Hashimoto\'s Thyroiditis Lifestyle Interventions for Finding and Treating the Root Cause

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These cells become activated in the presence of extracellular microbes, or
microbes that live outside of our cells such as fungi and some bacteria.


These cells produce IL-17 and IL-23, which are pro-inflammatory cyto-
kines active against Citrobacter, Klebsiella pneumonia, and Candida albi-
cans pathogenic species and can initiate autoimmunity.


IL-17a is pro-inflammatory cytokine and causes direct toxicity to the cells
it encounters. Th17 activation has been implicated in both Hashimoto’s
and Graves’ disease.


T Regulatory Cells


Formerly known as suppressor T cells, T regulatory cells (Tregs) return the
immune system to balance after an infection. They are produced in the thy-
mus and have anti-inflammatory and immunosuppressive actions as well
as promoting the immune tolerance of self. Tregs are associated with the
immunosuppressive cytokines TGF-beta and IL-10. Tregs seem to have an
inverse relationship with Th17 cells, meaning the more Th17 cells present,
the fewer cells will be differentiated into Tregs. A reduction of Treg cells
has been found in autoimmune conditions such as Hashimoto’s, while an
increase has been found in conditions like cancer and chronic infections.
These conditions trick the body into increasing Treg production so the
cancer cells and pathogens can blend in, unnoticed by the immune system.
Mouse models have shown that depletion of Tregs leads to hypothyroidism.


Immune Imbalance


Normally, the immune branches work together to overcome an infec-
tion. A healthy immune system is able to balance among each of these
branches, rapidly shifting the balance to the types of cells needed most
when battling an infection. It can also halt production of the fighter cells
when they are no longer needed. An imbalance of any of these branches
results in autoimmune conditions, or a lack of self-recognition.


Thus an immune “imbalance” has been proposed in most autoimmune
conditions. For example, an increased number of Th1 cells has been as-
sociated with Hashimoto’s, while an increased number of Th2 cells has
been associated with Graves’ disease and asthma.


However, this is not the case for all people affected, and some with
Hashimoto’s may have an overabundance of Th2 cells or not have a clear
predominating pathway.


An overabundance of inflammatory cytokines resulting from the Th1,
Th2, or Th17 system—in relation to insufficient immune suppressive

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