Hashimoto’s Autoimmune Thyroiditis

Hashimoto’s disease is an autoimmune disorder in which your immune system inappropriately attacks your thyroid gland, causing damage to your thyroid cells and upsetting the balance of chemical reactions in your body. The inflammation caused by Hashimoto’s disease, also known as chronic lymphocytic thyroiditis, often leads to an underactive thyroid gland (hypothyroidism). Hashimoto’s disease is the most common cause of hypothyroidism in the United States.

When You Are Diagnosed With Hashimoto’s

By the time you are diagnosed with Hashimoto’s, Hypothyroidism involving just the thyroid is no longer the primary factor. Any support you give for just the thyroid will provoke further attacks. So stop it!!! Look for the other non-thyroid factors and which of the other five patterns of low thyroid  are involved. You will respond much quicker in doing this.

Along the way, however, there can be periods where the thyroid sputters back to life, even causing temporary hyperthyroidism, then a return to hypothyroidism. This cycling back and forth between hypothyroidism symptoms and hyperthyroidism is characteristic of Hashimoto’s disease as the other Non-Thyroid Factors and/or conditions that cause the five patterns of hypothyroidism and/or 22 factors of low thyroid function caused by the neuroendocrine transmitters of the NEI Supersystem  flare up and/or calm down. Again, the thyroid is NOT directly involved.

So, for example, periods of anxiety/insomnia/diarrhea/weight loss may be followed by periods of depression/fatigue/constipation/weight gain. Did I mention the 22 different factors that can cause low thyroid function that are due to neuroendocrine transmitters of the NEI Supersystem? Again, the thyroid is NOT directly involved.

Hashimoto’s Thyroiditis Treatment Priorities

  1. Calm and Quite the immune system
  2. Quench inflammation in the body
  3. Reset the immune system
  4. Support the elimination of the other NON-Thyroid factors that provoke immune responses towards the thyroid. (Not mentioned by Kharrazian or Wentz)
  5. Address the Neuroendocrine transmitters imbalance that can cause 22 patterns of low thyroid function. (Kharrazian D. Why Do I Still Have Thyroid Symptoms. Chapter Ten, page 179; Not mention by Izabella Wentz)
  6. Support the underlying cause of whichever of the six patterns of low thyroid is present in the  body.  (Kharrazian D. Why Do I Still Have Thyroid Symptoms. Chapter Four, page 67; Not mention by Izabella Wentz)

The treatment of Hashimoto’s should not focus on the thyroid until the underlying factors provoking the immune attack are resolved. Any support that enhances the thyroid function will provoke aggressive attacks on the thyroid gland itself. Most of the factors involved in low thyroid function do not involve the thyroid gland.

It is like having a coworker that prevents you from doing your job and you have the job that gets all the attention and blame.

Hashimoto’s typically involves a slow but steady destruction of the gland  by the immune system and other NON-THYROID Factors that eventually results in the thyroid’s inability to produce sufficient thyroid hormone — the condition known as hypothyroidism. There are other NON-Thyroid factors that provoke immune responses towards the thyroid that take priority over supporting normal thyroid function.  There are six patterns of hypothyroidism (Low Thyroid) – five of which do not involve the thyroid that should be addressed.

Forbidden Cytokines Make Antibody Tests Confusing

Cytokine secretion by helper T cells is particularly important in autoimmunity because chronic autoimmune diseases, such as Hashimoto’s Thyroiditis, multiple sclerosis, diabetes, and rheumatoid arthritis are predominantly caused by Th1 cells. Th2 cells can antagonize Th1 functions and in numerous autoimmune conditions prevent autoimmune diseases from getting established.

After autoimmune conditions, such as those mentioned above, become established. Th2 is not only an inefficient suppressors of Th1, but can provoke and promote the onset of autoimmune conditions. Furthermore, neuropeptides (NPs): (somatostatin, calcitonin gene-related peptide, neuropeptide Y, and substance P), drive distinct Th1 and Th2 populations to a “forbidden” cytokine secretion: secretion of Th2 cytokines from a Th1 T cell line and vice versa. Such a phenomenon cannot be induced by classical antigenic/antibody stimulation.

Some of the NPs are produced by microbes as part of their defense strategy. Thus, focusing on restoring normal thyroid function to an autoimmune thyroid is futile.

Hypothalamic Sampling Hormones Requires Blood Flow

Sampling of hormones (including the sex hormones) by the hypothalamus requires consistent blood flow. In the body, blood carries hormones released by endocrine glands and carries them to body parts that need them.

In parasympathetic withdrawal, diagnosis is usually considered adrenal fatigue. The volume of blood shifts from the muscles and brain to the central abdominal compartment. The blood flow to the brain is not stopped when this occurs. The flow is reduced and Poiseuille’s Laws come into play.

The circulatory system provides many examples of Poiseuille’s law in action—with blood flow regulated by changes in vessel size and blood pressure. Blood vessels are not rigid but elastic. Adjustments to blood flow are primarily made by varying the size of the vessels, since the resistance is so sensitive to the radius. This is done by the Abdominal Brain through the release of NeuroEndocrine transmitters, i.e. Serotonin – sero = “blood”, tonin = “pertaining to”.

A 19% decrease in flow is caused by a 5% decrease in radius of the blood vessels. The body may compensate by increasing blood pressure by 19%, but this presents hazards to the heart and any vessel that has weakened walls.

This decrease in radius is surprisingly small for this situation. To restore the blood flow in spite of this buildup would require an increase in the pressure difference of a factor of two, with subsequent strain on the heart.

ISCHEMIC PENUMBRA OF PARASYMPATHETIC DOMINANCE

In severe and/or chronic illness, profound changes occur in the hypothalamic-pituitary-thyroid axis. Ischemia and inflammation disrupt the porous Blood-Brain-Barrier surrounding the hypothalamus. The observed decrease in serum concentration of both hormones and neuroendocrine transmitter (neurotransmitters in the blood) are not compatible with a negative feedback loop.

Ischemia is a restriction in blood supply to tissues, causing a shortage of oxygen and glucose needed for cellular metabolism (to keep tissue alive, healthy and functioning properly). Ischemia is generally caused by problems with blood vessels, with resultant damage to or dysfunction of tissue or organs. It also means local anemia in a given part of a body sometimes resulting from congestion (such as vasoconstriction, red blood cell aggregation due to insulin resistance/diabetes). Ischemia comprises not only insufficiency of oxygen, but also reduced availability of nutrients and inadequate removal of metabolic wastes.

Hepatic Portal Hypertension

Parasympathetic Withdrawal (vasodilation) with blood pooling in the Abdominal Compartment makes the Movement Compartment and Brain/Spinal Cord Ischemic. At the periphery of the ischemic region, the so-called ischemic penumbra, neuronal damage throughout the body develops more slowly because blood flow arising from adjacent vascular territories (collateral flow) keeps blood perfusion above the threshold for immediate cell death. In the ischemic core, the major mechanism of cell death is energy failure caused by Oxygen/Glucose Deprivation (O2/GD). The hypothalamus and midbrain are most vulnerable to ischemia.

Neuron Vulnerability

Neurons in the most vulnerable areas cease to respond or show only faint responses and develop irreversible ischemic or post-ischemic damage. The hypothalamus responds to ischemic insults rigorously without having irreversible ischemic or post-ischemic damage.

The thalamus-hypothalamus interface represents a discrete boundary where neuronal vulnerability to ischemia is high in thalamus (like more rostral neocortex, striatum, hippocampus). In contrast hypothalamic neurons are comparatively resistant, generating weaker and recoverable anoxic depolarization similar to brainstem neurons, possibly the result of a Na/K pump that better functions during ischemia.

