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Thyroid Disease: Functional Health at Life Change Health Institute – 5 Step Holistic Approach to Optimum Health

A thyroid disorder is an autoimmune condition related to the thyroid gland, a small gland that manufactures and stores thyroid hormones. A thyroid disorder impacts the metabolic processes and may be characterized by nervousness or tiredness, weight changes, weak muscles, impaired memory and irregular menstrual flow. Your thyroid is one of your body’s most important glands. When your thyroid doesn’t work properly, it can cause you to feel nervous or tired; make your muscles weak; cause weight gain or loss; impair your memory; and affect your menstrual flow. A thyroid disorder can also cause miscarriage and infertility. About 20 million Americans—more of them women than men—are affected by a thyroid disease or disorder, according to the American Thyroid Association (ATA). In fact, an estimated one in eight women will develop a thyroid disorder at some time in her life.
Thyroid Disease in Women
Women are five to eight times more likely to have thyroid dysfunction than men, but most don’t know they have it. Women often overlook their symptoms or mistake them for symptoms of other conditions. For example, women are at particularly high risk for developing thyroid disorders following childbirth. Symptoms such as fatigue and depression are common during this period, but these are also symptoms of thyroid disease. The ATA estimates that more than half of thyroid conditions remain undiagnosed.
How the Thyroid Works
The thyroid is a butterfly-shaped gland you can feel at the base of your neck, just below your larynx (voice box). Two lobes (the “wings” of the butterfly) fit on either side of your windpipe. The thyroid gland manufactures and stores thyroid hormone (TH), often referred to as the body’s metabolic hormone. Among other actions, TH stimulates enzymes that combine oxygen and glucose, a process that increases your basal metabolic rate (BMR) and body heat production. The hormone also helps maintain blood pressure, regulates tissue growth and development and is critical for skeletal and nervous system development. It plays an important role in the development of the reproductive system.
How to heal (HT)
Types of Thyroid Disorders
The thyroid gland can malfunction in one of three ways:
It can release too little TH, resulting in a condition known as hypothyroidism (underactive thyroid).
It can release too much TH, resulting in a condition known as hyperthyroidism (overactive thyroid).
Its tissue can overgrow, resulting in a nodule, a small lump in part of the gland. Most nodules are harmless growths, but some are cancerous. In fact, according to the ATA, less than one in 10 thyroid nodules are cancerous. However, despite this relatively low incidence, thyroid cancer is currently the fastest growing cancer in women.
When too little TH is released, the body’s metabolic rate decreases, and the body slows down. Hypothyroidism often goes undiagnosed because its symptoms are often mistaken for or attributed to other conditions.
Symptoms include:
low body temperature
weight gain
dry or itchy skin
thin, dry hair or hair loss
puffy face, hands and feet
decreased taste and smell
slow heart rate
poor memory
trouble with concentration
hoarseness or husky voice
irregular or heavy menstruation
muscle aches
high cholesterol
goiter (enlarged thyroid gland)
Hypothyroidism can occur spontaneously, develop during or after pregnancy or after treatment for hyperthyroidism. You can be born with it or it can be caused by Hashimoto’s thyroiditis, the leading cause of hypothyroidism in the United States. Named for the Japanese health care professional who first described it in detail, Hashimoto’s thyroiditis is an autoimmune disease. That means the immune system attacks the body’s healthy tissues instead of fighting off invading bacteria or viruses. In this case, the immune system produces antibodies to attack the thyroid gland as if it were a foreign substance that needed to be destroyed. The resulting damage leads to reduced production of TH. One of the leading practitioners in hypothyroidism treatment, Datis Kharrazian says hypothyroidism is caused by Hashimoto’s, the autoimmune disease that attacks the thyroid gland. Although the use of thyroid hormones may be necessary, he feels that they do not address the cause of dysfunction, which is an immune system that is attacking the body it was designed to protect.This is evidenced by the many people who still have symptoms even after the gland is surgically removed (because some tissue remains, providing a site for attack).
