Do you have symptoms of low thyroid function but have never been diagnosed with hypothyroidism? 

Some of the most telltale symptoms include the following:

• Low basal body temperature
• Cold extremities
• Feeling cold when others do not
• Unexplained weight gain and/or inability to lose weight
• Slow reflex relaxation phase
• Brittle hair and nails
• Dry elbows and heels
• Thinning of the hair at the temple
• Loss of the outer third of the eyebrows

If you have symptoms of low thyroid function but have not been diagnosed with it, then you might have "hidden hypothyroidism". Hidden hypothyroidism is simply a term I came up with for situations in which a person has hypothyroidism that has not been diagnosed because it "hides" from the methods used by most practitioners to test for hypothyroidism.

If you've ever suspected that you have hypothyroidism, but all of the practitioners that have "tested" you for it have said that everything looked "normal", this article might help to explain why.

When it comes to testing for hypothyroidism, most practitioners make one or more of the following mistakes:

• Relying only on TSH, T3, T4, and thyroid antibodies for diagnosis.
• Using outdated ideas about what levels of TSH could exist along with hypothyroidism.
• Using overly broad ranges of "normal" values for T3 and T4.
• Not looking at ratios between thyroid hormones.

Let's look at why each of these is a mistake.

Mistake #1: Relying only on TSH, T3, T4, and thyroid antibodies for diagnosis

The mainstream medical understanding of thyroid hormone regulation goes something like this:

When thyroid hormone levels are too low, the hypothalamus secretes thyrotropin-releasing hormone (TRH) to stimulate the pituitary gland to secrete thyroid stimulating hormone (TSH) to stimulate the thyroid gland to produce more T3 and T4. However, new research is demonstrating that much more is affecting thyroid signaling than the total amount of thyroid hormones and the regulation of thyroid hormone production by the hypothalamus and pituitary glands (R).

Thyroid hormone transport across cellular membranes plays an important role in intracellular T3 levels in body tissues and in pituitary tissues. And thyroid hormones have their effect inside of cells, not in the bloodstream. So what is most important is thyroid hormone signaling inside of cells.

Reduced T4 and T3 transport into the cells of the body occurs in many conditions, including chronic fatigue syndrome, fibromyalgia, neurodegenerative diseases, migraines, stress, anxiety, depression, bipolar disorder, insulin resistance, diabetes, hyperlipidemia (high cholesterol), chronic dieting, and aging, while the T3 level in the pituitary gland is often unaffected.

Thyroid transporters in the body are very energy-dependent and are therefore affected by low energy production, which is typically due to impairment or dysfunction of mitochondria, the energy-producing organelles in our cells. Mitochondrial impairment or dysfunction is present in many, if not all, health conditions, so low intracellular transport of thyroid hormones can be present in most health conditions.

Meanwhile, the pituitary gland is not vulnerable to these factors because its thyroid hormone transporters are not energy-dependent. The pituitary gland also has thyroid hormone receptors with higher affinity to thyroid hormones than those in other cells of the body. Therefore, the pituitary is able to maintain intracellular T3 levels and thyroid hormone receptor activity while the rest of the body may be experiencing significantly reduced intracellular T3 levels and receptor activity.

The consequence of this is that the pituitary gland may not be stimulated to secrete more TSH despite the presence of tissue hypothyroidism in other parts of the body. This makes TSH and other standard blood tests unreliable markers of the presence or absence of hypothyroidism.

Two additional situations are worth mentioning in which practitioners should not rely upon the hypothalamus-pituitary regulatory system and blood levels of thyroid hormones to portray an accurate picture of thyroid hormone signaling in the body.

First, benzodiazepine medications inhibit T3 uptake into the cells of the body but have no effect on the T3 transport into the pituitary gland. This leads to low thyroid signaling at the level of cell with a normal level of TSH produced by the pituitary gland.

Second, in mold illness inflammatory cytokines can cause dysfunction of the hypothalamus and pituitary glands, reducing their ability to respond to low levels of thyroid hormone by producing TRH and TSH. All other hormones regulated by the hypothalamus-pituitary regulatory system can also be affected, including adrenal hormones, sex hormones, and melatonin.

When practitioners use TSH to diagnose hypothyroidism (some only test TSH), they are relying on regulatory mechanisms to be working in a manner that actually is not occurring in the many conditions listed above.

In addition to the issues described so far, testing only TSH, T3, T4, and thyroid antibodies leaves out reverse T3 (rT3), an inactive thyroid hormone that blocks the action of T3 at receptors.

When the body perceive a stress or resource scarcity, it converts more of the pool of T4 to rT3 instead of T3 in order to put the brakes on metabolism and slow down the rate at which it utilizes fuel and other resources. So rT3 levels rise and T3 levels fall as more T4 gets converted to rT3 instead of T3. The level of T3 might remain int the "normal" range, but now the ratio of rT3 to T3 has increased, thereby reducing the degree of T3 signaling within cells, which leads to symptoms of hypothyroidism due to tissue hypothyroidism.