There is a well recognized but poorly understood caudal-to rostral increase in the brain`s vulnerability to neuronal injury caused by metabolic stress (insulin resistance).

Several brain regions, including the caudate, hippocampus, and hypothalamus, are vulnerable to hypoxic–ischemic brain injury. During O2/GD, hypothalamic neurons gradually depolarized during ischemic exposure. The O2/glucose deprivation (O2/GD) response induces failure of the Na+/K+ pump. The recovery is slow with chronic ischemic penumbrance

Without oxygen and glucose, neurons cannot generate the ATP needed to fuel the ionic pumps that maintain the ionic gradient across the neuronal membrane, mainly the Na+−K+ ATPase.

In the ischemic penumbra, the flow reduction is not sufficient to cause energy failure, and neurons remain viable for a prolonged period of time after the insult, but the neurons are stressed and critically vulnerable to pathogenic events that may tip their fragile metabolic balance. Excessive extracellular accumulation of glutamate is a major factor contributing to production of cytotoxic nitric oxide, free radicals and arachidonic acid metabolites. These events lead to necrosis or programmed cell death depending on the intensity of the insult and the metabolic state of the neurons. Injured and dying cells have a key role in post-ischemic inflammation because they release danger signals that activate the immune system.

Neurons that demonstrate particular vulnerability to ischemic challenges have been termed “selectively vulnerable neurons”. Of the entire forebrain, the neurons of the hippocampus are the most vulnerable.

Summary: Parasympathetic Dominance causes Ischemia to the Hippocampus, Hypothalamus, and Pituitary producing alterations in the HPA, HPT, HPD and HPG axis.

Fives Stages of Hashimoto’s Thyroiditis

Hashimoto’s is a progressive autoimmune condition and the Five stage of Hashimoto’s have been identified.

Stage 1

A person has the immune system imbalance that predisposes them to development of Autoimmune conditions, one of which is Hashimoto’s. For all intents and purposes they do not have thyroid disease or an autoimmune disease. Their thyroid function is normal and there is no attack on the thyroid.

  • Women are more at risk for autoimmune conditions due the monthly fluctuations of their hormones.
  • Women with severe morning sickness have an over active Th17 immune response.

    READ MORE... Th17

  • Women with “hip pain”, “sciatica” or “loose ligaments” during the last trimester have an overactive Th17 immune response causing bone marrow edema in the hip bones causing the aforementioned painful conditions.
  • Women put on bed rest during the last trimester have an overactive Th17 immune response.
  • Women that feel better during pregnancy are using their baby’s endocrine glands to support their NEI Supersystem deficiencies. The baby is born with over-worked, underdeveloped endocrine glands that will not be able to support them during adult life.
  • Immune / inflammatory and hormone messengers cross the placenta, which the baby’s immune and endocrine system responds to. The baby is born with an overactive immune system and possible “forbidden” Cytokines are actively disrupting the child’s immune responses. These are the children born with allergic responses or incessant crying.

Stage 2

Other Non-thyroid Factors begin provoking immune responses towards the thyroid gland. Bacteria can translocate from the mouth to the thyroid. Lectin can damage TSH receptors. Damage occurs to the thyroid gland. The immune system moves into to clear the damaged tissue. Because the oral infection is never addressed and eating a diet of non-seasonal fresh fruit and vegetables is considered healthy. The Non-thyroid factors continue to damage the thyroid with the help of the immune cells. A person will have symptoms, but their TSH, T3 and T4 may be normal. But thyroid medication will be demanded and prescribed anyway. At this point the thyroid antibody test may reveal thyroid antibodies are now being produced.

Stage 3

The neuroendocrine transmitters may lose the ability to control the blood supply. The blood may be predominantly in the abdomen with very little hormone messengers making their way to the head for sampling by the Hypothalamus. This will cause altered feedback signals to the thyroid gland.

The thyroid gland loses its ability to compensate and thyroid hormone production starts to become affected. The lack of T3 and T4 making in the blood stream to the Hypothalamus for sampling will cause a mildly elevated TSH (between 2 – 10). The T3 and T4 will be normal as they are used up by the body, decreasing their available supply. This is often described as subclinical hypothyroidism. The five Non-Thyroid patterns (underconversion, overconversion, resistance, hormone binding elevation or HPT axis), 22 patterns of Neuroendocrine transmitters imbalance and the Non-Thyroid factors will never be considered or addressed. Thyroid hormones will be prescribed leading to further inability of the thyroid gland’s need to produce thyroid hormones.

Stage 4

Ignoring the Non-Thyroid Patterns while taking Thyroid Drugs

Thyroid gland failure occurs when the thyroid gland loses its ability to make thyroid hormones. The thyroid hormone drugs are recognized during hypothalamus sampling. As far as the hypothalamus which controls the Hypothalamic-Pituitary-Thyroid Axis is concerned, you have all the thyroid hormones you need and there is no need to signal the thyroid gland by producing Thyroid Stimulating Hormone (TSH). Thus, it is expected that TSH is low while taking thyroid medications. This makes it a failure to stimulate the production of thyroid hormone problem. If you do not use it, you lose it. Your body sees no need to support unused thyroid tissue.

Too much of the thyroid gland is not maintained when the Non-Thyroid Patterns causing hypothyroidism symptoms are not addressed.

Ignoring the Non-Thyroid Factors while taking Thyroid Drugs

Thyroid gland failure occurs when too much of the thyroid gland is damaged or destroyed by the Non-Thyroid Factors and the subsequent Immune response. Too much of it has been damaged or destroyed. Supporting the “normal” function of the thyroid gland will enhance the immune response towards the thyroid gland. It is futile to cause more damage while expecting thyroid gland improvement.

Thyroid Drugs and Supplements

TSH will be low as there is no signals from the Hypothalamus for its production. T3 and T4 numbers will be ambiguous and confusing. Support will continue for the restoration of thyroid gland with confusing results.

Stage 5

You are allowed to have multiple autoimmune conditions simultaneously. It is not a matter of which came first. Most Doctors will only offer to test for autoimmune conditions based on their specialty. This leads to multiple Doctor visits, multiple diagnoses, and multiple treatment plans putting you on a slippery slope with a downward spiral.

Until the immune system is brought under control, thyroid supplements and drugs are futile. You do not worry about what color you are painting the kitchen when the house is on fire.

Hypothalamic Pituitary Thyroid (HPT) Axis

Hypothalamic – Pituitary – Thyroid Axis (HPT) AKA: Hypothyroidism Secondary to Pituitary Hypofunction

Another more appropriate name for the Hypothalamic – Pituitiary – Thyroid (HPT) Axis is Hypothyroidism Secondary to Decreased Pituitary Output. This is the label used in Dr. Kharrazian’s book Why Do I Still Have Thyroid Symptoms When My Lab Tests Are Normal.

The pituitary gland is often portrayed as the “Master Gland” of the body. Such praise is justified in the sense that the anterior and posterior pituitary secrete a battery of hormones that collectively influence all cells and affect virtually all physiologic processes.

The pituitary gland may be king, but the power behind the throne is clearly the hypothalamus. Some of the neurons within the hypothalamus – neurosecretory neurons – secrete hormones that strictly control secretion of hormones from the anterior pituitary. The hypothalamic hormones are referred to as releasing hormones and inhibiting hormones, reflecting their influence on anterior pituitary hormones.