Says Dr. Kharrazian:
My goal is to discover the exact nature of the immune imbalance, as it differs for each person, and then restore immune balance. This often means dietary changes, such as going on a gluten-free diet, as the literature establishes a clear link between gluten and Hashimoto’s. It also may mean giving up other favorite foods. Balancing blood sugar, addressing poor gut health, tackling chronic inflammation, and restoring adrenal health are fundamental aspects of this approach. Beyond that researchers have identified specific nutritional compounds that can be invaluable in modulating a dysregulated immune system. By addressing the immune system and not just the thyroid gland, we restore healthy thyroid function, reduce or remove the need for thyroid medication, restore healthy brain function, and perhaps most importantly prevent the development of future autoimmune diseases (particularly against brain tissue, which is sadly a site of future attacks for many of those with Hashimoto’s).
Even if it’s not autoimmune in nature, Dr. Kharrazian believes that hypothyroidism has its roots in some type of metabolic dysfunction, and, by reviewing the literature and through clinical observation, has identified what he believes are 24 different causes of low thyroid function. Says Dr. Kharrazian: “In addition to an autoimmune disorder they include elevated cortisol from chronic stressors; excess estrogen, such as from birth control pills or estrogen creams; excess testosterone in women, a common fallout from diets high in carbohydrates; PCOS; chronic inflammation; gut infections; and brain neurotransmitter deficiencies. Some of these don’t show up on lab tests at all, and most won’t show up on a test that screens TSH only. Knowing how to correctly order a thyroid panel and read it is integral.” Dr. Kharrazian also believes that it is important to understand that no one thyroid hormone medication is right for everyone. According to Dr. Kharrazian: “Although bio-identical hormones are always preferable, the exogenous T3 will be problematic for some people, such as those who overconvert T4 to T3. Also, different medications use different fillers, and reactions to those fillers can vary from person to person.”
Dr. Kharrazian believes that hypothyroidism is not only very common today, it’s a silent epidemic. But he believes that the reason for the condition varies significantly among the population, and the astute practitioner will first search for that person’s cause of hypothyroidism and address that, rather than apply a blanket treatment to all. Says Dr. Kharrazian: “It is not simple, quick, or easy, and it most often involves lifelong dietary and lifestyle changes, but a faltering thyroid is a warning that must be heeded before the person’s health deteriorates further.” Datis Kharrazian, DHSc, DC, MS, MNeuroSci, FAACP, DACBN, DABCN, DIBAK, CNS is considered one of the leading experts in non-pharmaceutical applications to chronic illnesses, autoimmune disorders, and complex neurological disorders. Patients from all over the world fly to his practice located in San Diego, California to learn and understand his perspective regarding their condition and to apply natural medicine alternatives to help them improve their quality of life. Dr. Kharrazian has become the referral source for many doctors nationally and internationally when their cases become too complex to evaluate and diagnose.


Understanding How the Thyroid Works

Your thyroid powers every cell in your body through the hormones it produces. These hormones determine the energy level and reproduction of each cell, keeping your organs powered up and managing your overall metabolism. The process of creating, regulating, and delivering these hormones is complex, and it all begins in your brain. The hypothalamus, which is responsible for managing hunger, thirst, sleep, hormones, and body temperature, among other important functions, continuously monitors the level of thyroid hormones present in your bloodstream. If it determines that energy levels are low, it sends out TRH, Thyroid Releasing Hormone, to your pituitary gland. Your pituitary gland, a pea-sized gland at the base of your brain, then releases TSH Thyroid Stimulating Hormone, which is sent directly to the thyroid. Your thyroid is then prompted to produce thyroid hormone using an amino acid called tyrosine and iodine (we will cover the importance and effect of iodine later in the series). It converts the tyrosine into thyroglobulin and then attaches between one and four iodine atoms, creating T1, T2, T3, and T4 respectively.
The primary output of your thyroid is T4 (thyroglobulin plus four iodine atoms), which is a storage form of the hormone. It is circulated throughout the bloodstream and stored in tissues so that it’s available when needed. A much smaller percentage of the hormones produced is T3, which is the active form of thyroid hormone. T2 and T1 make up an even smaller percentage, and researchers are still unsure of what role these two hormones play. When each local area of your body determines that it needs active T3 for more power, it converts the storage T4 to active T3 using an enzyme called deiodinase. This enzyme (which needs selenium, zinc, and iron to function properly) strips one of the outside iodine atoms off of the T4, turning it into Free T3 (FT3). Your body also uses a portion of the T4 to create Reverse T3 (RT3), which is done by stripping away one of the inside iodine atoms, creating another inactive form of thyroid hormone, but one that can attach to the receptors for Free T3.
