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. If you’re thinking you’re showing signs of periodontal disease and worry about your oral hygiene, depending where you’re located you may want to book an emergency dentist London.

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, there’s then no wonder as to why it would be important to wear protective gear such as an N95 Mask should you be exposed to any number of harmful chemicals or bacteria in your daily life. 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. DNA testing can help greatly in diagnosing conditions or predicting a potential future risk of something. There are DNA and Drug Testing Clinics Nationwide – Health Street for people to attend to check on anything they are worried about or want to check on.

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. 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.

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.

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.

Iodine and the Thyroid: Part 2 Iodine vs. Antibody Testing

In the post: Iodine and the Thyroid: Part 1, I stated that the proponents of iodine will quote studies supporting iodine use but start stammering and yammering like they have a swollen tongue (probably due to their iodine deficiency) when asked about the studies reporting autoimmune thyroid caused by iodine.

This post attracted responses by iodine proponents validating the point of my blog. Iodine proponents never mention any link between iodine and autoimmune thyroid or do any lab testing looking for autoimmune thyroid induced by iodine supplementation.

Concerned about your Health?
Iodine toxicity questions- Call today! 530-615-4083

Ironically the source of this response, a Laboratory Associate from a well-known lab could not have known that a patient brought in Iodine level reports from this lab last week. The lab results provided by this lab are good. I use them every time a patient brings them but I will not use their treatment recommendations for reasons you will see below.

“Hello Dr Peterson, 

I just finished reading your blog post about iodine and I have a couple of questions. 

First, my iodine related background. 

  • Developed an iodine test in dried urine that is now in production and used to detect dietary iodine deficiency.
  • Read through over 600 complete publications on iodine, the thyroid, and halides
  • Aware of both sides of the iodine supplementation argument (high and low dose)
  • Constantly following iodine blogs, forums, twitter etc.
  • Talked with many doctors, over the phone and at conferences, about their experience with iodine supplementation
  • Recently published a paper on Japanese iodine intake and the health of the Japanese people 
  • Completed a study on the iodine-loading test to determine why so many individuals fail and how a 50mg dose is excreted
  • Investigated whether iodine or other halides cause the side effects seen in those who take large amounts of iodine 

As I read through your blog post, I picked up that you were against high dosing of iodine, yet you mention supplementing with proper amounts when needed. 

For both an “iodine sufficient” (in this case, at least 150ug/day) and an “iodine deficient” individual, what dosing do you recommend? Do you see any benefits from supplementation with iodine or iodide outside of thyroid hormone production?”

I have to admit in Iodine and the Thyroid, I omitted their fall back excuse for recommending iodine – “Ya-but Japanese people eat kelp and kelp has iodine.” As you can read in the proponents email, there is no mention of autoimmunity. But admits to being aware of both sides of iodine supplementation – “high and low dose”. I didn’t see any mention of iodine dosage causing autoimmune thyroid. How do you read “over 600” complete publications and not find any mention of autoimmunity?

I will use the recommendations from this particular lab to answer this question. As you can see below, starting in July 2011 this patient was taking 50 mg of oral iodine/iodide for her “iodine deficiency”. She felt better for the first 30 days but soon after that began experiencing a severe decline in her health. Clumps of hair were falling out; fatigue, depression and when she reported this to her doctor ordered an iodine test. Her levels of iodine were 61,132. The normal range for iodine is 100-1,100 with the optimal being 150-300. If my math is correct that is 203 times the optimal level. When she questioned her iodine levels the doctor refused to take her call.

In addition to the iodine test, a blood test was done which included thyroid antibodies using the AtheNA methodology with ranges different from the microsomal antibody test. The older microsomal antibody test ranges for thyroid peroxidase antibodies are 0 – 34. The AtheNA ranges are a new methodology for measuring Thyroid Antibodies. These include thyroglobulin antibody and thyroid peroxidase antibody, which is a more specific test measuring the active antigen in the older microsomal antibody test.

As you can see this patient with 203 times the recommended levels using the “low dose” iodine supplementation has Thyroglobulin antibody levels of 192. This would be considered positive for Autoimmune Hashimoto’s thyroiditis, based on the strongly positive Thyroglobulin antibodies. This lab assistant and doctor fell into the Green Allopathy mind trap of “If I recommend it – it can do no harm.”