T3 and T4 regulation

The production of thyroxine (T4) and triiodothyronine (T3) is regulated by thyroid-stimulating hormone (TSH), released by the anterior pituitary. The thyroid and thyrotropes (cells in the anterior pituitary) form a negative feedback loop: TSH production is suppressed when the T4 levels are high, and vice versa. The TSH production itself is modulated by thyrotropin-releasing hormone (TRH), which is produced by the hypothalamus and secreted at an increased rate in situations such as cold (in which an accelerated metabolism would generate more heat).

Thyroid Hormones Pass Through Blood – Brain -Barrier

Thyroid hormones and neuroendocrine transmitters have important influences upon the hypothalamus, and to do so they must pass through the blood–brain barrier. The hypothalamus is bounded in part by specialized brain regions that lack an effective blood–brain barrier; the capillaries at these sites has perforations to allow free passage of hormones and even large proteins and other molecules. At these sites, the hypothalamus samples the hormone composition of the blood. Some of these sites are the sites of neurosecretion, where signals are sent from the nerve cells of the hypothalamus to the posterior pituitary. The hypothalamus secretes substances known as neurohormones that start and stop the secretion of anterior pituitary hormones. 

The neurons are in intimate contact with both blood and Cerebrospinal Fluid (CSF). These structures are densely vascularized, and contain receptive neurons that control hormones, regulation of fluid and electrolyte balance.

The hypothalamic-pituitary-thyroid axis (HPT axis) is a neuroendocrine system that regulates metabolism.  When the hypothalamus senses low circulating levels of the hormones T3 and T4 in the blood, it signals to the pituitary by releasing Thyroid Releasing Hormone (TRH) into the capillaries traveling to the anterior pituitary, which secretes Thyroid Stimulating Hormone (TSH) into the veins. The veins carry the TSH to the thyroid signaling the thyroid gland to release T3 and T4.  T4 normally is converted to the more active T3, but T4 can also be converted to reverse T3 (rT3).  Reverse T3 antagonizes the T3 receptor, so high levels can be detrimental.

 

Hypothalamic Sampling Requires Blood Flow

Sampling of hormones (including the sex hormones) by the hypothalamus requires consistent blood flow. In the body, blood carries hormones released by endocrine glands and carries them to body parts that need them. 

In parasympathetic withdrawal, diagnosis is usually considered adrenal fatigue. The volume of blood shifts from the muscles and brain to the central abdominal compartment. The blood flow to the brain is not stopped when this occurs. The flow is reduced and Poiseuille’s Laws come into play. 

The circulatory system provides many examples of Poiseuille’s law in action—with blood flow regulated by changes in vessel size and blood pressure. Blood vessels are not rigid but elastic. Adjustments to blood flow are primarily made by varying the size of the vessels, since the resistance is so sensitive to the radius. This is done by the Abdominal Brain through the release of NeuroEndocrine transmitters.

A 19% decrease in flow is caused by a 5% decrease in radius of the blood vessels. The body may compensate by increasing blood pressure by 19%, but this presents hazards to the heart and any vessel that has weakened walls.

This decrease in radius is surprisingly small for this situation. To restore the blood flow in spite of this buildup would require an increase in the pressure difference of a factor of two, with subsequent strain on the heart.

ISCHEMIC PENUMBRA OF PARASYMPATHETIC DOMINANCE

In severe and/or chronic illness, profound changes occur in the hypothalamic-pituitary-thyroid axis. Ischemia and inflammation disrupt the porous Blood-Brain-Barrier surrounding the hypothalamus. The observed decrease in serum concentration of both thyroid hormones and thyrotropin (TSH) are not compatible with a negative feedback loop.

Ischemia is a restriction in blood supply to tissues, causing a shortage of oxygen and glucose needed for cellular metabolism (to keep tissue alive, healthy and functioning properly). Ischemia is generally caused by problems with blood vessels, with resultant damage to or dysfunction of tissue or organs. It also means local anemia in a given part of a body sometimes resulting from congestion (such as vasoconstriction, red blood cell aggregation due to insulin resistance/diabetes). Ischemia comprises not only insufficiency of oxygen, but also reduced availability of nutrients and inadequate removal of metabolic wastes. 

Parasympathetic Withdrawal (vasodilation) with blood pooling in the Abdominal Compartment makes the Movement Compartment and Brain/Spinal Cord Ischemic. At the periphery of the ischemic region, the so-called ischemic penumbra, neuronal damage throughout the body develops more slowly because blood flow arising from adjacent vascular territories (collateral flow) keeps blood perfusion above the threshold for immediate cell death. In the ischemic core, the major mechanism of cell death is energy failure caused by Oxygen/Glucose Deprivation (O2/GD). The hypothalamus and midbrain are most vulnerable to ischemia.

Neurons in the most vulnerable areas cease to respond or show only faint responses and develop irreversible ischemic or post-ischemic damage. The hypothalamus responds to ischemic insults rigorously without having irreversible ischemic or post-ischemic damage.

The thalamus-hypothalamus interface represents a discrete boundary where neuronal vulnerability to ischemia is high in thalamus (like more rostral neocortex, striatum, hippocampus). In contrast hypothalamic neurons are comparatively resistant, generating weaker and recoverable anoxic depolarization similar to brainstem neurons, possibly the result of a Na/K pump that better functions during ischemia.

There is a well recognized but poorly understood caudal-to rostral increase in the brain`s vulnerability to neuronal injury caused by metabolic stress (insulin resistance).

Several brain regions, including the caudate, hippocampus, and hypothalamus, are vulnerable to hypoxic–ischemic brain injury. During O2/GD, hypothalamic neurons gradually depolarized during ischemic exposure. The O2/glucose deprivation (O2/GD) response induces failure of the Na+/K+ pump. The recovery is slow with chronic ischemic penumbrance

Without oxygen and glucose, neurons cannot generate the ATP needed to fuel the ionic pumps that maintain the ionic gradient across the neuronal membrane, mainly the Na+−K+ ATPase. 

In the ischemic penumbra, the flow reduction is not sufficient to cause energy failure, and neurons remain viable for a prolonged period of time after the insult, but the neurons are stressed and critically vulnerable to pathogenic events that may tip their fragile metabolic balance. Excessive extracellular accumulation of glutamate is a major factor contributing to production of cytotoxic nitric oxide, free radicals and arachidonic acid metabolites. These events lead to necrosis or programmed cell death depending on the intensity of the insult and the metabolic state of the neurons. Injured and dying cells have a key role in post-ischemic inflammation because they release danger signals that activate the immune system. 

Neurons that demonstrate particular vulnerability to ischemic challenges have been termed “selectively vulnerable neurons”. Of the entire forebrain, the neurons of the hippocampus are the most vulnerable.  

Summary: Parasympathetic Dominance causes Ischemia to the Hippocampus, Hypothalamus, and Pituitary producing alterations in the HPA, HPT, HPD and HPG axis.

HPT AXIS 

During illness, profound changes may occur in the hypothalamic-pituitary-thyroid (HPT) axis. The most consistent change is a decrease in serum tri-iodothyronine (T3) level, but in severe illness, serum thyroxine (T4) may also decrease. The persistence of a normal or even decreased serum level of thyrotropin (TSH) in the face of decreased serum thyroid hormone concentrations implies there is not an adequate concentration of T3 or T4 reaching the hypothalamus for sampling. 

Since these abnormalities of thyroid hormone concentration usually occur without any evidence of thyroid disease and disappear with recovery, they have been referred to as the `sick euthyroid syndrome’ or the `euthyroid sick syndrome’.