The T3 then enters cell membranes (with the help of cortisol) and regulates how much energy your mitochondria produce. Your mitochondria are the “power plants” of your cells and there are trillions of them in your body. The Free T3 acts as a gas pedal for the mitochondria, revving up power production, and the Reverse T3 acts as a brake pedal, slowing down the power. These micro-level reactions all work in concert to control hugely important metabolic factors such as heart rate, fatigue, weight regulation, brain function, and more. When your thyroid isn’t functioning properly it can affect any or all of these separate systems, creating a wide array of symptoms that might seem unrelated (which is why thyroid disease often goes undiagnosed), but can all be traced back to your thyroid.
Thyroid 1
Thyroid 2
Hypothyroidism – An Underactive Thyroid
The most common form of thyroid disease is hypothyroidism, which is when your thyroid is underactive and does not produce enough thyroid hormone. This can either be because your pituitary gland is malfunctioning and not sending enough TSH to your thyroid, or, more commonly, your TSH levels are normal, but for various reasons your thyroid isn’t producing enough T4 and T3 to adequately fuel your cells. Hypothyroidism causes a general slowing down of your metabolic processes, and can lead to these symptoms:

  • Fatigue
  • Brain Fog
  • Weight Gain or Inability to Lose Weight
  • Cold Hands or Feet
  • Hair Loss
  • Constipation
  • Poor Concentration
  • Infertility
  • Low Libido
  • Depression
  • Decreased Heart Rate
  • Decreased Body Temperature


When too much TH is released, the body’s metabolic rate increases, and your metabolism speeds up.
Symptoms of hyperthyroidism include:
weight loss
fast or irregular heart rate
heat intolerance or increased perspiration
changes in appetite
sleep disturbances (such as insomnia)
muscle weakness
trembling hands
more frequent bowel movements
shorter and scantier menstrual flow
exophthalmos (bulging eyes)
goiter (enlarged thyroid gland)
Hyperthyroidism can be caused by nodules composed of thyroid cells that produce TH without regard to the body’s need. It can also develop during or after pregnancy and may be caused by Graves’ disease. Symptoms of hyperthyroidism may also result from overtreatment of hypothyroidism with synthetic TH or from thyroiditis, an inflammation of the thyroid gland, which leads to an overproduction of TH. Graves’ disease, another autoimmune condition, is the leading cause of hyperthyroidism, accounting for 85 percent of hyperthyroidism cases. Graves’ disease differs from Hashimoto’s thyroiditis in that the antibodies turn the thyroid on, causing the thyroid gland to enlarge and overproduce TH. Other antibodies may also attack eye muscle tissue and the skin on the front of the lower leg. Graves’ disease was named for Robert Graves, an Irish health care professional who first discussed this form of hyperthyroidism. It is a completely treatable disease and is rarely fatal.
Thyroid nodules
Thyroid nodules are the most common thyroid disorder, occurring in up to 50 percent of people over the age of 50. Many of these nodules are small (less than 1 centimeter) but some can reach more than 5 centimeters with few, if any, symptoms. Indeed, many nodules are only discovered when people have imaging studies of their necks, such as a chest CT scan or a carotid ultrasound. An estimated one in 10 Americans will develop a significant thyroid nodule at some point in their lives. Ranging from as small as a millimeter to as large as several inches, thyroid nodules themselves don’t represent illness. Nodules do, however, indicate an underlying problem with the thyroid and should be evaluated if they are discovered. The majority of nodules are benign discrete clumps of thyroid cells, which don’t function like normal thyroid tissue. Other nodules turn out to be simple cysts. However, there is a slight chance that a thyroid nodule is cancerous—less than 10 percent of nodules are cancerous—so it is important to have a health care professional assess all growths. While most nodules have no symptoms, are never detected and are harmless, some can be large enough to press against the windpipe and cause difficulty swallowing or a cough. A nodule can also become overactive, suppressing the rest of the gland and causing hyperthyroidism.