Thyroglobulin and thyroid peroxidase antibodies are most typically associated with Hashimoto’s thyroiditis or Graves’ disease, but can also be found in myxedema, granulomatous thyroiditis, nontoxic nodular goiter, thyroid carcinoma, and rarely in some other conditions.

Since her doctor wouldn’t answer her questions she sought out a different opinion and found my office. Unfortunately this is not an isolated incident. Women and men come into my office with similar stories every week. They feel better initially and then fall apart. Some continue taking iodine because their doctor says it is good for them. While others stop it as this woman did when she could not get the answers she sought.

She started feeling better stopping the iodine but after an autoimmune response is stimulated it can continue for six months or more. The autoimmune attack doesn’t stop but continues with the signs and symptoms less noticeable. Damage to your body is still occurring.

After triaging her case, a protocol was designed to re-regulate her immune system to reduce the autoimmune attack on her body and support restoration of the metabolic processes contributing to her condition.

Autoimmune disease is a serious health condition that should not be taken lightly. I don’t remember being told of the link between iodine and autoimmune thyroid while in school. But once I was told of the link I immediately stopped recommending iodine inappropriately. If your healthcare provider isn’t aware of the connection, you should inform them. If they ignore the connection you have to ask yourself what you want to do. Are you willing to risk your health because they dismiss the connection between iodine supplements and autoimmune thyroid?

If you decide to continue taking iodine, I wish you the best. For those that want to take iodine and work with our office, you will be dismissed as our patient. If you are confused in need of help, we can help answer your questions and develop a program to get you feeling better.

Concerned about your Health?
Iodine toxicity questions- Call today! 530-615-4083

Iodine for the Thyroid?

The debate regarding Iodine for the Thyroid is more polarized than that of Democrats and Republicans within the healthcare community. With each side is very adept at supporting their view with numerous studies, it becomes very confusing as to whether iodine is good or bad. It is interesting to compare how their knowledge and expertise compare to reality.

To see what happens when their recommendations are compared to lab testing. Iodine and the Thyroid: Part 2 Iodine vs. Antibody Testing

My decision is based on two events that occurred in my life. While attending chiropractic college, we were told iodine was necessary for proper thyroid function, therefore use iodine for hypothyroid. As a result of this I recommended the iodine patch test to treat thyroid patients. One woman I made this recommendation to seemed to respond well intitially. I say initially because she returned six months later looking in horrible shape. Eyes protruding, almost bald, 30 pounds heavier complaining of constant fatigue. What happened? I noticed a brown spot on her arm and thought it was an old bruise. She replied, she had just applied her iodine and it had not absorbed in yet. When asked why she had continued the iodine, she said she felt so good on it in the beginning, she decided to stay on it. She had been on the web and self-diagnosed herself with Candida attributing that to her current state of health. I decided then and there to never recommend iodine again until I understood what had happened.

Concerned about your Health?

Iodine toxicity questions

– Call today! 530-615-4083

The second incident involved my own health. At the same time I recommended her use of iodine, I was using progesterone. Why, because a well known book recommended progesterone for men. Shortly after this I attended Dr. Kharrazian’s Functional Endocrinology course. Imagine my horror as he described what happens to those using progesterone inappropriately, which coincidentaly was how I was feeling. In addition to this, he described what occurs with inappropriate use of iodine, with shouting erupting from three doctors saying they have used iodine for 30 years of collective practice and not once had there been any ill effects. After the shouting subsided, Dr. K calmly said he would not debate the issue in that venue and asked them to order TPO antibody tests on all of their patients using iodine. Then next year he would discuss iodine with them. The following year, the three were again sitting together and as Dr. K brought up the iodine topic I turned to view their response. All three were shaking their head in unison agreeing with Dr. K.

“No battle plan survives contact with the enemy”

All nutritional or hormonal theories are based upon optimal body function through the vitalistic view where the nutrient or hormones interact in a perfect environment. Treatment plans for iodine and hormones are made based upon optimal function in a perfect environment. Who among us has optimal body function in a perfect environment, with disease and inflammation as are our enemies?