The downregulation at all levels of the HPT axis (decreased thyrotropin-releasing hormone (TRH) and TSH at the hypothalamic-pituitary level, and a decreased production of T3 at the peripheral extra-thyroidal level) in Non-Thyroid Illness is part of the neuroendocrine adaptation to Parasympathetic Withdrawal. In this view, attempts to restore thyroid hormone levels are detrimental and should not be undertaken. 

Immune Stimulation

There is a neuroendocrine component in the pathogenesis of the decreased activity of the HPT and somatotropic axes in prolonged critical illness. T3 can stimulate dendritic cell (DC) maturation, leading to DC-induced T cell proliferation and IFN-γ release. The cytokines IL-1β, TNF-α, IFN-γ, and IL-6 can inhibit the conversion of T4 to T3, thereby shunting T4 towards the production of the potentially detrimental rT3.

Early or Subclinical Hypothyroidism

[captainform id=”1220620″ lightbox=”1″ text_content=”Take%20the%20Early%20Hypothyroid%20Survey” bg_color=”FF0000″ text_color=”FFFFFF” position=”left” type=”floating-button”]Early or Subclinical hypothyroidism, also called low thyroid or hypothyroidism is diagnosed when thyroid hormone levels are with normal reference range but TSH is mildly elevated. 

Thyroid disorders are more common among women than men. Dr. David Peterson at Wellness Alternatives says, 

“Sex dependent hormonal fluctuations occur in women due to pregnancy, menopause, contraceptive use, and hormonal replacement therapy. Because hormone surges can occur, these contributing factors make women 7 times more likely to develop a thyroid condition than men. The body can interpret a hormone surge as an alarm to turn on or off other important signaling in the body that can lead to faulty thyroid function.” 

While screening patients for thyroid disease, physicians often order labs measuring only thyrotropin-stimulating hormone (TSH) levels in patients. Sometimes labs will show increased thyrotropin-stimulating hormone (TSH) levels in patients whose free thyroxine (T4) levels are not below normal. This state, termed “Subclinical Hypothyroidism,” is most commonly an early stage of hypothyroidism.

TSH can be elevated up to 3 to 5.5 mIU/L even if thyroxine (T4) levels are within the normal reference range, indicating subclinical hypothyroidism. At this stage, the TSH test is especially useful because it could be pointing to the underachieve thyroid function before some patients develop clinical findings, goiter, or abnormalities noticeable in other thyroid tests.

The most common early symptoms of hypothyroidism, such as fatigue, constipation, dry skin, and weight gain are ‘nonspecific? and could are associated with many other diseases and conditions. The symptoms can also be present in subclinical hypothyroidism, when TSH is in the range of 0.3 and 10 mIU/L but T4 and T3 hormones are normal.

 

If the only lab tests run are only thyroid markers. There is no way anything other contributors to “low thyroid” symptoms can be considered. 

Other Causes of Subclinical Hypothyroidism

Other causes of borderline hypothyroidism include mild thyroid failure due to thyroid surgery, previous radio iodine therapy and external radiation therapy as well as temporary subclinical hypothyroidism after pregnancy or silent and subacute thyroiditis. 

Other Patterns of Hypothyroidism

The symptoms experienced by the patients are caused by factors involved in five other patterns of Hypothyroidism described in Dr. Kharrazian’s book, “Why Do I Still Have Thyroid Symptoms? When My Lab Tests Are Normal”. None of which improve by thyroid drugs or supplements. The following bullet points introduces the patterns and their primary causes: 

  • Hypothalamic – Pituitary – Thyroid Axis (Hypothyroidism Secondary to Pituitary Hypofunction) )(page 78)
    • Primary Cause
      • Pituitary gland fatigue
      • Active Stress Response
      • Ischemic Penumbrae of Parasympathetic Withdrawal
        • Decreased blood flow to Hypothalamus, Pituitary and Brain
        • Hormones traveling through the blood stream needed for production of Thyroid Stimulating Hormone (TSH) never get to the pituitary 
    • Secondary Symptoms
      • Symptoms of Low Thyroid
  • Thyroid Hormone Underconversion (page 81)
    • Primary Cause
      • Oxidative stress
      • Inflammation in the body
      • Immune reactions
      • Detoxification processes
    • Secondary Symptoms
      • Symptoms of Low Thyroid
  • Thyroid Hormone Overconversion (page 82)
    • Primary Cause
      • Insulin resistance
      • Polycystic Ovarian Syndrome (PCOS)
      • Low DHEA
      • Increased androgens
      • Increased Testosterone
    • Secondary Symptoms
      • Fatigue
      • Weight gain
      • Hair loss
      • Symptoms of Low Thyroid
  • Thyroid Hormone Binding Elevation (page 83)
    • Primary Cause
      • Birth Control
      • Oral Contraceptives
      • Hormone Replacement Therapy
    • Secondary Symptoms
      • Symptoms of Low Thyroid
  • Thyroid Resistance (page 84)
    • Primary Cause
      • Elevations in cortisol
      • HPA axis
      • Adrenal Uncoupling
    • Secondary Symptoms
      • Symptoms of Low Thyroid

No part of the body can be understood separate from the whole. Patients experience varicose veins or hemorrhoids, inflammation, blood sugar imbalances, stress in their lives and may have used birth control or hormone replacement throughout their lives. Never once thinking that these Patterns of Hypothyroidism may be may be the cause of their symptoms as they are trained to associate everything with low thyroid.

If these condition remain untreated and unchanged, within a few years in some patients, overt hypothyroidism develops, with low free T4 levels as well as a raised TSH level. Thus becoming a “real” Thyroid problem. Unfortunately, for most they will have been prescribed Thyroid medications for years because no one bother to consider any other factors. Thus, creating an Iatrogenic Thyroid problem. 

For most, these patients may have never had a thyroid problem to begin with. Their “Low Thyroid” symptoms were caused by one or more of the five other patterns of Hypothyroidism described in Dr. Kharrazian’s book, “Why Do I Still Have Thyroid Symptoms? When My Lab Tests Are Normal”. Which are not true thyroid problems.

Immune Suppression

Too often, inflammation and immune response are suppressed with NSAIDS or Hydrocortisone drugs. The immune system becomes unregulated. This leads to the likelihood that Hashimoto’s will develop and detectable antithyroid antibodies will show up in lab tests. Thyroid Antibodies

Studies have shown that thyroid antibodies can be detected in 80% of patients with borderline hypothyroidism. Autoimmune thyroid disease or Hashimoto’s is the most common cause of elevated TSH. The majority of patients with subclinical hypothyroidism have THS lower than 10 mIU/L. 

SERUM LIPIDS

Patients with subclinical hypothyroidism sometimes have subtle hypothyroid symptoms and may have mild abnormalities of serum lipoproteins and blood sugar, which are indicators for insulin resistance. Only patients with definite and persistent TSH elevation should be considered for thyroid treatment. 

In patients with full-blown hypothyroidism, serum levels of triglycerides, total cholesterol and low-density lipoprotein (LDL) cholesterol are elevated. In patients with subclinical hypothyroidism, not surprisingly, the same changes are present but are less marked and less consistent. This pattern of lipid abnormalities, of course, is important because it is a risk factor for atherosclerotic cardiovascular disease.

Coincidently, the same elevation of serum levels of triglycerides, total cholesterol and low-density lipoprotein (LDL) cholesterol occurs. 

CARDIAC FUNCTION

In several studies, a sensitive measure of myocardial contractility, the ratio of pre-ejection period to left ventricular ejection time (PEP:LVET) was shown to improve significantly in patients with subclinical hypothyroidism who were treated with levothyroxine, compared with patients who were treated with placebo.

Should We Treat Subclinical Hypothyroidism?

