Symposium Q&A from Debbie Mitchell, MD

Here are the Questions and Answers from Debbie Mitchell, MD.

Q: Is it possible to have hypothyroidism without having elevated TSH? Is the TSH screening the end of testing or can other tests confirm hypothyroidism, such as full symptoms and family history of Hashimotos?

A. TSH is the most reliable test for primary hypothyroidism (meaning that the problem is that the thyroid is not working properly) as it reflects your own hypothalamus and pituitary gland’s impression of how much thyroid hormone is available in the body. In very rare circumstances, the pituitary gland is unable to make TSH properly – this is called central hypothyroidism. Central hypothyroidism is most commonly seen in the setting of congenital brain malformations, or a history of brain surgery or brain radiation, though can be seen in other conditions as well. In this setting, the TSH could be misleading.

Q. What is the best way to asses one’s risk of developing Type 1 diabetes?

A. In general clinical practice, we can assess someone’s risk by evaluating their family history and their own personal history of other autoimmune diseases. There are also ongoing research studies evaluating risk factors for diabetes – in some of these studies, antibodies against the pancreas are measured which can refine that risk estimate. If you have a family history of type 1 diabetes, I encourage you to consider enrolling in TrialNet (www.trialnet.org).

Q. How late in life can someone be diagnosed with type 1 diabetes?

A. There is no upper limit to the age at which someone can be diagnosed with type 1 diabetes, though it becomes increasingly rare with age and is fairly unusual (though definitely not impossible!) after age 45.

Q. Is there a risk of women’s heart disease and calcium supplementation?

A. Great question and one that clinical researchers are hotly debating! A few studies have suggested that there may be an increased risk, but many other studies have not found an increase in risk. The studies that have been done at this point were not primarily designed to look at heart disease, so more research definitely needs to be done. At least some studies have suggested that calcium through the diet (such as from dairy, tofu with calcium, etc.) may be safer than supplements. And with calcium – you should get enough, but more is not better. The recommendation for adults is to get 1000 mg per day – be careful not to get more than 2000 mg per day unless that is under the direction of your physician.

Q. Are there natural ways to regulate the thyroid for hypothyroidism?

A. There are several trace minerals that are important for thyroid hormone synthesis including iodine and selenium. In particular, some evidence suggests that adequate selenium may lower antibody levels and prevent certain kinds of thyroid disorders, though it probably does not have an effect in established hypothyroidism. As with almost all vitamins and minerals, getting it through the diet if possible is best. Selenium deficiency is quite rare in North America as it is very abundant in fish, meat, dairy, and several grains including rice. People with strict vegan diets or significant malabsorption may want to check their selenium levels. And, some would argue that levothyroxine, the standard treatment for hypothyroidism, is “natural” in that it is chemically identical to thyroid hormone made in the body.

Q. For those whose celiac disease was discovered later in life and who have low bone density, what are the best treatments to increase bone mineral density?

A. I can’t emphasize weight-bearing activity enough – particularly activities which put a lot of mechanical force on the bone such as running quickly and jumping. Adequate amounts of calcium and vitamin D are important as well. Both smoking and excessive alcohol can decrease bone density, so it is important to avoid these activities. If your bone density is so low that you are at high risk of a fracture, medical treatments such as bisphosphonates might be appropriate.

Q. Do unexpected fractures in kids heighten your suspicion for celiac disease?

A. Absolutely – celiac disease is something I screen for routinely in children who have evidence of skeletal fragility.

Q. Were the fracture studies you discussed done on individuals with celiac disease on a gluten-free diet or untreated (not on a gluten-free diet)?

A. They were done on people treated for celiac disease, but were very large database studies, so there is limited information about to what extent patients were adherent to the diet.

Q. Should a teenager diagnosed with celiac disease following a healthy gluten-free diet have a bone density scan for a baseline or wait until later years?

A. At this point, the current guidelines state to “consider” a bone density scan in children at the time of diagnosis of celiac disease. And for children not adhering to a gluten-free diet, some clinicians will recommend repeating a bone density scan. The information may be of use, particularly for children with unusually low bone density where more intensive counseling about dietary adherence, vitamin D and calcium, and physical activity may be warranted. On the other hand, all children with celiac disease should be taking these steps to maximize bone density no matter what the bone density scan shows. So, until new research emerges, I think it is an individual decision for each patient, family, and physician.

Q. Did you say the prevalence of type 1 DM in celiac is 1-3.81? What is the prevalence of celiac disease in Type 1 DM?

A. Studies suggest that the prevalence of type 1 diabetes among patients with celiac disease is in the range of 1-4%. Conversely, the prevalence of celiac disease among patients with type 1 diabetes is approximately 5-10%.

Q. For Hashimoto, does T4 replace everything the thyroid makes? Is there any evidence to support supplementing with T3, or other, in adult females?

A. This is an area of renewed interest among endocrinologists. The thyroid gland naturally makes quite a bit of T4 (so called because it has 4 iodine atoms attached to it), and only small amounts of other thyroid hormone metabolites including T3 (which is actually the most active version of the hormone). T3 is generated in peripheral tissues by specific enzymes which convert T4 to T3. For most people, treating with T4 is adequate, since the body will then convert appropriate amounts to T3 in a regulated fashion. Most research studies looking at treatment with a combination of T4 and T3 have not found any significant benefit either to laboratory test values or to patients’ symptoms when compared to T4 alone. However, there may be a small subset of people who do not generate T3 efficiently and might benefit from combination therapy. This is a question with ongoing research.