When your plan meets your enemies in the real world, the real world wins. Nothing goes as planned. Errors pile up. Mistaken suppositions come back to bite you. The most brilliant plan loses touch with reality. However, the reliance on these treatment plans, especially with the incongruence between plan and reality is usually an exercise in self-delusion. When plans meet the real world, it’s not the real world that will yield to your plan. You must adapt whatever you’re doing to the circumstances truly at hand. This is where Functional Medicine shines.

Before the 1920s, iodine deficiency was common in the Great Lakes, Appalachian, and Northwestern U.S. regions and in most of Canada. Treatment of iodine deficiency by the introduction of iodized salt has eliminated the “goiter belt” in these areas. To this day, iodine deficiency is almost none existant with the introduction of iodized salt. But the notion of iodine deficiency carries on today.

Iodine you may know is one of the most important minerals for proper functioning of the thryoid. Iodine is an essential element that enables the thyroid gland to produce thyroid hormones. The plan is then extrapolated by iodine proponents into iodine makes the thyroid work better therefore use iodine supplementation. While in reality, iodine, which is high up on the atomic scale requires near perfect pH for its assimilation into the body. But, the thyroid doesn’t get access to iodine unless the body pH is near perfect in addition to many other factors.

Why Do People Feel Better on Iodine?

If you are hyperthyroid you will feel better through the Wolff-Chaikoff effect. The Wolff-Chaikoff1-8 effect is used to describe hypothyroidism caused by ingestion of a large amount of iodine. Hyperthyroidism is the term for overactive tissue within the thyroid gland causing an overproduction of thyroid hormones (thyroxine or “T4” and/or triiodothyronine or “T3”).

It is an autoregulatory phenomenon which inhibits formation of thyroid hormones inside of the thyroid follicle. This becomes evident secondary to elevated levels of circulating iodide. Wolff-Chaikoff effect lasts several days (around 10 days), after which it is followed by an “escape phenomenon”, which is described by resumption of normal organification of iodine and normal thyroid peroxidase function. High levels of intracellular iodide are known to suppress the transcription of thyroid peroxidase (TPO) enzyme, along with NADPH oxidase. The suppresion of the enzymes that attach iodide to thyroglobulin causes a reduction in the production of the downstream product, thyroxin (T4).

Concerned about your Health? Iodine toxicity questions

– Call today! 530-615-4083

Wolff-Chaikoff is observed in individuals without an obvious thyroid disorder, and especially in patients with autoimmune thyroiditis or those previously treated for thyroid diseases (Graves’ disease, subacute or pospartum thyroiditis, iatrogenic thyroid dysfunction.)

 The hypothyroidism is transient and thyroid function returns to normal in 2 to 3 weeks if  iodine usage is withdrawn, but transient T4 replacement therapy may be required in some patients. The patients who develop transient iodine-induced hypothyroidism must be followed long term thereafter because many will develop permanent primary hypothyroidism. Continued use of iodine supplementation will cause the Jod-Basedow phenomenon to occur.

If you are hypthyroid, iodine usage increases thyroid production of T4. The thyroid gland actively takes up iodine and incorporates iodine into thyroid hormone. This provokes the thyroid into hyperfunction with out any feedback control. Think of it like putting your car in cruise control and never touching the brakes. Long term use of iodine then drives a person into the Jod-Basedow phenomenon AKA Iodine-Induced Thyrotoxicosis.

Jod-Basedow9-19 phenomenon, a thyrotoxic condition caused by exposure to increased amounts of iodine, has historically been reported in regions deficient in iodine. However, when a person is given iodine supplements combined with dietary intake on a continual basis without monitoring, they develop a hyperfunction autoimmune response. It causes an increased activity of TPO antibodies that multiply dramatically with iodine supplements.


In addition to driving a person first into a Wolff-Chaikoff effect, then into a Jod-Basedow phenomenon and eventually into iodine-induced autoimmune disease. The iodine supplementation or the skin patch test will not in any way show a person what their TPO antibodies are and will be different for each person due to different rates of absorption and elimination.


Knowing we don’t have an optimally functioning body in an imperfect environment, the rules for normal don’t apply. The urinary clearance tests are only as good as their liver is able to detoxify. This makes iodine clearance testing suspect.

