinese medicine, and promote cell-mediated immunity (CD4 type of T cells, killer T cells (CD8 type), natural killer cells, macrophages). Being in a Th1 dominant immune state directs killer T-cells (CD8) to attack microorganisms and abnormal cells at the sites of infection inside the cells, kills specific fungi, viruses, and bacteria, stimulates natural killer cells and cytotoxic lymphocytes to kill cancer cells. This state is enhanced by several immune communication chemicals, specifically Interluken-2 and 12, and gamma-interferon.
Th2 cells promote humoral immunity (B cells and antibodies) to produce antibodies (e.g., IgG, IgE) to neutralize foreign invaders outside of the cells. This state is enhanced by immune communication chemicals Interleukins 4, 5, 6, and 10, and alpha interferon.
Failure of Th1 and overactive Th2 is found in many chronic diseases, including AIDS, candidiasis, multiple allergies, multiple chemical sensitivities, some autoimmune diseases, viral hepatitis, and cancer. As many serious diseases, such as HIV infection, progess, the immune system shifts from the more effective TH1 state to the ineffective Th2 state.
DIETARY FACTORS THAT SUPPORT Th1
- Omega-3 Fatty acids (DHA/EPA) improve cell-mediated immunity, and reduce Interleuken-6 and triglycerides; found in all cold water fish, especially salmon, sardines, mackerel, halibut, and trout. Fish should be canned, boiled, or broiled instead of fried. Lesser amounts found in dark-green leafy vegetables and sea vegetables (blue green algae, chlorella. (Chlorella also increases cell-mediated immunity by other factors.)
- Oleic acids (monounsaturated) increase IgA antibody (immunity on mucus membranes/ Th3); found in cold-pressed extra virgin olive oil, hazelnut or filbert oil (or the whole nuts), green and ripe olives, and almonds. (Coconut oil neither suppresses nor enhances cell mediated immunity.)
- Vitamin A increases IgA; found in cod liver oil, cooked carrots, squash, pumpkin, and sweet potatoes/yams (any yellow/orange vegetable).
- Vitamin E induces interleuken-2, natural killer cell function, and gamma interferon, and acts as an antioxidant.
- Garlic activates natural killer cells, T-lymphocyte function, and the level of interlueken-2.
- Silica reduces excess IgG, which improves natural killer cell function and improves the integrity of the skin and mucus membranes; found in cooked oatmeal or millet, and the herb horsetail.
- Glutathione acts as an antioxidant and removes toxins from inside cells. It is increased by alpha lipoic acid, selenium, and the amino acids N-acetyl cysteine, L-cysteine, and L-glutamine. Good quality sources of protein can supply many of these amino acids through the diet.
- Proper digestion, including protein digestive enzymes, naturally found in fresh ginger root, raw pineapple, and kiwi fruit. Cayenne before meals stimulates hunger and digestive enzymes. Lemon juice or apple cider vinegar stimulates hydrochloric acid (vinegar also kills HIV). Most of immune system and neurotransmitter receptor sites are in our intestines!
- Healthy balance of intestinal flora increases Interlueken-2 and 12, and gamma interferon production, decreases IgE antibody production (associated with allergic reactions) and all Th2 factors, and increases the anti-tumor activity in macrophages.
- NOTE: One species of intestinal flora promotes Th2, which is streptococcus thermophilus, widely used in the making of commercial yogurt. So if the yogurt contains more thermophilus than acidophilus, there will be more Th2 than Th1!
Sunlight, water, exercise, touch, positive attitude, and acupuncture also increase Th1! Be cautious with echinacea and astragalus because they can increase both Th1 and Th2.
DIETARY FACTORS THAT INCREASE Th2
The three most common factors that increase Th2:
- Faulty digestion, leading to absorption of partially digested and unusable proteins, which increases the antibody immune response to these foreign food particles. This can be improved by proper stomach acid and digestive enzyme function, chewing slowly and eating only when hungry.
- White sugar, which directly weakens the functioning of macrophages, natural killer cells, and other white blood cells, and weakens systemic resistance to all infections.
- Trans-fatty and omega-6 acids, found in most heated and processed vegetable oils (soy, canola, safflower, corn, and sunflower), and the processed foods made from these oils. The trans-fatty acids weaken CD8 killer-T cell activity. Except for expeller pressed oils, nearly all other vegetables are processed with solvents, hexane or gasoline, to remove oils from the seeds. The process also twists the fatty acids out of their normal shape, so when they are incorporated into cell membranes, they produce membranes that are porous and vulnerable to viral infections. The heat, light, and oxygen in the process cause the oils to go rancid.