Indications for treatment in subclinical hypothyroidism are not established, but general guidelines can be offered. Also, patients who complain of fatigue, dry skin, constipation, muscle cramps or other common symptoms of hypothyroidism may possibly benefit from treatment of the five Patterns of Hypothyroidism, even if their TSH level is elevated.

The presence of symptoms that might be related to mild hypothyroidism also increases the potential benefit of treatment. However, these same symptoms may be related to one or more of the five Patterns of Hypothyroidism in the Kharrazian book, which are not truly a thyroid problem. In these five Patterns of Hypothyroidism, treatment is directed towards the underlying cause, which is not the thyroid

Treatment of Subclinical Hypothyroidism

Treatment is similar to that recommended in patients with overt hypothyroidism. But first and foremost, make sure it is hypothyroidism. As you can see from the Table 1, multiple issues can cause symptoms associated with hypothyroidism. 

Risk of harm to the patient by treating only the thyroid, against the potential benefits of supporting the Pattern of Hypothyroidism must be balanced. Clinical experience and success is the only way to determine which approach works. If the patient responds with treatment of the non-thyroid Patterns of Hypothyroidism, there is no reason to treat the thyroid.

Follow the Money!!!

But as they say – Follow The Money. Twenty, Thirty or more years on thyroid supplements or drugs is financially profitable. People are well trained to expect to be on supplements and drugs for a lifetime. Why let them think anything else. It is not only hypothyroidism, but insulin resistance would fall into this category. They call it “Pre-Diabetes” preparing you for the inevitable lifetime of drugs. It takes a little longer to get there but with all the “co-morbidities” associated with Diabetes. It is good for their business. But not so good for your health and quality of life.

Final Comment

At this point in time, the focus is only on routine laboratory screening for hypothyroidism, but very few will take the time to consider any other possibilities contributing to low thyroid symptoms. 

If you are tired of the status quo. It is time for a change.If you are doing the same thing over and over expecting your health to change.  Ask yourself. Are you ready for a different approach? If you are call today. 530-615-4083

Do You Have An Iatrogenic Thyroid?

Iatrogenic Thyroid conditions are created when every ill a person has is blamed on the thyroid.

While screening patients for thyroid disease, physicians often order labs measuring only thyrotropin-stimulating hormone (TSH) levels in patients. Sometimes labs will show increased thyrotropin-stimulating hormone (TSH) levels in patients whose free thyroxine (T4) levels are not below normal. This state, termed “subclinical hypothyroidism,” is most commonly an early stage of hypothyroidism.

The symptoms experienced by the patients are caused by factors involved in five other patterns of Hypothyroidism described in Dr. Kharrazian’s book, “Why Do I Still Have Thyroid Symptoms? When My Lab Tests Are Normal”. None of which improve by thyroid drugs or supplements. The following bullet points introduces the patterns and their primary causes:

  • Hypothalamic – Pituitary – Thyroid Axis (Hypothyroidism Secondary to Pituitary Hypofunction)
    • Primary Cause
      • Pituitary gland fatigue
      • Active Stress Response
      • Ischemic Penumbrae of Parasympathetic Withdrawal
        • Decreased blood flow to Hypothalamus, Pituitary and Brain
        • Hormones traveling through the blood stream needed for production of Thyroid Stimulating Hormone (TSH) never get to the pituitary
    • Secondary Symptoms
      • Symptoms of Low Thyroid
  • Thyroid Hormone Underconversion
    • Primary Cause
      • Oxidative stress
      • Inflammation in the body
      • Immune reactions
      • Detoxification processes
    • Secondary Symptoms
      • Symptoms of Low Thyroid
  • Thyroid Hormone Overconversion
    • Primary Cause
      • Insulin resistance
      • Polycystic Ovarian Syndrome (PCOS)
      • Low DHEA
      • Increased androgens
      • Increased Testosterone
    • Secondary Symptoms
      • Fatigue
      • Weight gain
      • Hair loss
      • Symptoms of Low Thyroid
  • Thyroid Resistance
    • Primary Cause
      • Elevations in cortisol
      • HPA axis
      • Adrenal Uncoupling
    • Secondary Symptoms
      • Symptoms of Low Thyroid
  • Thyroid Hormone Binding Elevation
    • Primary Cause
      • Birth Control
      • Oral Contraceptives
      • Hormone Replacement Therapy
    • Secondary Symptoms
      • Symptoms of Low Thyroid

No part of the body can be understood separate from the whole. Patient experience varicose veins or hemorrhoids, inflammation, blood sugar imbalances, stress in their lives and are using birth control throughout their life. Never once thinking that these may be may be the cause of symptoms they are trained to associate with the low thyroid.

If these condition remain untreated and unchanged, within a few years in some patients, overt hypothyroidism develops, with low free T4 levels as well as a raised TSH level. Thus becoming a “real” Thyroid problem. Unfortunately, for most they will have been prescribed Thyroid medications for years because no one bother to consider any other factors. Thus, creating an Iatrogenic Thyroid.

Alternative and Functional Medicine Iatrogenesis

Unfortunately, Alternative and Functional not exempt from creating iatrogenic problems for their patients. Hundreds of Alternative and Functional Doctors, Nutritionists and Herbalists have attended the Mastering the Thyroid class. Yet, they have failed to incorporate the course material.

Alternative and Functional Medicine Doctors are not exempt from creating Iatrogenic problems for their patients.

Patients have read Thyroid Self-help books come into their offices demanding to be treated for Hypothyroid symptoms. Too often after failing to respond to Hypothyroid drugs and/or supplements from previous Doctors. What is the definition of insanity? Doing the same thing over and over expecting the results to change. Like somehow, supplements from a different supplement company are going to miraculously work this time.

Are the Alternative and Functional Medicine Doctors capable of understanding the five Patterns of Hypothyroidism. Absolutely! Yet Professional and Social Media peer pressure keeps them from acting independently.

 

How easy would it be to follow the information. Dr. Kharrazian lays it all out in his book. Alas, his focus is on the brain and is not able to recognize the factors that cause the five Patterns of Hypothyroidism and neither are those following him.

If you are doing the same thing over and over expecting your health to change.  Ask yourself. Are you ready for a different approach? If you are call today. 530-615-4083

 

Using Thermography to Identify Thyroid Dysfunction

Over the years at our clinic, we have seen images of women with thyroid or Hashimoto’s using infrared thermography for breast health, in lieu of mammograms.

In almost all of the cases cases, we have clearly seen cases of inflammation in the dental area using this heat sensing technology. In all of those cases, a heat signature can be seen running from the area of oral infection down to the thyroid area.

Many of these cases are caused by a low-grade infection and inflammation and have, through further testing, been attributed to dental or oral issues, such as issues related to root-canal treated teeth. Invariably, some cases are very subtle, even asymptomatic for many years, but these cases slowly and continuously affect peoples’ health.

And she is mad at me because she spent $14,000 getting her amalgams removed.

With thermographic imaging, we can identify areas of suspected inflammation and infection because they present with heat. Once an area of concern is identified, it needs further investigation and resolution. People living with a chronic source of infection and inflammation will eventually find that their immunity is affected. This is because once the oral bacteria leave the mouth, they become invasive species and keystone pathogens.

In some cases, this chronic inflammation and invasive infection will actually promote the dysfunction of other organs in the body. Numerous studies have linked vaginosis (chronic yeast infections), miscarriages, pre-term birth, and gastrointestinal symptoms are linked to invasive oral bacteria.

