https://youtu.be/ckGGiSdf6jM

A Revolutionary Breakthrough in Understanding Hashimoto’s Disease and Hypothyroidism

Dr. Kharrazian’s academic and clinical research has been featured in numerous documentaries and his clinical models of functional medicine are used by several academic institutions and thousands of health care providers throughout the world.

In the following episode, with Datis:

• The research that led to Dr. Kharrazian writing his first book
• The majority of hypothyroid patients have Hashimoto’s
• How Hashimoto’s attacks the thyroid gland
• Balancing thyroid hormones doesn’t fully address Hashimoto’s
• What is cerebellar ataxia?
• The inspiration behind Dr. Kharrazian’s second book
• Many thyroid patients have brain impairments
• Breaking down TH1 and TH2
• Problems with conventional thyroid testing
• Symptoms of Hashimoto’s
• Finding the right treatment
• How lifestyle factors impact Hashimoto’s
• Gluten is the most common trigger for people with Hashimoto’s
• Infections that can cross-react with the thyroid
• How chemicals can impact thyroid function
• Every patient is uniquely different
• The Autoimmune Protocol (AIP)
• What are goitrogens?
• Why some patients react to proteins
• New research published about cross-reacting food proteins
• Iodine flares up symptoms in patients with Hashimoto’s
• Vitamin D is important for all autoimmune patients
• Addressing the adrenals
• The role of adaptogens
• The benefits of hydrochloric acid (HCl) & digestive enzymes

Dr. Amy Myers is a renowned leader in functional medicine and a New York Times bestselling author of The Autoimmune Solution. She received her Doctorate in Medicine from LSU Health Sciences Center and spent 5 years working in emergency medicine before training with the Institute of Functional Medicine. Amy has helped thousands around the world recover from chronic illness through her dietary-based program, The Myers Way®.

In the following episode, Amy Talks about:

• Before Amy was a thyroid doc, she was a thyroid patient
• Your thyroid regulates every cell in your body
• Hypothyroidism vs. hyperthyroidism
• The lab work Amy recommends for anyone suspecting they may have thyroid dysfunction
• If your conventional doctor says your thyroid is ok… they may be wrong
• What is functional medicine?
• The impact of stress on your thyroid gland
• Ways to combat psychological stress
• How infections can negatively impact your thyroid
• There isn’t a great way to test your iodine level
• Two ways gluten can cause thyroid dysfunction
• The diet that supports a healthy thyroid gland
• Most people are vitamin D deficient
• The impact of goitrogens on your thyroid
• Amy’s healthy morning routine

The Comprehensive Thyroid Assessment is a hormone test that provides a thorough analysis of thyroid hormone metabolism. It includes central thyroid gland regulation and activity, thyroid production and secretion, peripheral thyroid conversion, and thyroid autoimmunity. This hormone test allows the practitioner to pinpoint common imbalances that underlie a broad spectrum of chronic illness. This test analyzes serum levels of TSH, free T4, free T3, reverse T3, anti-TG antibodies, and anti-TPO antibodies to assess central and peripheral thyroid function, as well as thyroid auto-immunity. Thyroid hormones are essential and primary regulators of the body´s metabolism. Hormone imbalances can affect virtually every metabolic process in the body, exerting significant effects on mood and energy level.

Symptoms of thyroid hormone imbalances can include:

Fatigue
Depression
Coldness
Constipation
Poor skin
Headaches
PMS
Dysmenorrhea
Fluid retention
Weight gain
Anxiety/Panic attacks
Decreased memory and concentration
Muscle and joint pain
Low sex drive

Thyroid hormone function has a profound impact on overall health via:

Modulation of carbohydrate, protein, and fat metabolism
Vitamin utilization
Mitochondrial function
Digestive process
Muscle and nerve activity
Blood flow
Oxygen utilization
Hormone secretion
Sexual and reproductive health
Many other physiological parameters
Thyroid Hormone Testing

The Comprehensive Thyroid Assessment is a hormonal test which reveals imbalances that often go undetected with more limited assessments.

