Liz Sutherland, ND, editor-in-chief of the Journal of Restorative Medicine had the pleasure of interviewing Kent Holtorf, MD, who will be presenting at the 2019 Restorative Medicine Conference in San Diego
Sorce: Restorative Medicine DigestJune 20, 2019
LS: Dr. Holtorf, please share some information with us about your background.
KH: I went to Berkeley and then UCLA as an undergrad. From there I went to St. Louis University Medical School. It was during that time I started feeling like something was wrong. I was so fatigued. I felt mentally and physically exhausted. The university doctor said I was just stressed and depressed and that this was very common. But I knew something was wrong. I couldn’t think. Everything was so difficult. I had anxiety like never before. I tried all kinds of conventional therapies and nothing really helped. When I went back to UCLA for my residency, I felt worse and worse.
I’ve always been very evidence based, and it was ingrained in me not to go to any so-called alternative medicine conferences because they’re not based on science. But I wasn’t functioning and had to do something. So against my better judgment I went to some of these alternative conferences and saw that they were more evidence based than what we were being taught in the residency! I started incorporating hormone optimization, especially T3, into my own treatment plan and it saved my life. That’s when I realized that learning how to properly treat the thyroid can help so many people. In my practice, we’ve also developed many new treatments for Lyme disease, such as peptide therapies. Every single patient with Lyme disease has low thyroid, by the way, just like every Hashimoto’s patient has low thyroid.
LS: Thank you very much for sharing that context with us. How do you determine tissue thyroid levels in your practice?
KH: It’s a little complicated, but once you learn the pattern you can pick it out. The typical pattern we see is a low-normal TSH, a high-normal T4, a low-normal T3, and a high-normal reverse T3.
Educated doctors when they see low-normal TSH and high-normal T4 will tell their patients about reduced T4 and T3 conversion, but the key is actually thyroid transport. T4 and T3 have different transporters and T4 is much more energy dependent. If a patient with this profile (low-normal TSH, high-normal T4, low T3, and high reverse T3) goes to their doctor, a third of the doctors will say they’re high, a third will say they’re low, and a third will say they don’t know what to make of it! In general an endocrinologist only looks at TSH and T4, and if they see a low-normal TSH and a high-normal T4, they tell the patient it’s subclinical hyperthyroidism. It’s actually the opposite. If you examine all these other parameters you see it’s a sign of low thyroid function. Hundreds of studies show this.
As soon as you have a little less mitochondrial function, which is caused by so many things including infections, pollutants, toxins, pesticides, aging, and so on, then T4 does not get into the cell. T3 is also limited, but not nearly as much. You’ll see people with high T4 because it’s not getting into the cell. The only thing TSH tells is the level of T3 in the pituitary, which is different than any other cell in the body. The pituitary pulls in T3. It doesn’t transport it. It doesn’t convert it, so it’s probably the worst measure to use to determine tissue thyroid levels. The textbooks say reverse T3 is an inactive metabolite, but it’s an active competitor of T3. It lowers T4 to T3 conversion. If you infuse reverse T3 into a patient their metabolism drops. Reverse T3 blocks the thyroid. In my talk I’ll highlight studies that show every obese patient has low thyroid.
One of the best ways to look at tissue levels of thyroid is via sex hormone binding globulin (SHGB). SHBG increases in response to estrogen levels and to the amount of thyroid in the liver. There are also studies that show that PCOS basically leads to low intercellular levels of T3.
On our nonprofit site, the National Academy of Hypothyroidism, I’ve looked at hundreds of articles from major peer-reviewed journals that show it’s completely inaccurate to use TSH to diagnose low thyroid function. It becomes more inaccurate basically the sicker the patient. If there’s a totally healthy patient on Earth who hasn’t been exposed to pesticides or stress, you can probably use TSH.
LS: How do you treat patients with Hashimoto’s disease?
KH: Hashimoto’s is probably the least likely cause of low thyroid function! Most Hashimoto’s patients do not have typical antibodies. They have antibodies against their pituitary, but it’s an activating antibody, and so it lowers TSH. I’ve found that giving thyroid hormone results in a better outcome than lowering the antibodies. In my talk I’ll explain why T3 is far superior for patients with Hashimoto’s. If you do it right, and do it safely, the chances of side effects are extremely low. A lot of practitioners use T4-T3 combinations and natural desiccated thyroid. I will talk about that. Certainly it’s better than some options, but in general the sicker the patient the more T3 is needed. T3 is a key part of treatment for patients with, for example, chronic pain syndrome, Lyme disease, and fibromyalgia who also have so many other issues.
LS: In general how long would a really sick patient have to stay on T3?
KH: That’s a tough question because it’s very broad and everyone’s different. We’ve seen the sickest, most complex patients who have been everywhere, but never had their thyroid appropriately treated, and all of a sudden they’re better in a couple of weeks. Patients often feel better within weeks and do very well. Some sicker patients have thyroid resistance so it takes a little longer, but T3 is a vital part of a multisystem treatment for these people. If you get patients better and improve all of these issues, then they don’t need to stay on T3. But almost everyone is suboptimal and they want to stay on thyroid because they feel better. One study I’ll discuss in San Diego suggests that low-normal thyroid is basically a greater risk factor for heart disease than diabetes, high cholesterol, and obesity. T3 is also a better antidepressant than antidepressants.
LS: What tests do you use to determine thyroid function?
KH: We use serum testing. I think salivary testing, especially the four-point cortisol is helpful, but we find we don’t need it because we can tell what’s going on from a morning cortisol and clinical symptoms. We also check people’s metabolic rate, especially overweight patients. Almost without exception, they have a 25% lower baseline metabolism. They’re burning 500 calories less a day, so they’ve got to be pretty much starving just to stay even. If a patient is nervous on their first visit, their metabolic rate might be slightly up, but it’s still low. We also use the Thyroflex test. This is a computerized test that measures the velocity of the brachioradialis reflex, which correlates with intercellular thyroid levels.
LS: Thank you very much, Dr. Holtorf, for these intriguing insights. We look forward to your presentations in San Diego.