Thyroid antibody levels more than halved

I initially saw this client in April 2018. She wanted to work with me to uncover root causes for her chronic eczema which was really quite pronounced on her face, her weight, and to reduce the increasing amount of time she was experiencing hives.

She had been prescribed numerous topical creams for her eczema, all to no avail. After taking a detailed case history, as I do with all new clients, I ran a comprehensive  metabolic blood test - why? 

A comprehensive blood chemistry panel is the single most efficient and effective tool for evaluating your health, it screens for a wide range of conditions including several types of anemia, indications of gut, viral and bacterial infections, insulin resistance and hypoglycemia, liver and kidney issues, and thyroid and adrenal function. Having all these markers run collectively rather than disparately allows me to move forward and identify underlying foundational mechanisms. In this case, her vitamin D was “deficient” and I uncovered a pattern suggestive of Hashimoto's Autoimmune Hypothyroidism. Her TSH was out of range “high” and she had incredibly high Anti-Thyroglobulin antibodies and Antithyroid Peroxidase, as seen here:

And so we got to work…..

I always have to balance supporting the failing “system or gland”, in this case the endocrine system and thyroid as well as the immune system, because it is betraying her.  AND dig deeper to ask the question why? Why is her immune system betraying her. 

A general outline of how Hashimoto’s Autoimmune Hypothyroidism develops, is best explained by an analogy that has been adopted in functional medicine as the ‘The three legged stool of autoimmune disease’.

  1. Genetic predisposition: certain genes make individuals more likely to develop certain diseases.

  2. A trigger: specific antigen, or protein, that the immune system recognises as a threat (real or not), that sets off the cascade of over-activation. In the case of celiac disease, the trigger is gluten. In the vast majority of autoimmune diseases the trigger remains unknown, but in HAH we have some robust published research on some viral and bacterial triggers such as the Epstein Barr Virus and Yersinia Enterocolitica (a gram negative bacteria that is a common cause of human gastroenteritis).

  3. Immune dysregulation and Intestinal permeability (also referred to as ‘leaky gut’): this increased permeability means that the normally tightly-knit cells of the intestines are weakened and ‘leaky’. This allows large compounds, such as proteins from food or bacteria, entry into our bloodstream. The immune system is highly dependent on the health of the intestinal barrier..

If all of these three components lineup, then the scene is set for a perfect storm of an autoimmune fire.

Triggers and root causes

I group triggers or root causes into six areas. Triggers can both cause and/or contribute to the development of symptoms:

  1. Food intolerances or sensitivities - e.g gluten, casein, lactose, histamine, lectins, AGGULINTINS, additives, gums as an example.

  2. HPA dysregulation and adrenal health/impaired ability to handle stress - stress to our biochemistry is: dysregulated blood sugar control, mental and emotional stress, managing an infection, lack of adequate sleep.

  3. Gut Permeability & immune dysregulation.

  4. Nutrient depletions - vitamin D, iron/ferritin, zinc, essential fatty acids, magnesium, B1, B12, B9, and selenium being the most common.

  5. Environmental toxins - such as mercury, pollen etc.

  6. Infections:

    1. ​Viral

    2. Gut ‘infections’: Dysbiosis or SIBO

    3. Stealth (e.g. Lyme)

    4. Bacterial

How do triggers work?

Whenever the immune system recognises a foreign invader, it will form antibodies against it.

Hashimoto’s has been classified as a Type IV hypersensitivity, which is delayed. The damage to the thyroid tissue is NOT antibody mediated, but rather the antibodies “mark” the thyroid cells, and the actual attack is performed by antigen specific cytotoxic T lymphocytes.

Lymphocytes begin to enter the thyroid and begin to destroy it, causing scarring, which leads to a decreased ability to function and produce hormones, resulting in symptoms. Additionally, antibodies can also be formed to thyroglobulin, the protein that is an intermediary in thyroid hormone production. 

In this case, we started working on the following triggers: 

1. Nutrient depletions - repleting vitamin D and also providing selenium which has been shown to help lower thyroid antibodies.