This thyroid hormone testing measures:

Unbound levels of T4 and T3 which reflect the bioactive portion of thyroid hormone. This hormone assessment can identify not only overt hyper-and hypothyroidism, but subtle sub-clinical manifestations of thyroid dysfunction. Reverse T3, levels of which can increase when peripheral conversion to T4 to active T3 is impaired. Peripheral thyroid imbalances may arise from nutrient shortages, heavy metal exposure, adrenal stress, enzyme deficiencies, and other chronic illness. Thyroid antibody levels, which help gauge autoimmune response and may reflect metabolic irregularities and hypothyroidism even when TSH and T4 levels appear normal. Thyroid antibody levels may rise in response to trauma, dysbiosis, inflammation (including thyroiditis) or progressive thyroid degeneration. Ensuring healthy thyroid function is clinically essential. Optimal thyroid function may help safeguard against the pathogenesis of diabetes, obesity, heart disease, and depression. Thyroid hormones also play central metabolic roles in healthy sexual and reproductive function in both women and men. Because they are essential for IGF-1 production, thyroid hormones significantly affect lipid metabolism.

TWENTY-TWO PATTERNS OF LOW THYROID FUNCTION

1. Hypothalamus paraventricular defect relates to central nervous system deficiency of serotonin, leading to low TSH: The hypothalamus is the part of the brain that directs hormone function, including that of the thyroid, via the pituitary gland. Dysglycemia (hypoglycemia, insulin resistance, and diabetes) is the most common cause of a serotonin deficiency, which hampers communication between the brain and thyroid gland. People with this type of low thyroid function will have symptoms of serotonin deficiency, a TSH below the functional range of 1.8, and a T4 below 6.

2. Hypothalamus paraventricular defect relates to central nervous system deficiency of dopamine, leading to low TSH: The hypothalamus is the part of the brain that directs hormone function, including that of the thyroid, via the pituitary gland. Dysglycemia (hypoglycemia, insulin resistance, and diabetes) is the most common cause of a dopamine deficiency, which hampers communication between the brain and thyroid gland. Also, the importance of methylation cannot be overlooked with a dopamine deficiency and should be addressed as well. People with this type of low thyroid function have symptoms of dopamine deficiency, a TSH below the functional range of 1.8, and T4 below 6.

3. Hypothalamus paraventricular defect promoted by cytokines, leading to low TSH: Inflammation from gut infections, chronic viral infection, Lyme disease, food intolerances, molds, or environmental compounds can damage the hypothalamus and affect its ability to communicate with the thyroid gland. These patients typically will have low white blood cell counts, a TSH below the functional range of 1.8, and a T4 below 6.

4. Hypothalamus paraventricular defect promoted by elevated prolactin: The hormone prolactin is very sensitive to shifts of dopamine, thyroid hormones, progesterone, and serotonin. These shifts can elevate prolactin, suppressing both TSH, and the luteinizing hormone (LH), leading to depression of the sex hormones in women and men. Prolactinoma, a benign pituitary tumor, may also elevate prolactin, again suppressing TSH.

5. Pituitary suppression from cortisol leading to low TSH: This pattern occurs when elevated cortisol from adrenal stress suppresses pituitary function and thus TSH levels. These patients will have a TSH below the functional range of 1.8, and T4 below 6. The main causes for this pattern are active infection, dysglycemia, unrelenting stress, and, most commonly, hypoglycemia or insulin resistance.

6. Thyroid tissue disorder related to thyroid peroxidase (TPO) autoimmune response:  TPO is the enzyme in the thyroid responsible for the production of thyroid hormones and is a common site for autoimmune attacks. A positive TPO antibody test suggests Hashimoto’s disease.