The proponents of iodine will quote studies supporting iodine use but start stammering and yammering like they have a swollen tongue (probably due to their iodine deficiency) when asked about the studies reporting autoimmune thyroid caused by iodine. I have to question why iodine proponents discredit testing for thyroid antibodies. I think an autoimmune disease takes precedence over an alleged deficiency. To paraphrase the Lay’s Chip ad, “You can’t have just one autoimmunity.” Wouldn’t you want to know?

The other side is not anti-iodine but pro-proper use. There are cases where a person is found to be Primary Hypothyroid through lab testing, where limited supplementation of iodine is recommended. Hashimoto’s disease is the most common cause of hypothyroidism in the United States. 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).

Most people who have Hashimoto’s thyroiditis never actually develop overactive thyroid symptoms. Over time they start to develop the symptoms of low thyroid function and have their TSH measured. Their TSH will usually be found to be high and they are typically diagnosed as primary hypothyroid and placed on thyroid hormone replacement.

The issue of their autoimmune attack is not addressed. Instead, the medical community considers your thyroid condition managed by having a normalized TSH from thyroid hormone replacement. While the alternative and iodine proponents consider it managed by iodine supplementation. At least the medical community is using lab testing.

You decide whether you want someone managing your health were everything is an iodine deficiency or someone who looks for the true underlying cause of your health condition.

Concerned about your Thyroid? Call 530-615-4083 Today

  1. Markou K, Georgopoulos N, Kyriazopoulou V, Vagenakis AG.,  Iodine-Induced hypothyroidism. Thyroid. 2001 May;11(5):501-10.
  2. Lesher JL Jr, Fitch MH, Dunlap DB., Subclinical hypothyroidism during potassium iodide therapy for lymphocutaneous sporotrichosis. Cutis. 1994 Mar;53(3):128-30.
  3. Wémeau JL.,  [Hypothyroidism related to excess iodine], Presse Med. 2002 Oct 26;31(35):1670-5.
  4. Eng PH, Cardona GR, Previti MC, Chin WW, Braverman LE.,  Regulation of the sodium iodide symporter by iodide in FRTL-5 cells. Eur J Endocrinol. 2001 Feb;144(2):139-44.
  5. Alexandrides T, Georgopoulos N, Yarmenitis S, Vagenakis AG., Increased sensitivity to the inhibitory effect of excess iodide on thyroid function in patients with beta-thalassemia major and iron overload and the subsequent development of hypothyroidism. Eur J Endocrinol. 2000 Sep;143(3):319-25.
  6. Bando Y, Ushiogi Y, Okafuji K, Toya D, Tanaka N, Miura S., Non-autoimmune primary hypothyroidism in diabetic and non-diabetic chronic renal dysfunction. Exp Clin Endocrinol Diabetes. 2002 Nov;110(8):408-15.
  7. Frey H. Hypofunction of the Thyroid Gland, due to Prolonged and  Excessive Intake of  Potassium Iodide. Acta Endocrinol (Copenh). 1964 Sep;47:105-20.
  8. Reinhardt W, Luster M, Rudorff KH, Heckmann C, Petrasch S, Lederbogen S, Haase R, Saller B, Reiners C, Reinwein D, Mann K.  Effect of small doses of iodine on thyroid function in patients with Hashimoto’s thyroiditis residing in an area of mild iodine deficiency. Eur J Endocrinol. 1998 Jul;139(1):23-8.
  9. El-Shirbiny AM, Stavrou SS, Dnistrian A, Sonenberg M, Larson SM, Divgi CR. Jod-Basedow syndrome following oral iodine and radioiodinated-antibody administration. J Nucl Med. 1997 Nov;38(11):1816-7. Erratum in: J Nucl Med 1998 Mar;39(3):489.
  10. Navarro FA. [Jod-Basedow phenomenon: who was Dr. Jod?] Rev Clin Esp. 1997 Jul;197(7):531. Spanish.
  11. Goday-Arnó A, García Rico A, Martínez-Riquelme A, Cano-Pérez JF. [Graves Basedow disease following treatment with magistral formulae for obesity. Jod-Basedow phenomenon?] Rev Clin Esp. 1996 Aug;196(8):536-8.
  12. Gómez de la Torre R, Enguix Armada A, García L, Otero J. [Thyroid nodule disease in a previously endemic goiter area] An Med Interna. 1993 Oct;10(10):487-9. Spanish.
  13. Yamada T. [Jod-Basedow (iodine-induced hyperthyroidism)] Ryoikibetsu Shokogun Shirizu. 1993;(1):367-9. Review. Japanese.
  14. Woeber KA. Iodine and thyroid disease. Med Clin North Am. 1991 Jan;75(1):169-78.
  15. Maberly GF, Corcoran JM, Eastman CJ. The effect of iodized oil on goitre size, thyroid function and the development of the Jod Basedow phenomenon. Clin Endocrinol (Oxf). 1982 Sep;17(3):253-9.
  16. Maberly GF, Eastman CJ, Corcoran JM. Effect of iodination of a village water-supply on goitre size and thyroid function. Lancet. 1981 Dec 5;2(8258):1270-2.
  17. Livadas DP, Koutras DA, Souvatzoglou A, Beckers C. The toxic effect of small iodine supplements in patients with autonomous thyroid nodules. Clin Endocrinol (Oxf). 1977 Aug;7(2):121-7.
  18. Birkhäuser M, Burer T, Busset R, Burger A. Diagnosis of hyperthyroidism when serum-thyroxine alone is raised. Lancet. 1977 Jul 9;2(8028):53-6.
  19. Spaulding SW, Burrow GN, Ramey JN, Donabedian RK. Effect of increased iodide intake on thyroid function in subjects on chronic lithium therapy. Acta Endocrinol (Copenh). 1977 Feb;84(2):290-6.

