Cover of Rethinking Hypothyroidism: Why Treatment Must Change and What Patients Can Do on left; headshot of Dr. Antonio Bianco in a black jacket, white shirt, and dark tie on right.
Cover of Rethinking Hypothyroidism; Dr. Antonio C. Bianco Credit: University of Chicago Press/Jean Lachat Photography

My throat was slit. It was back in the dark ages of the 20th century, but if you take a close look at me you can still see the scar—a fine line running along the base of my neck, from ear to ear.  It’s the necklace I can’t take off, the trail of a scalpel.

The cut was made to remove a nodule from my thyroid gland. I later had a long and jerky dance with the brand-name, “gold standard” pill for thyroid deficiency.

So when the glaze-over title Rethinking Hypothyroidism appeared on a list of new books published by University of Chicago Press late last year, it lit up for me.

But you wouldn’t have to have my history to be interested. Everybody’s got a thyroid gland—it’s that butterfly-shaped lump that sits front and center in your neck. And it’s in the driver’s seat, so to speak, controlling the activity of all your other organs. If it malfunctions, you could grow a goiter or morph into something like cretinism; if it stops working totally, you’ll die.

Rethinking Hypothyroidism: Why Treatment Must Change and What Patients Can Do by Antonio C. Bianco, MD, University of Chicago Press, 296 pp., paperback $22/hardcover $99,

Rethinking Hypothyroidism is the work of Antonio C. Bianco, MD, PhD., and professor of medicine at the University of Chicago, where he runs a National Institutes of Health-funded  lab devoted to the study of thyroid hormones, a subject he’s been researching for more than 40 years. A former president of the American Thyroid Association and a consultant to pharmaceutical companies, he’s a longtime member of the medical establishment, so it was a surprise to find that this book—a combination of detailed medical science history, patient user manual, and professional memoir—is unflinching in its analysis of why hypothyroidism now needs to be rethunk. 

First, a nutshell version of the science: The thyroid gland uses iodine to produce the hormones that activate your organs, including your brain. These hormones were identified in the early 20th century and long thought to be two separate entities: T4, which is sort of a warm-up act, and T3, the power-packed main performer. T4 is actually transformed into T3 in various human organs, but no one knew that until 1970, when, Bianco writes, its discovery had a huge impact on treatment (more about that in a bit).

The thyroid gland needs a supply of iodine to make these hormones. Humans and animals ingest iodine from their food, which absorbs it from soil. In areas of the world where iodine is scarce, the gland can’t function properly. It attempts to compensate by enlarging, producing those egglike neck lumps known as goiter. Goiters have been endemic all over the globe, including Bianco’s native Brazil, where they turned up in 10 to 20 percent of the patients he saw there as a medical student in the 1970s.   

In much of the world, this problem has been addressed by the addition of iodine to the food supply—particularly in salt. Iodine insufficiency is no longer a significant cause of hypothyroidism in the United States, Bianco says. But hypothyroidism is still common here, mostly due to autoimmune disease and thyroid cancer (which requires removal of the gland). He estimates that there are currently about 15 million hypothyroid cases under treatment in the U.S., and—thanks to a lowered threshold for treatment—another ten million subclinical cases receiving thyroid supplements.

For most of human history, the function of the thyroid gland was a mystery. Its connection to ailments like cretinism and goiter, and to symptoms like cold intolerance, weight gain, and mental and physical sluggishness, wasn’t understood until the last quarter of the 19th century. After the connection was made, initial attempts at treatment included transplanting animal glands to humans (the glands didn’t survive); serving up a daily chunk of sheep thyroid gland to be eaten (said to taste “disgusting”); and providing oral doses of desiccated animal thyroid extract (bingo).  In the early 20th century, commercially produced animal thyroid extract—mostly from the Armour company’s Chicago stockyards, and mostly from pigs—became the standard hypothyroidism treatment. 

But the potency of pig extract was difficult to standardize, and there were concerns that it might have negative effects after long-term usage. In the late 1950s, a subsidiary of Baxter Travenol Laboratories introduced Synthroid, a new synthetic version of T4 (which had been identified and first synthesized a few decades earlier). The U.S. Food and Drug Administration (FDA), whose standards for new drugs would later become more rigorous, approved it without clinical trials that would have tested its effectiveness against the animal extract, which contains both T4 and T3. When more stringent FDA standards were later adopted, Synthroid was grandfathered in. 

Initially Synthroid was one of several synthetics on the market, and doctors weren’t necessarily likely to use any of them, sticking with the animal extract they were used to. But research published in 1970 proved what some had previously suspected: that T4 is converted to T3 in human organs. This discovery was interpreted to mean that T4 alone, conveniently available in tablets of standardized potency, was the optimal way to treat hypothyroidism. Synthroid’s manufacturer, seizing the opportunity, embarked on a famously aggressive marketing campaign, influencing physicians directly and through support of their professional associations, and before long, physicians who were still prescribing pig thyroid extract were themselves branded as “old-fashioned.” Brand-name Synthroid (and, eventually, its generics) became the go-to treatment, and a blood test (the TSH test) superseded patients’ reports of symptom relief as the measure of its success. 

This worked for most patients, but many others remained fatigued and brain-fogged, even when their blood tests fell within the normal range. Bianco writes that the failure to test the efficacy of T4 alone in comparison to T4 plus T3 was a mistake. The amount of influence allowed to pharmaceutical companies at the time was inappropriate and had unfortunate results. And physicians’ willingness to discount patients’ complaints of continuing hypothyroid symptoms if their blood tests looked normal was a decades-long disservice to those patients. He apologizes for having done so himself. Recent research has shown that not all patients are able to convert T4 to T3 efficiently, and those people—perhaps as many as 20 percent of those diagnosed as hypothyroid—would likely benefit from the addition of T3 to their regimen. He calls for more research on every aspect of this.

In a phone interview last week, Bianco told me he hopes that “if something good should come out of this book, it will be some reshaping of the relationship between the pharmaceutical companies and the professional societies. And also, more attention to the patients. We should trust the patients, not dismiss them. They’re telling us something, and we should listen. That was a lesson for me.”