The Eight Thyroid Patterns by Datis Kharrazian DC, MS, FAACP, DACBN, DIBAK, CNS, CSCS, CCSP
We can simplify altered thyroid metabolism into eight patterns. These patterns include expression of altered thyroid metabolism from primary thyroid deficits, and alterations in thyroid metabolism secondary to other metabolic shifts. Please note that sometimes two patterns may coexist at the same time. For example, a patient may have thyroid underconversion at the same time as secondary hypothyroidism due to primary pituitary hypofunction. It is not realistic in the clinical setting to order a thyroid panel with all of the markers for thyroid results. So, the clinician must make decisions based on history, medication use, and possible influences of other metabolic shifts on the thyroid. For example, if a patient is on oral contraceptives the panel must include a TSH an T3U and or FT4 and/or FT3. It is always necessary to order a TSH with all panels, since it is the key marker that will distinguish primary thyroid tissue deficits from secondary influences from other metabolic disorders. Please also note that positive antibodies may be concomitantly involved with any one of these thyroid patterns, although it is always positive with thyroid hyperfunction.
1. Hypothyroidism
Thyroid Stimulating Hormone (TSH) = Elevated Total T4 (TT4) = Normal or Low
Free T4 (FT4) = Normal of Low
Free Thyroxine Index (FTI) = Normal or Low Resin T3 Uptake (T3U) = Normal or Low
Free T3 (FT3) = Normal or Low
Reverse T3 (rT3) = Normal
Thyroid Antibodies = negative or positive
An elevated TSH is all that is required to diagnose primary hypothyroidism. The T3 and T4 levels either protein bound or free fraction are irrelevant. Remember, the pituitary will increase its TSH release if the thyroid tissue is dysfunctional. Many times the thyroid may compensate at the time of the test by presenting normal T3 and T4 levels, but if the TSH is elevated it is a primary hypothyroid case because the pituitary is overworking in attempt to improve thyroid output.
Nutritional Considerations with Primary Hypothyroidism: 1. K-12 Thyroxal: 2 capsules, 3x a day
2. K-9 Thyro-CNV: 2 capsules, 3x a day
Many thyroid hypofunction patterns may be managed functionally with proper nutritional support. The clinician must repeat the TSH in 30 days while the patient is on the above protocol to make sure the patient is capable of functional management. If the TSH is reduced to a normal limit, the patient may decrease the dosage of the above protocol and have repeat testing of TSH. At some point the clinician should be able to determine the proper dosage of supplementation to maintain the TSH.
At times, the patient may not respond to the above protocol, and the clinician may need to consider natural thyroid replacement, or rule out an autoimmune thyroid. Remember, anytime a patient has positive thyroid antibodies, nutritional or replacement support for the thyroid will not make major changes in reducing thyroid symptoms. Patients with positive antibodies against their thyroid must be treated as an immune patient. Note that the most common cause of hypothyroidism in the United States is secondary to post Hashimoto’s.
2. Hyperthyroidism
Thyroid Stimulating Hormone (TSH) = Low Total T4 (TT4) = Normal or Elevated
Free T4 (FT4) = Normal or Elevated
Free Thyroxine Index (FTI) = Normal or Elevated Resin T3 Uptake (T3U) = Normal
Free T3 (FT3) = Normal or Elevated Reverse T3 (rT3) = Normal
Thyroid Antibodies = Positive
A patient that presents with hyperthyroidism must be co-managed by a physician with the scope of practice to manage the acute thyroid pharmaceutically. The clinician that ignores the progression of hypothyroidism may be putting the patient at increased risk for complications such as thyrotoxicosis. Also, if the patient’s auto- inflammatory reaction is not quenched immediately the patient will have an increased potential to have thyroid tissue lost. Natural agents may be used adjunctively with appropriate medical management based on individual cases.
Nutritional Adjunct Support:
1. K-17 Testanex: 1⁄2 teaspoon, 3-6x a day
2. K-23 Super Oxicell: 1⁄2 teaspoon, 3-6x a day
3. Secondary Hypothyroidism to Primary Pituitary Hypofunction
Thyroid Stimulating Hormone (TSH) = salivary is below reference range or serum is below 1.8
Total T4 (TT4) = Normal or Low
Free T4 (FT4) = Normal or Low
Free Thyroxine Index (FTI) = Normal or Low Resin T3 Uptake (T3U) = Normal
Free T3 (FT3) = Normal or Low
Reverse T3 (rT3) = Normal
Thyroid Antibodies = Negative
These patterns are common with many patients with subtle symptoms of low thyroid function. These patterns are usually related to one of four causes. The first and most common cause is from chronic adrenal axis dysregulation. Elevations in cortisol have been found to have suppressive impacts on the pituitary. Many times patients with adrenal exhaustion (low cortisol) have this thyroid/pituitary pattern, because on their way to adrenal exhaustion their pituitary was exposed to chronic elevations of cortisol in the alarm and maladaptation phases. Clinically, it appears in addition to supporting their thyroid/pituitary axis the adrenal disorder (hyper of hypofunction) must be resolved.