7. Thyroid tissue disorder related to thyroglobulin (TGB) autoimmune response:  TGB is produced in the thyroid gland and is used to produce thyroid hormones. It is also a common site for autoimmune attacks. A positive TGB antibody tests suggests Hashimoto’s.

8. Down-regulated TPO activity related to progesterone deficiency Progesterone increases TPO activity: This is why a woman’s body temperature is higher when she ovulates — progesterone surges at ovulation, stimulating TPO activity and overall metabolism. Low progesterone can lead to low thyroid hormones, although their levels of TSH, T4, and T3 will not fall outside of normal lab ranges. Dysglycemia is a common culprit for low progesterone.

9. Down-regulated TPO from deficiency of cofactors : Various nutrients are important for the manufacture and function of adequate levels of TPO, which is responsible for thyroid hormone production. Poor diet and gut function can lead to a deficiency in these nutrients.

10. Down-regulated 5’ deiodinase activity from deficiency of cofactors: The 5’ deiodinase enzyme is responsible for converting T4 to T3, the only form of thyroid hormone the body can use. Poor diet and gut function can lead to a deficiency in the nutrients responsible for adequate function of this enzyme.

11. Down-regulated 5’ deiodinase from gastrointestinal dysbiosis and lipopolysaccharides: About 20 percent of the body’s T3 depends on healthy gut flora for conversion. Dysbiosis and bacterial infections down-regulate the 5’ deiodinase enzyme, which hampers this conversion.

12. Down-regulated 5’ deiodinase activity from elevated cytokines: Inflammation from gut infections, chronic viral infection, Lyme’s disease, food intolerances, molds, or environmental compounds can disrupt the conversion of T4 to T3. Inflammation elevates the levels of cytokines, which down regulates the 5’ deiodinase enzyme. Because T3 levels do not affect TSH levels, it should be standard to measure T3. Normal TSH, normal T4, and a depressed T3 strongly suggest down-regulation of the 5’ deiodinase enzyme.

13. Down-regulated 5’ deiodinase activity from elevated cortisol: Elevated cortisol from chronic stress down-regulates the 5’ deiodinase enzyme, inhibiting the conversion of T4 to T3. In the past it was believed T4 was shunted into irreversible and inactive T3. New research shows that there is not an increase in reverse T3, but rather poor clearance of reverse T3 due to elevated cortisol. 

14. Down-regulated 5’ deiodinase activity from peripheral deficiencies of serotonin: Serotonin influences the hypothalamus-pituitary-thyroid axis, as well as T3 conversion. Peripheral serotonin deficiency down-regulates these functions.

15. Down-regulated 5’ deiodinase activity from peripheral deficiencies of dopamine: Dopamine influences the hypothalamus-pituitary-thyroid axis as well as T3 conversion. Peripheral dopamine deficiency down regulates these functions.

16. Up-regulated 5’ deiodinase activity from elevated testosterone:  Elevated levels of testosterone in women create this pattern of too much T4 being converted into T3. The excess production of T3 overwhelms the cells and they develop a resistance to the thyroid hormone. This pattern is most often found in women with insulin resistance and PCOS or in men who use testosterone creams.

17. Elevations of thyroid binding globulin (TGB) leading to decreased production of thyroid hormones: TGB is the protein responsible for transporting thyroid hormones. When TGB levels increase, the percentage of free-faction thyroid hormones drop. This is evidenced by a depressed T3 uptake or low free thyroid hormones, despite a normal TSH. This pattern is typically due to a source of exogenous estrogens, particularly oral contraceptives or Premarin. 

18. Depression of thyroid-binding globulin (TGB) leading to increased production of thyroid hormones and resistance: When TGB drops, the amount of free thyroid hormones rises. In this pattern, the TSH is normal. The free thyroid hormone elevation is typically subtle and does not create hyperthyroid symptoms. Instead, the person develops symptoms of hypothyroidism due to thyroid receptor-site resistance. This pattern is typically caused by elevations of estrogens associated with insulin resistance and may also be promoted by high testosterone, such as occurs in women with insulin resistance or in men who use testosterone creams and medications. 