Other factors that increase Th2 include:
- asbestos, lead, mercury, and other heavy metals, pesticides,
- morphine, tobacco, alcohol, steroids,
- pathogens (including HIV, Hepatitis C, and candida), streptococcus thermophilus,
- continuous stress, negative attitudes and suppressed emotions,
- sedentary lifestyle, lack of water, low body temperature, and chronic insomnia.
Lectures by Satya Ambrose, L.Ac, N.D.
Konlee, Mark. “A Consumer’s Guide to Immune Restoration: The Search for ‘Th1’.” Positive Health News. Report No. 18. Spring 1999.
In Chinese medicine, infections are divided into two main types: wind-heat invasions and wind-cold invasions. Symptoms that help differentiate between the two types include:
|Fever||Light||Can be high|
|Aversion to cold||Pronounced||Slight|
|Headache||Deep, severe||At the back of the head|
|Sweating||None||Slight to profuse|
|Thirst||None or lowered||May be increased|
|Tongue||Body color normal||Red tip or sides of tongue|
The general treatment philosophy for treating a wind-cold invasion is to use warming foods and herbs to cause sweating to open the surface and release the pathogens. For w wind-heat invasion, cooling foods and herbs are used to reduce heat and open the surface.
Eat cool or neutral foods that will cool heat in lung and resolve phlegm. Use mostly liquids (juices, soups, teas) at neutral temperatures (very cold food and drink will weaken the body as they cool it) and maintain fluid intake.
Grains: Millet, barley, wheat, rice, amaranth (especially in soup)
Legumes: Soy, mung beans and sprouts, alfalfa sprouts
Vegetables: Watercress, seaweeds, mushroom, dikon radish, radish, carrot, pumpkin, cabbage, bok choy, cauliflower, white fungus, eggplant, water chestnut, lettuce, summer squash, cucumber, celery, asparagus, Swiss chard, spinach, broccoli, zucchini
Fruits: Apple, banana, Cantaloupe, persimmon, peach, pear, strawberry, citrus, papaya, pomelo, winter melon, watermelon, tomato
Herbs: Chickweed, horehound leaf, nettles, mullein leaf, peppermint, dandelion (greens and root), honeysuckle flowers, lemon balm, cilantro, marjoram
Warming foods: coffee, alcohol, chicken; any foods listed for wind-cold
Wind foods: chicken
Congesting foods: dairy, sugar
Eat warm or neutral foods that will warm the lung and resolve phlegm. Eat food at neutral temperature, avoiding cool or very hot food.
Grains: Oats, spelt, quinoa, sweet brown rice, rice, corn, buckwheat, rye
Legumes: Black beans, aduki beans, lentils
Vegetables: Garlic, green onion, and onion, parsnip, parsley, mustard greens, winter squash, cabbage, kale, leek, chive, peppers (hot peppers in small amounts)
Fruits: Cherry, citrus peel, date
Nuts: Walnut, sunflower seed, sesame seed, pine nut, chestnut
Meat: Beef, lamb
Herbs: Fennel, fenugreek, cayenne, horseradish, fresh ginger, elecampane root, coriander, cinnamon bark or twig, cloves, basil, rosemary, angelica root, dill, anise, caraway, cumin
Cooling foods: raw foods; any foods listed for wind-heat
Wind foods: chicken
Congesting foods: dairy, sugar
* Although coffee and alcohol are warming, they should be avoided as they suppress the immune system.
Cai, J. 2002. Oriental Dietetics Class Notes.NationalCollegeof Naturopathic Medicine. Fall 2002.
Maciocia, Giovanni. 1989. The Foundations of Chinese Medicine. Churchill Livingstone:London.
Pitchford, P. 1993. Healing with Whole Foods: Oriental Traditions and Modern Nutrition. North Atlantic Books:Berkley,CA.
A diet to maintain bone health should focus on adequate, high quality protein and foods high in vitamins and minerals necessary for bone rebuilding.
A vegetarian diet is associated with a lower risk of osteoporosis because animal protein generally contains higher amounts of phosphorous, which mobilizes calcium from bone. Calcium is also mobilized from bone to buffer the acidic breakdown products of protein. However, protein is required to build bone so an adequate amount of high-quality, non-meat protein should be maintained.
- Soy, including tofu, tempeh, soy nuts, miso, fresh edamame beans
- High protein grains (e.g., quinoa)
- Eggs (a complete protein source)
Vitamins and Minerals
A variety of vitamins and minerals are required to support formation and maintenance of healthy bone.