Mistake #2: Using Outdated TSH Reference Ranges

Until recently in mainstream endocrinology, TSH levels were not considered to be pathologically high unless they were above 10. More recently, endocrinologists started using 4.5 as the threshold for considering TSH high and indicating hypothyroidism. In contrast, in functional medicine it is common to consider TSH high if it is above 2.0, 2.2, or 2.5 and normal if it is below these thresholds.

But this still leaves out the many situations described previously in which regulatory mechanisms are not functioning as expected to increase TSH production. And there are still other causes of "normal" TSH levels in the presence of hypothyroidism.

The bottom line is that TSH is not a reliable marker of hypothyroidism.

Mistake #3: Using Overly Broad Ranges of "Normal" Values for T3 and T4

Lab companies set the range of "normal" values for lab test markers based on a statistical calculation of two "standard deviations" from the mean (average value), which automatically includes 95% of the range of values for that lab test marker.

This means that among the population of people getting lab tests from that lab, it is automatically assumed that 95% are "normal"/healthy and only 5% are unhealthy for that lab test marker (e.g. TSH, T3, T4, etc).

Does anything seem a little bit off about that assumption, the assumption that 95% of the people getting lab tests are perfectly healthy, when in fact most of the population of the United States has one or more chronic health condition?

Although functional medicine practitioners use a narrower "functional" range of "normal" values for markers like T3 and T4, this still leaves out something very important: thyroid hormone ratios. 

Mistake #4: Not Looking at Ratios Between Thyroid Hormones

According to Kent Holtorf, MD, "... the free T3/reverse T3 ratio is the most accurate method to determine cellular thyroid levels in the presence of physiologic stress, illness, depression or obesity." (R)

As mentioned earlier, rT3 blocks the action of T3 at the thyroid receptor. So the less T3 there is and/or the more rT3 there is, the lower the activity of T3 at the receptor. The level of T3 activity at the receptor can be lower than normal even when both T3 and rT3 are in the normal functional range. This would occur if T3 is in the low end of the "normal" range and rT3 is in the high end of the "normal" range. What matters is the ratio because that is what affects how much T3 is able to trigger signaling at the thyroid receptor.

Thyroid System Function and Signaling

We need to be thinking about thyroid system function and signaling, not just the function of the thyroid gland and the levels of thyroid hormones. Thyroid signaling at the level of the cells is affected by hormone ratios, thyroid hormones transport into cells, and thyroid receptor availability versus being blocked by something like rT3 or cytokines. 

Treating Low Thyroid System Function and Signaling

Practitioners should be treating the client, not just lab test results. If a client has symptoms of low thyroid function, a "trial" treatment could be the logical next step. There is little risk, and the response or lack of response to appropriate treatment further helps to determine whether or not there is tissue hypothyroidism. 

This begs the question, "What is 'appropriate' treatment?"

And there is another issue ... "Should hypothyroidism always be treated?"

In some situations, it may be best to not treat low thyroid function/signaling until certain other issues are addressed first. For example, if adrenal hormones and/or sex hormones are low, then increasing thyroid signaling could worsen symptoms associated with low adrenal and sex hormones because increased thyroid signaling increases metabolic rate and increases the rate at which adrenal and sex hormones are cleared. So fatigue might increase. Hot flashes might increase.

On the other hand, adrenal and sex hormone production could be low because thyroid signaling and metabolic rate are low. So it can be challenging to know which move to make ... support thyroid signaling now, or support it later after first supporting adrenal hormone and/or perhaps sex hormone signaling?

When trying to support thyroid system function and thyroid hormone signaling, choosing appropriate treatments depends in part upon whether the problem is related to hypothalamus or pituitary gland signaling, thyroid gland health, autoimmune thyroid disease, gastrointestinal issues, nutrient deficiencies, toxicities, current life stress, past trauma, or other factors.

Ways of supporting thyroid system function and signaling can include ...

• Nervous system regulation (e.g. increasing ventral vagal tone)
• Homeopathic treatments targeting the pituitary gland and/or thyroid gland
• Botanicals that support thyroid gland function, increase thyroid hormone conversion enzymes (e.g. for conversion of T4 to T3), or reduce thyroid autoimmune antibody production
• Pituitary and/or thyroid glandular products
• Thyroid hormones
• Increasing the intake of certain nutrients involved in thyroid hormone production
• Restricting the intake of certain nutrients involved in thyroid hormone production (in the case of Hashimoto's thyroiditis)

Keep in mind that thyroid system function and signaling are influenced by many "upstream" factors, all of which may need to be resolved before thyroid function normalizes. Thyroid issues pretty much never occur in isolation. They are essentially symptoms of other factors that need to be identified and addressed as well.

Thyroid issues are usually related to gastrointestinal conditions, toxicity with heavy metals and other toxicants, chronic infections, and sometimes nutrient deficiencies. Fully resolving a thyroid condition requires a detailed, whole systems analysis, such as the one at the core of the approach that I use to help people recover from many types of health issues.

The system I use is organized into the Bio-Individual Blueprint Roadmap and walkthrough video, which you can download and access here. If you have already downloaded the Roadmap document and watched the walkthrough video and would like to discuss getting support on your health journey, you can schedule a free 15-minute consultation or a free 45-minute Breakthrough Session.