19. Thyroid resistance promoted by an elevation of cytokines Pro-inflammatory TH-1 cytokines have been shown to decrease a cell’s sensitivity to thyroid hormones, causing symptoms of hypothyroidism: This is especially apparent with people on thyroid replacement hormone medication who are still suffering from symptoms of low thyroid activity. The effect of a chronic inflammatory immune response on thyroid receptor sites should be considered in this case. Thyroid resistance promoted by elevations of cortisol: Chronic elevations in the adrenals hormone cortisol have been shown to decrease the sensitivity of cellular receptor sites to thyroid hormones.

21. Thyroid resistance promoted by deficiencies of vitamin A: Thyroid hormone receptor sites must be sufficient in vitamin A in order to activate thyroid hormone. A deficiency in vitamin A hampers receptor site function so that the cell is resistant to thyroid hormones, leading to hypothyroidism symptoms. Vitamin A deficiency should be suspected with anemia, liver disease, cirrhosis, and alcoholism. The key clinical symptom of vitamin A deficiency is difficulty with night vision not related to astigmatism.

22. Thyroid resistance promoted by homocysteine: Elevated homocysteine has been shown to dampen the expression of thyroid hormones at the receptor site. Elevated homocysteine should always be considered in individuals who take antacid medications, oral contraceptives, and estrogen, or who have hypochlorydria and H.pylori infections. This pattern is difficult to identify since the patient has hypothyroid symptoms but normal blood tests. Since elevated homocysteine produces no symptoms, a blood test should be run to identify this pattern.

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

Commentary:

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: 

Further Commentary:

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

Commenttary:

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

Commentary:

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

Commentary:

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 ***

Commentary:

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

Commentary:

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)

Is Thyroid Disease a Risk for your Heart?

The relationship between thyroid health and cardiac health has been known since 1883¹. In mainstream medicine, it is typical to treat each organ system as its own entity hence the creation of a specialist in an “ology” practice. Yet, the body is a whole. This is especially true with thyroid and cardiac health. A patient could typically see an endocrinologist only to be referred to a cardiologist. If you have thyroid disease, you should know there are risks with either having an overactive or underactive thyroid gland. It is more often seen with hyperthyroidism and/or Graves’ disease. But, it can reveal itself in patients with Hashimoto’s thyroiditis. Studies suggest that too much thyroid hormones can lead to high blood pressure and clotting problems. On the other hand too little can instigate high cholesterol and inflammation.

Risks for Underactive Thyroid and Heart Disease

In a recent meta-analysis of over 55 cohort studies, with approximately 2 million people involved, patients that had hypothyroidism compared to euthyroidism (normal thyroid function) had higher risks of ischemic heart disease and cardiac mortality⁴.

Key Insight: Low thyroid hormone levels can slow your heart down. They can then cause the arteries to become less elastic leading to high blood pressure.

Thyroid hormones help the liver break down lipids and reduce the number of triglycerides (fat in the blood). Thyroid hormones also assist in cellular metabolism. If there is a reduction in the amount of circulating thyroid hormones, this will slow down metabolism.

This can occur for a number of reasons, including:

• Hashimoto’s thyroiditis
• Surgery
• Trauma to the thyroid gland

Some case-controlled studies have demonstrated that having TSH levels > 4, the higher the chances of coronary heart disease seen. If you are low in thyroid hormones, you can have elevated cholesterol levels, especially the low-density one called LDL. In addition, higher TSH levels are typically present in obese patients.

Risks for Overactive Thyroid and Heart Disease

Too much thyroid hormones such as T4 and T3 can cause heart palpitations and predispose you to a heart condition known as Atrial Fibrillation (A-Fib). This leads to overstimulation of thyroid hormones on the heart. Ultimately, this causes it to beat irregularly.