- Vitamin B6
- *Breaks down homocysteine, a protein which promotes osteoporosis, decreases fracture healing time
- Found in: Bran cereals, granola; Watermelon, banana, pineapple; Salmon, rainbow trout, steelhead, mackerel, halibut, tuna, herring; Almonds, sunflower seeds; Tomato, sweet potato, potato, broccoli; Soybeans
- Vitamin C
- *Promotes formation and cross-linking of structural proteins in bone
- Found in: Oranges, grapefruit (and juice), watermelon, cantaloupe, honeydew melon, papaya, kiwi, mango, guava, strawberries, blackberries, blueberries, cherries; Peppers, including red chili, green, sweet; Dark leafy greens, including turnip greens, kale, mustard greens, spinach; Brussel sprouts, cauliflower, broccoli, tomato, sweet potato, cabbage; Mung bean sprouts
- Vitamin D
- *Enhances dietary calcium absorption
- Found in: Vitamin-D fortified dairy products; Fish; Eggs; Liver
- Folic Acid
- *Breaks down homocysteine, a protein which promotes osteoporosis
- Found in: Brewer’s yeast; Blackeyed peas, lentils, lima beans, kidney beans; Peanuts; Turnip greens, Romaine lettuce, dandelion greens, Swiss chard, parsley; Leeks, broccoli, bok choy, acorn squash, tomato, brussel sprouts;Orangejuice; Wild rice, oat bran; Tofu
- Vitamin K
- *Attracts calcium to bone tissue
- Found in: Dark, leafy greens, including kale, collard greens, Romaine lettuce, spinach, Swiss chard; Broccoli, cauliflower, tomatoes, alfalfa; Wheat, oats, rye
- *Reduces urinary excretion of calcium and magnesium
- Found in: Dark, leafy greens, including kale, collard greens, Romaine lettuce, spinach, Swiss chard; Tomato; Pear, apple, prunes, raisins, dates; Peanuts, almonds, filberts; Honey; Seafood
- *Essential in bone formation
- Found in: Dark, leafy greens, including kale, collard greens, Romaine lettuce, spinach, Swiss chard, turnip greens, dandelion greens, beet greens, mustard greens; Sea vegetables, kelp, dulse; Swiss/cheddar/cottage cheeses, goat’s milk, buttermilk, yogurt; Carob flour, dates, figs, raisins; Black-strap molasses; Almonds, brazil nuts, sunflower seeds, sesame seeds, walnuts; Brewer’s yeast; Parsley, watercress, broccoli, celery, rutabaga; Tofu, soybeans; Wheat bran, buckwheat; Olives
- *Inhibits bone resorption
- Found in: Rye, whole wheat, millet; Beans, refried beans; Brazil nuts, cashews, sunflower seeds, almonds, pecans, peanuts; Black strap molasses; Tofu; Prunes, banana; Halibut
- * Influences both matrix and mineral metabolism in bone, and is required for proper calcium metabolism
- Found in: Dark, leafy greens, including kale, collard greens, Romaine lettuce, spinach, Swiss chard, beet greens; Kelp, dulse; Wheat bran and germ, buckwheat, millet, whole wheat, rye;
- Almonds, cashews, Brazil nuts, filberts, peanuts, pecans, walnuts; Molasses; Brewer’s yeast; Tofu; Coconut; Celery, asparagus, cabbage; Bananas, oranges, prunes; Legumes; Nuts, seeds- cashews, almonds
- *Increases amount of calcium laid down in bone
- Found in: Dark, leafy greens, including kale, collard greens, Romaine lettuce, spinach, Swiss chard; Celery, beets, asparagus; Bran, whole grains; Pineapple, banana; Egg yolks; Legumes
- *Reduces urinary excretion of calcium
- Found in: banana, raisins; Potatoes; Salmon, halibut; Carrots; Almonds; Soybeans
- *Essential for bone formation and enhances vitamin D action
- Found in: Wheat germ; Pumpkin seeds, sunflower seeds; Seafood; Nutritional yeast; Soybeans
Additional lifestyle changes, such as weight bearing exercise, and supplementation for hormone balance or additional nutritional needs should be addressed with dietary changes. Any organ system imbalance and energetic patterns underlying the development of osteoporosis also need to be treated.
- Refined sugar
- Processed foods
- High sodium, high fat
- Soda (any high phosphorous beverages)
In Chinese medicine, osteoporosis may be associated with yin deficiency and/or liver blood and/or yin deficiency.