A second cause of this pattern is related to post-partum expression. During pregnancy there are fluctuation and demands place on all hormones and feedback loops. Sometimes women will have this pattern develop after a pregnancy. In their history, they will usually exhibit symptoms of low thyroid function and metabolism after the birth of their child.
A third cause of this pattern is a patient that was inappropriately placed on thyroid hormones. Many doctors today are placing patients on thyroid hormones to manage symptoms of slow metabolism, despite a normal thyroid panel. Their logic being that the low thyroid symptoms are subclinical and therefore the labs are not demonstrating the thyroid dysfunction. Many of these patients feel better initially, but after several months many of them develop thyroid receptor site resistance and have a reoccurrence of their symptoms and therefore stop replacement. Some of these patients in the process develop an altered pituitary/thyroid feedback loop that does not resolve normal function again and therefore develop this pattern.
A fourth cause of this pattern is secondary to heavy metal toxicity, but it is not a common cause of this pattern. It would be wise for the clinician to investigate and manage the three previous patterns before attempting to identify and manage patterns of heavy metal burden. Not to say that the management of a heavy metal burden is not common or important, but rather the three previous causes are more common for the expression of this pattern.
4. Thyroid Underconversion
Thyroid Stimulating Hormone (TSH) = Normal
Total T4 (TT4) = Normal, High End of Normal Range or High
Free T4 (FT4) = Normal, High End of Normal Range or High
Free Thyroxine Index (FTI) = Normal, High End of Normal Range or High Resin T3 Uptake (T3U) = Low
Free T3 (FT3) = Low
Reverse T3 (rT3) = Low
Thyroid Antibodies = Negative
Nutritional Support:
1. K-22 Oxicell: 1⁄4 to 1⁄2 teaspoon, 3x a day
2. K-9 Thyro-CNV: 2 capsules, 3x a day
3. K-16 Adrenacalm: 1⁄4 to 1⁄2 teaspoon, 3x a day
Thyroid underconversion is a very common pattern and it is usually found with elevations of cortisol or increased lipid perioxidation. Elevations of cortisol are found in adrenal alarm and maladaptation patterns. However, if a patient is found in adrenal exhaustion, many times the 5’ diodinase enzyme has been down-regulated from prior expressions of elevated cortisol. Increased lipid perioxidation also has the potential to exhibit and underconversion pattern. Lipid perioxidation is the consequence of an inflammatory event or reduced antioxidant status. The Oxidata Test from Apex Energetics can be used to measure MDA levels, which are a marker for lipid perioxidation status. With all patterns in which increased lipid perioxidation is suspected, until the source of infection/inflammation is identified and managed, Oxicell is recommended.
5. Thyroid Overconversion
Thyroid Stimulating Hormone (TSH) = Normal
Total T4 (TT4) = Normal, Low End of Normal Range, or Low
Free T4 (FT4) = Normal, Low End of Normal Range, or Low
Free Thyroxine Index (FTI) = Normal, Low End of Normal Range, or Low Resin T3 Uptake (T3U) = High or High End of Normal Range
Free T3 (FT3) = High or High End of Normal Range
Reverse T3 (rT3) = Normal
Thyroid Antibodies = Negative
Nutritional Support
(Manage Insulin Resistance)
1. Glysen: 2-3 tablets, 3x a day with meals
2. Omega Co-3: 2 tablespoons, 3x a day
3. Adaptocrine: 2 tablets, 3x a day
4. Adrenacalm: 1⁄4 to 1⁄2 teaspoon, 3x a day
Nutritional Support
(Manage Androgen Replacement Overload)
1. K-10 Metacrin-DX: 2 tablets, 3x a day
2. K-11 Bilemin: 2 tablets, 3x a day
3. K-14 Methyl-SP: 2 tablets, 3x a day
Commentary: Androgenic overexposure tends to up-regulate the expression of 5’diodinase, the enzyme responsible for converting T4 into T3. Chronic elevations of T3 have been found clinically to cause thyroid resistance syndromes, therefore although the elevation of T3 may seem beneficial, the patient presents with symptoms of low thyroid function due to resistance from increased T3 production. This pattern is usually found in women suffering from the androgenic drives caused by insulin resistance in polycystic ovary syndrome (PCOS). Chronic elevations of insulin tend to up-regulate the enzyme 17,20 lyase in the theca cells of the ovaries and promote androgenic drives. The management of this thyroid disorder is to manage the insulin resistance.