The Link Between Hashimoto’s Thyroiditis and the Herpes Rash?

The link between Hashimoto’s and the Herpes rash is this. If you have any thyroid issue whether it is Hashimoto’s, low thyroid or hyperthyroid. You will have an issue with gluten sensitivity.

Is Your Herpes Break Out Really a Gluten Rash?

Are you suffering from occasional herpes out breaks on areas of your body but not on the genitals? Those with a sensitivity to gluten, often develop blistering rashes that are often mistaken for a herpes outbreak.

A Local Dermatologist told us he is upsetting the GI docs because he is diagnosing gluten sensitivity/celiac more than they are. He is sending patients out to be tested for gluten sensitivity/celiac when he sees these blistering rashes. He says if the fluid from one of these blisters is collected and tested it comes back very frequently positive for gluten sensitivity. However, most these rashes are so itchy, patients scratch and break the blisters before it can be collected.

Call today! 530-615-4083

Are you frustrated because the herpes medication doesn’t seem to control it or provide any relief? A good way to control the outbreaks would be to identify the causes, and take effective measures to ensure that they remain out of your daily life. How was your herpes diagnosed? What if your herpes outbreak wasn’t caused by virus. What then?

Dermatitis herpetiformis (DH), an itchy, stinging, blistering skin rash, occurs when your skin reacts to gluten antibodies circulating in your system. Some people call dermatitis herpetiformis a “gluten rash” or a “celiac disease rash” because it occurs in conjunction with a sensitivity to gluten. Regardless of the presentation or symptoms, a positive diagnosis of DH always indicates that a gluten sensitive enteropathy is occurring.

Antibody Testing

The current dogma is that Immune cells are stimulated by Antibodies. They believe as long as antibodies are present, the antibodies are constantly stimulating an immune response. They also are lead to believe the presence of antibodies are from an ongoing infection. Typically, IgG antibodies are produced in the first phase of immune responses. However, the immune response to IgA, IgG, and IgM declines or is terminated along the course of the disease in most patients. IgM antibodies are indicative of an ongoing immune response., Studies have shown the detection of IgA and IgM antibodies in 62% and 61% of IgG antibodies in autoimmune patients, and after 7 years.,

A resolution of the disease is not associated with a decrease in antibodies. Only those with a short disease duration are likely to experience a decrease in antibodies levels. For most autoimmune patients there is no significant change in antibody levels, However, patients with immune calming/quieting treatment, experienced a 20% decline in their antibody levels. Normalization in the levels of antibodies with treatment intervention occurs in less that 7% of patients. The success of clinical interventions in lowering antibody levels (and thus likely minimizing the pathogenic effects of autoantibody binding) appears to be dependent on disease duration. The association of shorter disease duration with greater declines in antibody levels is highly consistent with the growing body of evidence that shows improved clinical outcomes with earlier disease intervention in autoimmunity.,,

Approximately one-half of patients with Rheumatoid Arthritis had positive IgM-RF and/or antibodies on at least 1 occasion, almost 5 years prior to disease onset. More than 50% of autoimmune patients may have positive antibodies upwards of 13 years after disease resolution, regardless of treatment.

