Healthy Beginnings

Hashimoto’s and Graves’ Disease: The X Factor in Thyroid Diagnosis and Treatment

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Last month we discussed the six main patterns of thyroid dysfunction – five of which are very confusing to today’s endocrine world doctors, and which frequently defy a proper diagnosis and treatment. A general discussion of the proper diagnosis and treatment was discussed. This month in completing the “CliffsNotes®” version of thyroid diagnosis and treatment we will discuss the 800-pound gorilla in the room – Hashimoto’s autoimmune thyroid and why, though it is being diagnosed far more frequently in the last 3-5 years, successful treatment seems to remain beyond the grasp of most clinicians.

In the United States, the no. 1 cause of hypothyroidism is Hashimoto’s autoimmune thyroid. It may cause hyperfunction symptoms (heart palpitations, insomnia, anxiety, night sweats, being nervous and emotional, increased pulse at rest) or it may lead to hypofunction (tired/sluggish, feet cold, require excessive sleep, gains weight easily, depression, constipation, thinning eyebrows or hair on scalp, face or genitals, dryness of skin or mental sluggishness). It’s an immune problem first, a thyroid problem second. When the immune attack against the thyroid becomes exaggerated, this condition is then called Hashimoto’s thyroiditis and presents with the thyroid hyperfunction symptoms listed above. This can be confusing to your clinician, as hyperfunction symptoms are mostly considered to be Graves’ disease and when presenting with these symptoms (which can also be mistaken for just being stress-related) Graves’ must certainly be ruled out. Graves’ disease is also an autoimmune condition against the thyroid. The key to differentiate Graves’ from Hashimoto’s is a tissue biopsy, however running antibodies may be useful. In Graves’ disease, thyroid-stimulating antibodies (also known as thyroid-stimulating immunoglobulins or TSI) will be very high. In Hashimoto’s thyroid peroxidase, autoantibodies (TPO) will be the highest with or without TSH or TSI autoantibodies. So, in Hashimoto’s, both antibodies can be high. This is very confusing to many thyroid-based clinicians.

In Hashimoto’s there is not usually an immediate immune response leading to the hyperthyroid symptoms. In most cases of Hashimoto’s there is a slow, gradual attack against the thyroid, eventually leading to loss of enough thyroid cells that the condition presents as primary hypothyroidism (elevated TSH) due to the patient experiencing the previously mentioned hypothyroid symptoms and lab signs (also previously mentioned). Thus, most people who have Hashimoto’s never actually develop intermittent overactive thyroid symptoms. Over time they gradually develop symptoms of low thyroid function and have their TSH measured. Their TSH will usually be found to be elevated and they are typically diagnosed as primary hypothyroid and are placed on thyroid medications. Therefore, the main issue of autoimmunity is not addressed. Instead they are considered managed by having a normalized TSH lab finding from hormone replacement therapy. In a sense, patients are having their TSH managed, not the underlying immune attack that is responsible for the loss of their thyroid tissue and their low thyroid function. In most cases the autoimmune responses are ignored, and over time they lose more thyroid cells and their requirements for hormone replacement continue to rise. Even more important –most individuals with Hashimoto’s eventually do develop hypothyroidism, despite the fact that their TSH is managed with hormone replacement therapy, and they continue to have all of the symptoms of thyroid hypo-function. Indeed, researchers have concluded that a positive correlation between TPO (autoimmune marker) antibody titers and TSH levels in euthyroid (a thyroid whose labs are normal and that is working correctly) suggests that TPO antibodies are a predictor of future thyroid failure in people with normal thyroid function. So all hypothyroid patients should be checked for autoimmunity. Always! Even on their standard yearly checkups.

What’s the solution? Find out if you’re one of the 90 percent of hypothyroid patients who actually have Hashimoto’s as your condition, and then find a doctor who understands this condition and its clinical approach. And what is the clinical approach? The approach is to identify all mechanisms of the immune system that are exacerbating attacks against thyroid tissue and make attempts to modulate its expression. These factors could include gut issues, blood sugar imbalances, gluten sensitivities, other food allergies and more. Much more. And thus, it is beyond the scope of the article to discuss this approach in an in-depth matter at this time.

If you would like further information complete with actual research references on the non-drug approach to this matter you may go to and search for Hashimoto’s. Here you will find several hours of presentations on the specifics on this evaluative and clinical approach. For more information, call Power Health at 775-329-4402.


Risk factors for and prevalence of thyroid disorders in a cross – sectional study among healthy female relatives of patients with autoimmune thyroid disease, Clin Endocrinology (OXR) 2003 Sep, 59 (3) 396-401

Thyroid peroxidase antibodies predict poor metabolic control and need for thyroid treatment in pregnant IDDM women. Diabetes care 1997, Oct 20 (10) 1524-8