Early or Subclinical Hypothyroidism

Subclinical hypothyroidism, also called low thyroid or hypothyroidism is diagnosed when thyroid hormone levels are with normal reference range but TSH is mildly elevated. 

If the hypothalamus is getting a poor sampling of thyroid hormones in the blood, messages are sent hormonally in the blood to the pituitary that the thyroid isn’t doing its job. The pituitary will pump out extra TSH, giving the thyroid notice to produce more thyroid hormones. Primary Hypothyroidism is a true thyroid dysfunction and is the only pattern that can be effectively managed through thyroid replacement hormones or short-term dosage of iodine supplementation.  

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.” 

David Peterson, DC
  • Early or Subclinical Hypothyroidism is the only time to use Iodine or Selenium to restore normal Thyroid Function.
    • Primary Hypothyroidism is a thyroid treatable condition.

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. 

Thyroid Underconversion

Thyroid Under-Conversion due to Inflammation

Thyroid Under-Conversion occurs when the cell membranes of the body are damaged due to chronic infection or inflammation. Many fail to recognize inflammation is the result of an immune response. Many more continue to blame only the thyroid.

Inflammation and Immune Response are not separate issues.

Oxidative stress can cause lipid peroxidation. Oxidative stress is a natural byproduct of the use of oxygen by biological systems. It is also caused by various biological processes such as inflammation, immune reactions, and detoxification processes. Unsaturated fatty acids (especially in cell membranes) are very susceptible to damage by oxidative stress. This damage results in lipid peroxidation (literally – ‘fat oxidation’). Antioxidants (especially vitamin E) work to prevent excessive levels of oxidative stress in cell membranes and therefore, help prevent lipid peroxidation. Lipid peroxides can lead to damage to DNA. DNA damage can contribute to the risk of developing various cancers.

If a patient is found in adrenal uncoupling , the enzyme responsible for converting thyroid hormones has been down-regulated for prior exposure to elevated cortisol.

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

Oral Bacteria Translocating to Thyroid

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. These pictures of swollen thyroid gland can show you what the gland looks like when damaged. 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.

Order the MicrobeLink DX Kit

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.

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

Multiple Autoimmune Conditions

Hashimoto’s Autoimmune like all other Autoimmune diseases is not an entity, ghost or poltergeist with the name of the disease that enters your body to cause it harm. Though many treat it as such. All of the Autoimmune disease have ONE thing in common. Your Immune system.

You are expecting Classical and the Immune System is doing Punk Rock.

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

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.

In this pattern, the hypothalamus, which sits in the base of your brain is not getting a good sample of thyroid hormones in the blood. This is likely due to ischemia (decreased blood flow) to the brain. 

In this pattern the pituitary gland, which sits at the base of your brain, is getting inaccurate supply and demand messages from the hypothalamus. Consequently, the pituitary will then send the thyroid erroneous signals about the need to produce more thyroid hormones.

There’s nothing wrong with the thyroid itself, it’s just not being told to get to work! This pattern is associated with a Vasomotor Control imbalance of the blood flow in the body. Blood vessels in the abdomen are dilated resulting in a reduced sampling of hormones by the hypothalamus. Vasomotor Control imbalances can be caused by metabolic conditions, chronic stress levels or chronic bacterial and viral infections.

As you can see, thyroid physiology is complex and unique to the individual. There’s no such thing as a magic pill for everyone, and we need to get a comprehensive diagnosis to gain insight as to why someone is struggling with the symptoms they have. I consult people all over the world via Skype and phone consultations, clinically investigating these underlying factors.

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. If the blood supply to the heart is reduced you risk going into cardiac arrest, for which you would need emergency first aid attention.

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-? release. The cytokines IL-1?, TNF-?, IFN-?, and IL-6 can inhibit the conversion of T4 to T3, thereby shunting T4 towards the production of the potentially detrimental rT3.

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.