Dermatitis Herpetiformis

Dermatitis herpetiformis (DH) can often be misdiagnosed and frequently confused with skin conditions such as: allergies, bug or mosquito bites, contact dermatitis, diabetic pruritus, eczema, herpes, shingles, hives and psoriasis.

Reddened skin, circular bumps, and blisters filled with clear, neutrophil (white blood cell), containing liquid are very common. Skin lesions and scarring can also appear, particularly in patients that scratch and irritate the skin during outbreaks.

The onset of DH may be acute or gradual, appearing in the same location every time. DH outbreaks are very often mirrored, meaning that the rash will occur on both sides of the body in exactly the same place. The hallmark sign of DH is an intensely itchy, blistering skin rash. For people that seem to suffer more often than not with these outbreaks, trying to use cold sore medicine variations could potentially decrease the itchiness and halt the outbreak before it gets any worse.

DH can appear anywhere on the body; however, It most frequently present in the following areas:

  • Buttocks
  • Elbows
  • Knees
  • Lower back
  • Scalp

Dermatitis herpetiformis sufferers usually experience to rash in the same location every time. The rash might be continuous, or it might come and go.

Before the actual dermatitis herpetiformis breaks out, your skin may itch in that location, or it might feel is if it’s burning. The rash itself usually includes reddened skin plus multiple small, pimple like-bumps which contain a clear liquid.

The dermatitis herpetiformis bumps usually take several days to heal (during which time new bumps usually appear nearby), and once healed, only behind small purple marks that lasts for weeks or months. People with long-standing dermatitis herpetiformis usually have continuously reddened skin where the rash occurs.

As the name implies, dermatitis herpetiformis (DH) looks herpetic and is sometimes mistaken for a herpes virus. Red plaques erupt in groups of blisters, in the resulting intense itch can disturb sleep.

Who does dermatitis herpetiformis affect?

Unlike gluten sensitive enteropathy or celiac disease, which is diagnosed more often in women, dermatitis herpetiformis is more common in men. In fact, some studies show a male-to-female ratio of up to 2-to-1 in dermatitis herpetiformis patients. Men are more likely to have a typical oral or genital lesion.

DH can affect people of all ages but most often appears for the first time between the ages of 15 and 40. People of northern European descent are more likely than those of African or Asian heritage to develop DH.

Dermatitis Herpetiformis is an autoimmune blistering disorder associated with a gluten sensitive enteropathy. People with DH have a condition of the intestinal tract identical to that found in gluten sensitive enteropathy or celiac disease, although gastric symptoms might be absent. Autoimmune processes can be arrested if the interplay between the Neuro-Endo-Immune Supersystem and environmental triggers is prevented by re-establishing intestinal barrier function.

How does a disorder that damages the intestines show up on the skin?

When a person has gluten sensitive enteropathy consumes gluten, the mucosal immune system in the intestines responds by producing a type of antibody called Immunoglobulin A. As IgAs enters the bloodstream, they can collect in small vessels under the skin, triggering further immune reactions that result in the blistering rash of DH.

The first clue that a skin eruption may be DH is that “it itches like crazy.” People are digging at themselves. As a result the blisters are almost always broken open by the time the DH suffer seeks medical help.

The second characteristic sign of DH is its location on the body. Lesions most often appear on the extensor surfaces – the forearms near the elbows, the knees, and the buttocks. The outbreak of the lesions also tends to be bilateral, meaning it appears on both sides of the body.

The grouping of the lesions provides a final clue. Although DH is not caused by a herpes virus, its lesions resemble those of herpes and hence the word herpetiformis. In both conditions, lesions are formed in small groups. Still, DH is often confused with eczema, a common inflammatory skin disorder that, like DH, results in an itchy rash that is often scratched raw.