Foods that tonify yin
- Millet, barley, wheat germ, wheat, teff, quinoa, amaranth
- Seaweeds, algae
- Black beans, kidney beans, mung beans and sprouts
- Beets, string beans
- Persimmon, grapes, blackberry, raspberry, mulberry, banana, watermelon
- Dairy, egg
Foods that build liver blood and yin
- Mung beans and sprouts
- Chlorophyll-rich foods
- Flax, borage, evening primrose oils
- Grapes, huckleberry, blackberry, raspberry
- Black strap molasses
Hudson, T. 1999. Women’s Encyclopedia of Natural Medicine. Keats Publishing:Los Angeles,CA.
Marz, R. 1999. Medical Nutrition from Marz, 2nd Edition. Omni-Press:Portland,OR.
NationalCollegeof Naturopathic Medicine. Dietary Guidelines for the Prevention of Osteoporosis.. Patient Handout.Portland,OR.
Pitchford, P. 1993. Healing with Whole Foods: Oriental Traditions and Modern Nutrition. North Atlantic Books:Berkeley,CA.
There are four different types of allergic, or hypersensitivity, reactions and most common type is called a Type I response. In this type of reaction, when a person is first exposed to an allergen, several cells of the immune system start a cascade of reactions. The Th2 type of T helper cells (or lymphocytes) present the allergen to B cells, which then produce IgE antibodies. These IgE antibodies attach strongly to receptors on basophils and mast cells, two other types of immune cells, sensitizing them to future exposures.
When the person contacts the allergen again, the interaction between the allergen and the IgE antibodies on the mast cells and basophils stimulates these cells to release chemicals that intensify the inflammatory response causing allergy symptoms. Eosinophils, another type of white blood cell, are stimulated later in the process and release chemicals that further activate mast cells; this can increase and continue the inflammatory response even without additional exposures to the allergen.
There are many treatment options for allergies that stabilize the mast cells and basophils so they can’t release the inflammatory chemicals, including vitamin C and Quercetin. I feel the more important treatment goal is to shift the immune system balance away from the Th2 helper cells to the Th1 helper cells. This will reduce the initial step in the allergic response and improve other aspects of health. The Th1 helper cells are better able to fight bacteria and viruses and detect and destroy cancer cells; the Th2 helper cells are also implicated in many other diseases besides allergies, including asthma and some types of auto-immune diseases. However, Th2 helper cells, basophils, and eosinophils aren’t all bad; antibodies are one way the body fights infections and eosinophils are important in killing parasites.
The body produces many different chemicals to signal which type of immunity (Th1 or Th2) should be stimulated, and these chemicals can be influenced by many dietary and lifestyle factors. The three most common factors that significantly increase Th2 are:
- faulty digestion, leading to absorption of partially digested and unusable proteins, which increases the antibody immune response;
- white sugar, which directly weakens the functioning of immune cells, and weakens resistance to all infections; and
- trans-fatty and omega-6 acids, found in most heated and processed vegetable oils (e.g., soybean, safflower, corn, sunflower, and canola oil) and foods. The trans-fatty acids weaken killer-T cell activity. Vegetable oils are acceptable IF they are cold or expeller pressed oils, and stored in the dark.
Other factors to avoid include chronic infections, Candida (yeast), Streptococcus thermophilus (commonly found in yogurt), asbestos, heavy metals, pesticides, tobacco, alcohol, steroids, stress, negative emotions, sedentary lifestyle, lack of water, low body temperature, chronic insomnia, and weight lifting to excess.
There are also many factors that increase the Th1 immunity, including:
Probiotics change the Th2-Th1 balance of the immune system to re-establish the normal immune tolerance, in other words, the immune system knows what to respond to (i.e., bacterial infection) and what not to respond to (i.e., food). This is the same mechanism as allergy shots. It will take a longer time to re-establish this immune tolerance if it wasn’t initially created as a child, and symptom reduction can take up to 3 months.
Continued use of a probiotic is necessary because the entire surface of the upper intestines replaces itself every 72 hours and the colon replaces itself every 12 days. These new surfaces need to be recolonized because the bacteria are lost with the cell shedding; there will be a loss of colonization over time if there is no replenishing. There are different forms of probiotics and the most important factors are that the organisms are alive and are in the correct balance and amounts of the Bifidus and Lactobacillus bacteria. For example, much higher levels are needed after antibiotics because Lactobacillus and Bifidus are highly sensitive to broad-spectrum antibiotics. Antibiotics can eliminate 90% of these beneficial flora, allowing pathogenic bacteria, parasites, and yeast to increase. Many probiotics also contain fructo-oligosaccharides (FOS), which is a soluble fiber. FOS can cause gas for some patients, which is an indicator of a bacterial imbalance in the intestines because pathogenic bacteria produce gas when they encounter FOS. Gas will decrease as the balance changes back to the beneficial bacterial types because Lactobacillus and Bifidus produce acid in the presence of FOS, not gas.