The natural defense mechanism to fight development of organ dysfunction is impaired since their immune system is busy dealing with inflammation that has no chance of resolving on its own. In addition to this, the symptoms are far away from the mouth and people are using supplements or treatment for where the symptoms are occurring. The only way this problem can be resolved is by identifying and removing the cause. The infected area has to be properly dealt with before the body can be restored to health.

Conclusion

The IR imaging procedure provided enormous information about the physiological processes through examining the temperature of the body that can be related to the internal process of inflammation or irritation. The early signs provided by the IR imaging can be used as a prognostic indicator in detecting inflammation and subclinical pathology. The merits of a non-invasive IR imaging modality are important in identifying early stages of inflammation not visible by other imaging modalities. There is a high confirmation rate of ninety (90%) percent indicating strong correlation between thermographic and dental exams.

Oral Bacteria Damage the Thyroid

Those suffering from thyroid conditions may experience recurrent gum bleeding, easy bruising, and chronic fatigue. Hypothyroid patients have capillary blood supply alterations in gum tissues. Those suffering from thyroid issues also have enhanced periodontal bone loss as tooth-supporting alveolar bone is less sensitive to hormonal signals.

Oral Bacteria Damage the Thyroid

Oral Periogenic bacteria can cross into the blood stream through the bleeding gums causing a systemic inflammatory infection. The tissue of the gums can also become infected. This allows periodontal bacteria to enter into the blood stream, which translocate to organs of high metabolic activity, i.e. the Thyroid.

And she is mad at me because she spent $14,000 getting her amalgams removed.

If an oral bacterial infection is not able to establish drainage through the skin surface or into the oral cavity, it may spread diffusely through the neck’s soft tissue. Once the infection descends into the neck, it may reach the thyroid gland. The spread of the oral infection to the thyroid can cause thyrotoxic symptoms: temperature changes, pale skin, excessive sweating, tremors, tiredness, rapid heart beat. The swelling of the thyroid gland can cause trouble swallowing and speaking. Dental treatment would be required to stop the infectious drainage to the thyroid.

Oral bacteria causing infections in gum tissue may threaten more than your teeth and gums. Research has established associations between oral bacteria and systemic diseases including:

  • Chronic Inflammation
  • Autoimmune Diseases
  • Thyroid issues
  • Hair loss
  • Gastrointestinal disease
  • Degenerative Disc disease
  • Arthritis and Joint Pain
  • Type 2 Diabetes
  •  Heart Disease
  • Respiratory Disease
  • Blood Clots
  • Strokes
  • Preterm and Low Birth Weight Babies
  • Miscarriage
  • And many more.

The theories linking oral bacteria to other diseases explain that the mouth may be a portal for bacteria to spread to the rest of your body. These theories have been confirmed through the use of microbial DNA testing with an added wrinkle. There are more than just acid loving-cavity causing bacteria in the mouth.

Multiple Conditions – One Body

You are allowed to have more than one dysfunction occurring in your body at the same time. Too many Professional and Social Media Influencers promoting their version of low thyroid or Hashimoto’s make everything a result of thyroid dysfunction. In fact, some of the diseases occurring in the body, i.e. oral bacteria periodontitis contribute to thyroid symptoms.

Patients with long standing hypothyroidism may have increased subcutaneous mucopolysaccharides due to decrease in the degradation of these substances. The presence of excess subcutaneous mucopolysaccharides may decrease the ability of small blood vessels to constrict when damaged or cut and may result in increased bleeding from infiltrated tissues, including mucosa and skin.

Patients suffering from Hypothyroidism also have poor gingival microcirculation with a reduction in the diameter of capillaries, as well as a greater number and tortuosity of capillary loops.

The successful management of periodontal conditions is beneficial for the successful treatment of thyroid conditions. The length of time from periodontal disease onset to treatment of thyroid disorders may be critical, since uncontrolled periodontal disease resulting in destruction of the specialized tissues that both surround and support the teeth, maintaining them in the maxillary and mandibular bones.

After removal of thyroid due to cancer, a oral bacterial infection is seen by thermography. Radiating from the mouth to the thyroid area and into the gut. The micro-IDent and Metametrix GFP 2100 confirm the species of bacteria involved.
After removal of thyroid due to cancer, a oral bacterial infection is seen by thermography. Radiating from the mouth to the thyroid area and into the gut. The micro-IDent and Genova GIFX confirm the species of bacteria involved.

Oral Bacteria Translocation

Flossing, brushing or especially dental scaling can easily create bleeding. Many dentists claim this is normal and insignificant in terms of regular dentistry. If you experience oral bleeding you should be concerned, especially if you are suffering from an autoimmune condition. This opens a two-way street for blood to escape, and for bacteria to enter the blood stream. The blood stream provides access to all of the organs and tissues of the body while the bacteria (influenced by chemotaxis) looks for lodging.

Biting something hard like almonds, raw crunchy veggies or any hard food flushes these bacteria – if present – to the gingival crevice where they are liberated into the lymphatic drainage or into the blood circulation when chewing food or gum.If an infection is not able to establish drainage through the skin surface or into the oral cavity, it may spread diffusely through fascial planes of the neck’s soft tissue. Once the infection descends into the submandibular space, it may extend to the lateral pharyngeal space, and then to the retro-pharyngeal space. From here, it may reach the thyroid gland.

Dirt Tooth Powder

The damage caused to the gland results in the release of a conspicuous quantity of thyroid hormones, thus causing a thyrotoxic pattern: temperature, cutaneous pallor, excessive perspiration, tremor, tiredness, weight loss, increased appetite, and tachycardia.

Additionally, the thyroid gland’s edema caused difficulty swallowing (dysphagia) and speaking (dysphonia) commonly seen with thyroid gland enlargement. After dental treatment consisting of ultrasonic scaling, PerioProtect and appropriate anti-inflammatory and antibiotic therapy determined by dental PCR testing, administration of oral beta-blockers and corticosteroid therapy may be performed to counteract thyrotoxicosis in order to prevent recurrences. A root canal may be necessary, once the thyrotoxicosis had been resolved.

Simply using nutritional support for the thyroid will have no impact on oral bacteria induced damage to the thyroid. Call 530-615-4083 for more information.

What are the Effect of Dietary Lectins on Thyroid TSH Receptors

Lectins can attach themselves to Thyroid Stimulating Hormone (TSH) receptor sites and play havoc in two ways. The first is that the Lectins are able to “fit” the receptor sufficiently enough to stimulate the thyroid but the effects are different in those with hyperthyroid or Autoimmune Hyperthyroid and low thyroid or Hashimoto thyroiditis. The second effect is that the immune response to the lectin stimulation starts an autoimmune response to the thyroid stimulating hormone (TSH) receptorson the thyroid.

I want the Lectin eBookAutoimmune Diet Lectin Avoidance Guidelines
This 38 year old woman experience significant changes in her health by going on a Lectin Free Diet. The diet didn't stop the Cytokine Storms but significantly reduced their frequency.
I am 38 years old and throughout my life I have been to countless numbers of doctors dealing with digestion issues, parasites, migraines, allergies, blood sugar sensitivities, lack of energy, etc… By January 2013, my health had severely taken its toll, doctors given no explanation and I was barely able to walk by this point.  From what I believe is an absolute miracle, I came across an article from Wellness Alternatives.  I cannot thank you and your staff enough for saving my life and for getting my health back onto the road of recovery.  It has truly been a blessing to having met you.  I am absolutely amazed that through the blood work and quick turnaround analysis you were able to target the problem that I have had for years. Your knowledge,  professionalism and support throughout the past few months that I have met you has been truly inspirational.  I really am most grateful for what you have done for me and our family.
Sincerely, R. K.
Using the results from the Neuroscience Stimulated Cytokine Panel and NeuroEndocrine Comprehensive Panel, a protocol specifically designed for her has further reduced the occurrence of  the Cytokine Storms.