A gluten sensitive enteropathy is different from celiac disease in that a gluten sensitivity is the result of a microscopic colitis. The damage to the gastrointestinal lining in microscopic colitis is not bad enough for a biopsy or endoscopy to see enough damage to be called celiac disease. Many patients report they have been checked by their doctor and were told their lining was red or irritated. So they did not have a gluten sensitivity because they did not have celiac. Many healthcare providers also assume a person’s immune system is always working at 100% optimal efficiency. When in fact, the immune system is so fatigued from constant exposure to gluten. It cannot create a response in the normal fashion.

Breaking with Bread

A strict gluten – free diet may take weeks to clear up an outbreak. Accidental ingestion of gluten will cause symptoms to recur. Hidden sources of gluten can prolong the outbreak.

For some it will be as easy as maintaining a gluten free lifestyle. Others will require our help in quenching the immunoglobulin reaction, controlling the immune response, restoring the digestive chemistry and repairing the gastrointestinal lining to enable them to maintain themselves through diet and lifestyle.

Call today! 530-615-4083

Melatonin Suppresses Thyroid Hormones

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, it signals to the pituitary, which then signals 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 works against the T3 receptor, so high levels can be detrimental.

Melatonin supplementation inhibits the TSH content in the pituitary. However, Melatonin supplementation blocks the stimulatory effect of TSH on thyroid cells responsible for the production and secretion of thyroid hormones thyroxine (T4) and triiodothyronine (T3).

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, thyroxine (T4) may also decrease. The persistence of a normal or even decreased level of thyrotropin (TSH) in the face of decreased serum thyroid hormone concentrations implies a major change in HPT axis set-point regulation. 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’.

TSH serum levels are lower and those of free T4 are greater at night, when melatonin levels are higher, so that the response of pituitary to hypothalamic TRH and of thyroid to pituitary TSH is influenced by the pineal hormone melatonin, which alters the hypothalamic-pituitary-thyroid (HPT) axis function. Melatonin drives the molecular clockwork in the pituitary.

Melatonin & Thyroid Function

Melatonin has a suppressing action on thyroid function. Both hypothyroid and thyrotoxic patients have disturbed pineal function, which is not the case in those with weight issues. Those with hypothyroidism were found to have higher peak melatonin levels, total nighttime melatonin secretion, and urinary elimination of melatonin than normal individuals. Although thyrotoxic patients released a normal amount of melatonin during the night, their melatonin secretion peak occurs earlier in the night.

The molecular clockwork in the pituitary is strongly dependent on melatonin. Melatonin drives the rhythmic expression of clock genes in the pituitary, and the length of daytime light as well as melatonin supplements are involved in melatonin signaling.

Melatonin plays a role in the regulation of TSH release from the pituitary. Short days and long nights are correlated with decreasing levels of TSH in the pituitary. Moreover, chronic treatment with melatonin suppresses TSH release from the pituitary.

Melatonin has an inhibitory action on the Hypothalamic-pituitary-thyroid (HPT) axis. Long nights result in reduced levels of circulating thyroxin (T4). An active pineal gland produces melatonin, which inhibits thyrotrophin-releasing hormone (TRH) release from the hypothalamus. The effects of melatonin on the Hypothalamic-pituitary-thyroid (HPT) axis are similar to its effects on the Hypothalamic-pituitary-gonadal (HPG) axis.

Melatonin supplementation inhibits the TSH content in the pituitary. However, Melatonin supplementation blocks the stimulatory effect of TSH on thyroid cells responsible for the production and secretion of thyroid hormones thyroxine (T4) and triiodothyronine (T3). Free T3, T4 and TSH levels are lower with melatonin supplementation.

Melatonin is Not Just for Sleep Anymore

While most consider melatonin to be only produced by the pineal gland. It is produced throughout the body in much greater quantity (400x more in the gut). Melatonin is much more involved than previously thought. From enhancing autoimmune flairs during cytokine storms, to playing a role with infertility, melatonin and melatonin supplements used for ‘sleep problems’ enhances these conditions and not in a good way. It even plays a role in hot flashes and night chills.

If you have questions about sleep and you are having thyroid, autoimmune or infertility concerns with your health. Please contact my office.