For babies, breast feeding decreases incidence of allergies by establishing the correct balance of Bifidus and Lactobacillus bacteria. In breast fed babies, Bifidus accounts for 95% intestinal bacteria by 7 days and 97% by 19 weeks; formula-fed babies have only 22% by 7 days and only 77% at 19 weeks. Without probiotic supplementation, formula-fed babies never reach the levels of Bifidus seen in breast-fed babies. Supplementation of probiotic in babies should focus on higher levels of Bifidus than Lactobacillus and can start at birth to support healthy levels from breast-feeding and supplement formula feeding.
Omega-3 Fatty acids are found in all cold water fish, especially salmon, sardines, mackerel, halibut, and trout, with lesser amounts in dark-green leafy vegetables and sea vegetables and algae.
Oleic acids are best found in cold or expeller pressed extra virgin olive oil. Secondary choices include hazelnut or filbert oil (or the whole nuts), green and ripe olives, and almonds. Coconut oil can be used alternately with the other beneficial oils, especially for cooking.
Green foods, including spirulina and chlorella, are rich in antioxidants, vitamins, minerals, and enzymes needed for detoxification and optimum nutrition.
Digestive enzymes break up proteins into usable amino acids and levels can be increased with supplemental enzymes and/or pancreatic support. Apple cider vinegar stimulates hydrochloric acid, which is required to digest protein and activate enzymes. Eating slowly to allow natural salivary enzymes to work and eating only when hungry will also support good digestion. B vitamins are also required to support hydrochloric acid production and magnesium is required by the pancreas to produce enzymes to digest proteins. Both B vitamins and magnesium are also necessary for proper adrenal functioning. L-glutamine is an amino acid that serves as the major fuel for the cells of the intestines and is necessary for intestinal immunity. Chronic infections can also shift immunity toward Th2 and create an additional burden for the immune system, so investigating and treating chronic infections, especially in the digestive tract, is another key step.
DHEA is one of the adrenal hormones and the precursor to estrogen and testosterone. DHEA stimulates the Th1 immune chemicals, which indicates that an adrenal imbalance (exhaustion or overstimulation) may actually cause an immune imbalance. Therefore, knowing your adrenal status and using appropriate adrenal support, including DHEA if you are deficient, is an essential part of balancing the immune system. Many of the most common adrenal support treatments, such as licorice and ginseng, also have their own beneficial effects on immunity.
Glutathione acts as an antioxidant and is essential for balancing the Th1 and Th2 immune states.
Sunlight, water, touch, positive attitude, and acupuncture also have a positive effect on immunity.
- Eat nutrient-rich foods that will provide you energy and the building blocks to make the hormones and neurotransmitters you need. Processed foods are empty calories that create inflammation and increase toxicity.
- Drink enough water, which means half of your body weight in ounces of WATER (E.g. a 100 pound person would drink 50 ounces of water).
- Create a “meal time”.
- Slow down when you eat and chew each bite 31 times before you swallow so you can taste and savor your food.
- Sit at the table, turn off the TV and listen to music.
- Create a calm environment that allows your body to receive the nourishment and take it in.
- Alternate hot and cold water in your shower. Do 3 minutes of hot water and 30 seconds to 1 minute of cool to cold water (but not so cold that you’re freezing). You can alternate this as many times as you want during your shower. Just make sure to always end on cold. This is an easy hydrotherapy treatment that helps with elimination and gets your energy moving!
- Pay attention to your breathing. Put your hand on your lower abdomen. Does your hand rise when you inhale? Are you expanding your abdomen slowly as you inhale and allowing air out as you exhale? Is your breathing slow and rhythmic?
- Check in with your breath when you feel particularly tired, stuck, or disconnected from yourself or others. Take a few slow, deep breaths.
- In Chinese medicine, depression is often caused by stagnation, so get yourself moving when you’re feeling down. Take a brisk walk outside, put on some favorite music and dance around the living room, do some yoga, T’ai Chi, or Qi Gong, or even just shake your body wherever you are.
- Your thinking is a very powerful tool. Use it to create affirmations that are meaningful for you. Write them down and post them around your house, car, or office- anywhere you will see them. For example: “I am lovable, loving, and loved.” “I feel calm and centered within myself.”
- Find ways to connect in your community. Make a list of things you enjoy or are good at, and volunteer. You’ll help others with your unique skills and gifts while you are spending time with others doing something that is meaningful to you.