Surks, Goswami and Daniels -- Don't Change the TSH Reference Range
How these researchers could come to such a definitive conclusion that treatment is not warranted for subclinical hypothyroidism is inexplicable, given that in the same journal where their research is published, an article appeared just a few years earlier that demonstrated that treatment of patients with subclinical hypothyroidism could help with cholesterol levels and potentially reduce cardiovascular mortality risk by 31%. ["TSH-controlled L-thyroxine therapy reduces cholesterol levels and clinical symptoms in subclinical hypothyroidism: a double blind, placebo-controlled trial (Basel Thyroid Study)," Journal of Clinical Endocrinology and Metabolism, 2001 Oct;86(10):4860-6]
There is also evidence in the literature that levels above 2.0 during pregnancy can potentially complicate pregnancy, and that upper level normal TSH levels can inhibit fertility. For example, in early 2005, Drs. Casey and colleague wrote in the journal Obstetrics and Gynecology that "Pregnancies in women with subclinical hypothyroidism were 3 times more likely to be complicated by placental abruption."
There is also a Norwegian study just published in the International Journal of Obesity that found that there is a positive association between serum TSH within the normal range and body mass index, and the higher the TSH level, the higher the body mass index and likelihood of overweight or obesity.
These are just a few of the many examples of peer-reviewed literature in respected medical journals that discredit the argument that treatment is not recommended or warranted for subclinical hypothyroidism. The authors also state "The only documented adverse health outcome for individuals with TSH levels between 3.0 and 5.0 is progression to overt hypothyroidism. Levothyroxine treatment would clearly prevent that outcome, but at what price?"
However, it must be asked, why is preventing progression to overt hypothyroidism not a desired health objective, given that overt hypothyroidism most definitely can contribute to obesity, heart disease, depression, infertility, and host of other health problems?
Prevention of disease is a major focus of much of today's medicine, with exercise, diet and medications to prevent heart disease, obesity, stroke, and many other conditions. Some of these preventative approaches, particularly drug therapies, come with some risk factors, but the risks are presented along with benefits, so patients can make an informed choice.
Even if there is a small risk to treatment of subclinical hypothyroidism (and the existence of such a risk is a theory, not a proven fact) then why is this same approach not used for thyroid patients, who could be given the opportunity to prevent overt hypothyroidism, realizing that the prevention also comes with some risk?
Wartofsky and Dickey: The New Range is More Accurate
Drs. Wartofsky and Dickey defend the shift to the new range, with some caveats. They say: "We will probably never have an absolutely cutoff value for TSH distinguishing normal from abnormal, but recognition that the mean of normal TSH values is only between 1.18 and 1.4 mU/liter and that more than 95% of the normal population will have a TSH level less than 2.5 mU/liter clearly imply that anyone with a higher value should be carefully assessed for early thyroid failure."
"...the decision as to whether to initiate a trial of levothyroxine therapy is based more upon the 'art of medicine' at this time than the science."
In their article, they point to some key facts, including:
- In an iodine-sufficient population, the mean TSH is 1.5
- In African-Americans with low incidence of Hashimoto's thyroiditis, the mean TSH is 1.18, which suggests that "this is close to the true normal mean for a normal population"
- When people with positive antithyroid antibodies or family history of autoimmune thyroid disease are excluded from the "reference range" cohort, the normal reference range becomes .4 to 2.5
We are also befuddled by the practice of supporters of the recommendations of the consensus panel [the panel that recommended that the reference range not be changed] who promote a target TSH range of 1.0-1.5 mU/liter in patients already receiving T4 therapy, whereas they refuse to accept TSH levels of 3-10 mU/liter as abnormal in patients not receiving T4 therapy.