Call today! 530-615-4083

Are Edible Enemies contributing to poor health and inflammation? Lectins cause a plethora of damage to the body, promoting chronic inflammation and sensitivity. Take the Edible Enemy Quiz to test your knowledge on lectins.

Use the Lectin Control Formula to reduce the inflammatory response that occurs due to lectin consumption. Take two capsules with each meal.

Use Registration Code: DP283 to get access to the Doctor's Supplements Store.
I want the Lectin eBookAutoimmune Diet Lectin Avoidance Guidelines

What Are Lectin?

The production of lectins, alkaloids and secondary metabolites are a defense mechanism to protect themselves and their seeds from consumption while the plant is growing and before the seeds are ready for dispersal. For the purposes of this blog the listed secondary metabolites listed below will be referred to as Lectins unless specifically mentioned. Lectins occur naturally in organic and conventionally grown vegetables and fruit. Lectins occur artificially in Genetically Modified and Selectively Bred - organically or conventionally grown vegetables and fruits.

Plants are naturally genetically modified to survive in the primal environment of nature and are artificially genetically modified to survive their trip to the grocery store.

Plant Lectin Regulation of Vegetable & Fruit Consumption

Plants invest energy into the production of seeds. Plants have evolved to encourage vegetable and fruit seed dispersal but also evolved mechanisms to decrease consumption of vegetables and fruits when unripe and from non-seed dispersing predators. To this end, plants have developed physical and chemical deterrents.

Physical deterrents:

  • Cryptic coloration (e.g. green fruits blend in with the plant leaves)
  • Unpalatable textures (e.g. thick skins made of anti-nutritive substances)
  • Resins and saps (e.g. prevent animals from swallowing)
  • Repellent substances, hard outer coats, spines, thorns.

Chemical deterrents 

When immature or out-of-season, the seed, grain, vegetable or fruit are protected by chemical deterrents such as lectins to keep themselves from being eaten to extinction. Chemical deterrents in plants are called secondary metabolites, i.e.trypsin inhibitor, chymotrypsin inhibitor, α-amylase inhibitor, phytohemagluttinin (lectin), phytic acid, oxalic acid, nitrate and nitrite, L-mimosine, canavanine, L-DOPA, glucosinolates, cyanogenic glucosides/cyanogens, tannins, gossypol, chlorogenic acid, saponins, phorbol esters and alkaloids. 

Damage Caused By Lectins:

  • They bind to the thyroid TSH-receptorsacting as long-acting thyroid stimulator (LATS)stimulating the activation of TSH-receptor antibodies.
  • Lectins acting as LATS stimulate overproductionof thyroid hormones in those suffering from Hyperthyroid or Graves disease.
  • Lectins acting as LATS block productionof thyroid hormones in those suffering from low thyroid or Hashimoto’s thyroiditis.
  • Lectins are toxic to wounded cells and inhibit the natural repair system of the GI tract.
  • Lectins are known to “unlock” (breakthrough) the barrier variables of the GI lining and allow large undigested protein molecules into the bloodstream.
  • Lectins serve as a "Trojan horse" allowing intact or nearly intact foreign proteins to invade our barrier variables (natural gut defenses) and enter behind the lines causing damage well beyond the gut and into the joints, brain and skin of affected individuals provoking cytokine immune responses.
  • They can bind to red blood cells causing the cells to clump together resulting in a form of anemia.
  • They can damage collagen and connective tissues in joints.
  • They are directly related to Rheumatoid Arthritis.
  • They can bind to the stomach lining even when the pH is 3 or less.
  • They stimulate abnormal thickening of the pancreas interfering with exocrine cells production of enzymes and endocrine cells production of insulin.
  • They stimulate abnormal thickening of the lining of the gut.
  • They damage the villi lining the gut.
  • They stimulate the shift the microbial ecology promoting the overgrowth of E. coli.
  • The abnormal thickening of the pancreas and gut lining plus the microbial shift exacts a nutritional penalty on the absorption of nutrition.
  • They can provoke IgG and IgM antibodies causing Type 2 Hypersensitivity immune responses.
  • They provoke a direct cytokine driven immune response causing cytokine storms, invisible illness symptoms and cytokine-induced sickness behavior.

Effects of Dietary Lectins on the Thyroid

Lectins can attach themselves to a thyroid receptor site and play havoc in two ways. The first is that the Lectins are able to "fit" the receptor sufficiently enough to stimulate the thyroid but not enough fit sufficiently to produce thyroid hormones. The second effect is that the immune response to the lectin stimulation starts an autoimmune response to the thyroid.

Concerned about your Thyroid?

Thyroid stimulating hormone (TSH) at various concentrations significantly increased the response of lymphocytes to both lectins found in legumes and in other vegetables and fruit. Lectins may cause the activation of ‘long-acting thyroid stimulator (LATS)’also known as thyroid stimulating immunoglobulins, or TSI, in the blood.  TSI or LATS are antibodies that bind to special receptors on the thyroid gland than normally bind to thyroid stimulating hormone (TSH). TSH is the hormone that stimulates the thyroid gland to secrete thyroid hormones.  TSIs mimic the effect of TSH, thereby causing the thyroid to secrete excessthyroid hormone. LATS mimic the effect of TSH only stimulating the thyroid but not producing any thyroid hormones.

Lectins act as Long-Acting Thyroid Stimulators (LATS) and cause the activation of Thyroid Stimulating Hormone Receptor Antibodies (TSH-R Ab). These LATS appear to act similarly to TSH after attaching to the TSH receptor. The LATS are able to "fit" the receptor sufficiently well to stimulate the thyroid while blocking the production of thyroid hormones. This activates the immune system to produce TSH-R Ab to the thyroid stimulating hormone receptors. TSH-R Ab Autoantibodies act as thyroid stimulator agonist in autoimmune hyperthyroid (Graves disease) mimicking the effects of TSH and causes the overproduction of thyroid hormones with hyperthyroid symptoms. TSH-R Ab act as TSH antagonist in autoimmune hypothyroidism (Hashimoto thyroiditis) causing an inverse reaction blocking the production of thyroid hormones making it seem as if the individual is suffering from a low thyroid.

For those with low thyroid, their TSH levels will be low but the thyroid is being stimulated resulting in swelling, tenderness and irritation to the thyroid. Those who have Hashimoto’s, hyperthyroid or Grave’s disease the TSH-R antibody will stimulate the production of TPO antibodies resulting in an immune attack on the thyroid causing further destruction. This is often the case for those with elevated TPO antibodies who are doing all the right things but still have high TPO Ab.

Lectin excited T cells, which produce immunoglobulin excited thyroid function, causing hyperthyroidism. Although pituitary TSH release is suppressed, thyroid-stimulating antibodies not subject to negative feedback maintain the hyperthyroidism. These antibodies appear to act similarly to TSH and via the TSH receptor.

Lectin Exposure  Symptoms

Symptoms could be obvious, such as gas, bloating, diarrhea, or constipation (or both, alternating). Less obvious food related symptoms may include headache, fatigue, 'indigestion,’ skin problems including hives, psoriasis, acne, swollen joints, or water retention. While some symptoms will resolve quickly after eliminating an offending family, other symptoms may take 6-12 months. Be patient. If you are genetically intolerant, you will never be able to consume that group of foods safely.