If a patient is type II diabetic and on exogenous insulin replacement, this pattern is also possible. With these patients, attempts made to decrease their insulin needs via diet, nutritional supplementation, and exercise are crucial. Sometimes the elevations of androgens causing this pattern are not from androgenic drives from hyperinsulinemia, but rather from increased intake of exogenous testosterone or precursors such as testosterone. In these cases the dosage needs to be modified and support of both phase I and II liver detoxification is recommended.
6. Thyroid Biding Hormone Elevations
Thyroid Stimulating Hormone (TSH) = Normal Total T4 (TT4) = Normal
Free T4 (FT4) = Low
Free Thyroxine Index (FTI) = Low or Normal Resin T3 Uptake (T3U) = Low
Free T3 (FT3) = Low
Reverse T3 (rT3) = Normal Thyroid Antibodies = Negative
Nutritional Support for Elevated Estrogens:
1. K-5 Estrovite: 2 capsules, 3x a day
2. K-14 Methyl-SP: 2 capsules, 3x a day
3. K-10 Metacrin-DX: 2 capsules, 3x a day 4. K-11 Bilemin: 2 capsules, 3x a day
*** Eliminating exposure to exogenous estrogens needs to be considered ***
This pattern is common from elevations of estrogens. It is usually from exogenous estrogen exposure such as oral contraceptives or hormone replacement therapy. Elevations of estrogen increase thyroid hormone binding and therefore the free T3, T4 and T3 Uptake are reduced. At times this pattern may be found in males if they are aromatizing their testosterone into estrogens, but it is not common.
7. Thyroid Resistance
Thyroid Stimulating Hormone (TSH) = Normal Total T4 (TT4) = Normal
Free T4 (FT4) = Normal
Free Thyroxine Index (FTI) = Normal
Resin T3 Uptake (T3U) = Normal Free T3 (FT3) = Normal
Reverse T3 (rT3) = Normal Thyroid Antibodies = Normal
This pattern is found in patients that present with symptoms of low thyroid hormone function but with perfectly normal lab tests. These patterns are usually caused by elevations in cortisol. Elevations in cortisol down-regulate the thyroid alpha 1 and 2 receptor sites. Management of these patterns require correction of the adrenal axis drive and adjunct support to decrease cortisol like Adrenacalm. Vitamin A and D inadequacy may alter thyroid receptor rite resistance. Thyroxal is abundant in vitamin A and D and should be considered in these cases. Elevated homocysteine may also cause some degree of thyroid resistance and using Methyl-SP should be considered. Thyroid resistance is also created at times when a patient’s exogenous replacement of thyroid hormones is not being be appropriately monitored.
Nutritional Considerations for Thyroid Resistacne
1. K-14 Methyl-SP: 2 capsules, 3x a day
3. K-12 Thyroxal: 2 capsules, 3x a day
4. K-16 Adrenacalm: 1⁄4 to 1⁄2 teaspoon, 3x a day 5. K-2 Adaptocrine: 2 capsules, 3x a day
8. Autoimmune Thyroid (Not Hyperthyroid)
Thyroid Antibodies = Positive
Any other thyroid pattern may co-exist
Commentary: Any time you see antibodies (TPO Ab) for the thyroid as positive you must manage the patient as an autoimmune patient not a thyroid patient. Any potential causes for an individual immune expression should be considered such as heavy metals, infections (virus, parasite, bacteria, yeast), dysglycemia, food intolerances, chemical exposures, liver detoxification, etc. These patients may benefit from Oxicell and Thyroxal as adjunct nutritional support until the causes are found. Performing the clearvite program may be a great place to start. It will help decrease gastrointestinal-hepatic- immune wind-up and act as elimination/provocation diet.
Adjunct Nutritional Support:
1. K-12 Thyroxal: two capsules, three times a day 2. K-22 Oxicell: 1⁄4 to 1⁄2 teaspoon, 3x a day
3. K-21 Clearvite Program (three weeks)

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