2. Remove foods that may trigger or exacerbate an immune response.

The immune system uses IgA, IgE, IgG, and IgM immunoglobulins to help protect us from the outside world. An IgE antibody reaction can trigger anaphylaxis and is the most well-known cause of “food allergy.” However, you may also have delayed food sensitivities (probably involving IgG antibodies and others), or you may have intolerances to foods which are not immune-mediated, such as antigen complexes.Factors such as nutrition, environmental exposure, medications, low Vitamin A and D and the diversity of the microbiota, can break down the mechanism and predispose the system to IgE and IgG food immune reactivity. Repeated exposure to food “triggers” or antigens through broken barriers (leaky gut) can produce IgG food immune reactions.

Antibody-antigen complexes can accumulate and cause symptoms if one continues to eat a problem food, eventually depositing in organs or tissues. Food sensitivities may also cause chronic inflammation or irritation, preventing healing on other fronts. In this case, I was dealing with skin complaints both in the form of eczema and hives, so my thinking was that food triggers, through broken barriers and loss of tolerance was at play. I didn’t test for IgG antibodies (I use Cyrex testing), I created a food plan that removed higher histamine foods, and provocative proteins such gluten and casein together with high levels of fibre dense foods to support microbiome diversity.

3. ​Increase nutrients that promote optimal immune function, re-establish “tolerance” and better modulate the immune system

There are two primary types of immunity: cellular and humoral. Cellular immunity is our first line of defence against pathogens like viruses and bacteria. It includes immune cells that directly attack and destroy these pathogens, regardless of whether or not the body has seen them before.

Humoral immunity is our second line of defence. It involves immune cells that produce antibodies, which bind to specific pathogens that the body has been exposed to in the past.

In autoimmune disease, there is often an imbalance between the cellular and humoral branches of the immune system. An optimum immune status would be one that is balanced between cellular and humoral immunity.

Specialised populations of T lymphocytes (called regulatory T cells) balance the immune response. They promote tolerance, help to prevent autoimmune diseases, and limit chronic inflammatory diseases such as asthma and inflammatory bowel disease. If regulatory T cells are not doing their job, the immune system can become overactive, which is a hallmark of autoimmune disease. People with autoimmune disease often have low levels of T regulatory cells, and improving T regulatory cell function can improve autoimmune disease. .

Foods and nutrients that support T Reg cells, then support the tolerance necessary for immune homeostasis. Different vitamins do this is different ways: cruciferous vegetables, vitamin A, vitamin D, probiotics, Butyrate all do their positive part, and I integrated all into her bespoke plan. 

4. Better manage the stress response and remove the more antigenic foods, and prescribed a suitable food plan. I also prescribed Antioxidant support to reduce oxidative stress in thyroid gland itself.

At her four month follow up, her skin had improved dramatically and she’d lost a stone in weight.

The next stage of the approach was to work on the gut, and this had a dramatic impact.  Through running a PCR based gut stool test, the GIMAP, a number of LPS “laden” bacteria where uncovered. LPS are large molecules that are found in the outer membrane of Gram-negative bacteria, and elicit strong immune responses. This was interesting to me on two fronts in her case: weight and inflammation.

One of the mechanisms leading to weight gain, with evidence from both mouse models and humans, incorporates both the gut microbiota and inflammatory processes. 

According to this theory, a key feature for initiating weight gain is permeability of the gut barrier, i.e. the layer of cells in the intestine that normally controls which substances can go deeper into the body. But when the barrier is breached, these large molecules found in the outer membranes of certain bacteria, called lipopolysaccharide (LPS for short) get past and start to circulate widely around the body. This causes the immune system to release protein messengers that initiate the cascade of reactions leading to inflammation (known as cytokines). The chronic low-grade inflammation sets off metabolic effects, including disrupted glucose metabolism and fat absorption, and weight gain is the end result.

I have worked with this client for 18 months now, peeling back the multiple layers of triggers in her case. There have been great improvements - she reports huge increase in energy, better sleep, 3 stone in weight loss and no eczema on her face at all. Of course, there have been some set backs, it hasn’t all been plain sailing, but another wonderful result this month was re-testing her thyroid.

Her TSH is down 2 points to nearly within range , but the most impressive improvement is the Anti-Thyroglobulin antibodies, down from 1697 to 401 and Anti-Thyroid Peroxidase, now negative.

September 2019:-

I wanted to share this with my community as an example of how taking a broader view and working to connect the dots can help to better optimise health and facilitate the body to come back to a place of balance. It takes time, and commitment though, this has been 18 months of work!

As always- in health, Tanya x 

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SIBO part 2: Open Wide…..say ahhhh