Some symptoms may occur chronically and may seem unrelated to a gut/food or lectin intolerance reactions. This group of symptoms includes the so-called degenerative diseases and autoimmune diseases like those mentioned in the list at the beginning of this report including ‘Invisible Illness,’ Cytokine-Induced Sickness Behavior, atherosclerosis, hypertension, osteoporosis, senile dementia, osteoarthritis and Rheumatoid Arthritis, inflammatory joint diseases, fibromyalgia, chronic fatigue, and adult onset diabetes. Obesity has been associated with consumption of 'edible enemy' lectins.

Are Edible Enemies contributing to poor health and inflammation? Lectins cause a plethora of damage to the body, promoting chronic inflammation and sensitivity. Take the Edible Enemy Quiz to test your knowledge on lectins.

Use the Lectin Control Formula to reduce the inflammatory response that occurs due to lectin consumption. Take two capsules with each meal.

I want the Lectin eBookAutoimmune Diet Lectin Avoidance Guidelines
Use Registration Code: DP283 to get access to the Doctor's Supplements Store.

Lectin Toxicity Evades Antibody-Based Blood Tests

The type of harm lectins do is harder to diagnose than in classically defined food allergies or sensitivities. In other words, confirmation of intolerance will not be found in IgA, IgG, IgE antibody, allergy or intestinal biopsy testing because the damage done is a direct cytokine driven response, and not necessarily immune-medicated or only secondarily so. Intestinal biopsy testing may be suspect because lectins cause a thickening of the intestinal lining. The medical community is looking for thinning and damage to the intestinal lining.

The diagnostic “invisibility” is why lectin consumption is rarely linked to the ailments that afflict those who consume them. While lectins are not the sole or primary cause of a wide range of disorders, them are a major factor in sustaining or reinforcing injuries or diseases once they are initiated and/or established in the body. This response will deplete your anti-inflammatory cytokines and inhibitory neurotransmitters. Many will suffer cytokine storms during flair-ups. Some will develop into an invisible illness known as Cytokine-Induce Sickness Behavior.

Once lectins make it through a compromised mucosa and/or digestive lining. It can exert systemic effects which can easily become overlooked as being caused by eating legumes, fruits or vegetables. The best tests to determine how lectins are affecting your cytokine immune status and neurotransmitter levels are the:

  • Neuroscience Stimulated Cytokine Analysis Comprehensive
  • Neuroscience NeuroEndocrine Comprehensive
Base: General Overall Immune Response
PHA (Lectin): Immune Response when exposed to Lectins
LPS (Bacteria): Immune Response when exposed to Bacteria
Blue: Immune Suppressed or Immunocompromised
Red: Immune Activated or Stimulation

Four Different Hashimoto Patients - Four Different Immune Responses

All had bad reactions with the Th1/TH2 challenge. Why? All suffered a lectin driven immune response. All have an overactive Th17 immune response. Three have a suppressed TH1 response. One has a suppressed TH2 response. The upper right is immunocompromised. The lower right is immune stimulated to everything. The lower left is a raw vegan over-consuming Soft and Hard Lectins. The upper left TH1 immune system collapses when exposed to bacteria driving straight into TH17.

Systemic Effect of Lectins 

Lectins may influence absorption, metabolism and systemic availability of nutrition by two different but possibly simultaneous mechanisms.

Lectins can indirectly influence hormones (the endocrine system of the body) by binding to the neuroendocrine cells of the gut and as a consequence of this input, release message molecules (hormones) to the blood. Alternatively, lectins can pass through the gut wall into the blood circulation and thus may directly influence peripheral tissues and body metabolism by mimicking the effects of endocrine hormones. The organs most often affected are the pancreas, skeletal muscle, liver, kidneys and thymus.

Thymus, spleen and other organs: Overconsumption of Soft Lectins causes the thymus and spleen to begin decreasing in size wasting away. Some of these are irreversible with potentially serious consequences for the immune system, especially T cell-mediated immunity.

Effects of Dietary Lectins on Inflammatory Cytokines

Cytokines are several different types of substances that are produced by cells within the immune system. These substances relay signals between the immune system cells. By relaying messages between the cells, these cytokines help to trigger the immune system’s response to whatever threat is present.

Lectins strikingly increase levels of multiple pro-inflammatory cytokines (especially interleukin 2 receptor (IL-2), tumor necrosis factor alpha (TNF-α), IL-6, IL-8).

Cytokines, (mediators of acute inflammation) are generated to induce cell breakdown and death. Cytokines can produce an inflammatory response to food independent of the allergic reaction that most are familiar with.  Food allergy or cross-reactive testing will not detect a cytokine induced inflammatory response to food. This requires specialized testing done with the NEI Stimulated Cytokine panel that measures these cytokine and chemokines.

A phenomenon involving the function of inflammatory cytokines is known as a cytokine storm. Essentially, this is a situation where the balance of communication between immune cells and the cytokines present is interrupted.

When the inflammatory cytokines are involved in some sort of storm situation, there is a loopback created between both types of cytokines and the immune cells. The pro-inflammatory cytokines go wild – like college students on Spring Break. There are several common signs that indicate that a storm is present, including fever, body aches and nausea, along with stronger symptoms that are related directly to the ailment itself. Similar to how the college student feels after a week long binge that does not wear off.

Immune Supportive Supplements

A person is said to be immunocompromised when their immune system is incapable of working at full capacity. The immune system is how the body fights off diseases and protects itself against new infections, so someone who is immunocompromised will usually get sick more often, stay sick longer, and be more vulnerable to different types of infections. They may be more inclined to use supplements to stimulate the immune system. Until they become immune suppressed. Then they rarely get “sick.” Immunosuppressed individuals never feel well and start developing symptoms associated with Cytokine Induced Sickness Behavior (CISB).

Information from secondary sources suggests that supplementing with immune stimulating supplements, i.e. thymus gland extracts, have been shown to enhance responsiveness to Lectins and have been able to produce an cytokine storm in immunocompromised patients.

Lectins: Edible Enemies

Being realistic regarding diet is that there is always a sliding scale of lesser evils that we exchange for the experience of enjoying our foods and obtaining the comfort they provide. Because some food toxins cannot be removed from foods and other may be created during processing or cooking, consumption of small quantities of food toxins is unavoidable.

How problematic or reactive lectins are for you depends upon the health of your gastrointestinal lining, the behavior of your microflora and your immune status. If you have a Ghetto Gutwhere the gut lining is impaired, the microbes are misbehaving, and your ability to produce digestive chemistry is less than optimal. Any food you commonly eat will provoke a reaction including organic foods. This combination of factors will change your immune status depleting the inhibitory neurotransmitters and anti-inflammatory cytokines necessary to control the Neuro-Endo-Immune Super-system. When it comes to the immune response, small insignificant changes in lectin exposure can mean the difference between being reactive or not.

The Autoimmune Diet Lectin Avoidance Guidelines will reduce your exposure to lectins, GMOs. The Seasonal - Four Day Rotation diet will add variety to your diet while reducing your risk of creating food sensitivities.

Your chances of eating your way out of this will be significantly increased by following these guidelines. You will still need help re-regulating your neurotransmitters, cytokines and restoring the sequencing of your digestive tract.

Are Edible Enemies contributing to poor health and inflammation? Lectins cause a plethora of damage to the body, promoting chronic inflammation and sensitivity. Take the Edible Enemy Quiz to test your knowledge on lectins.

Use the Lectin Control Formula to reduce the inflammatory response that occurs due to lectin consumption. Take two capsules with each meal.

I want the Lectin eBookAutoimmune Diet Lectin Avoidance Guidelines
Use Registration Code: DP283 to get access to the Doctor's Supplements Store.