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Alan Cohen, M.D. on Depression and Thyroid Disease
The Depression/Thyroid Disease Connection Explored

by Mary Shomon

Alan Cohen, M.D. is board certified in neurology and psychiatry, and his research focuses on utilizing the latest research protocols for the treatment of a wide variety of emotional and physical disorders. Dr. Cohen has generated patent protected treatment protocols to advance the latest innovations in modern psychopharmacology. He is the author of a research study presented to the Third International Conference on Refractory Depression, titled Psychostimulant Augmentation Of Antidepressants In Anergic Depression Associated With Hypothyroidism. .

Can you tell us a little about your medical background and why hypothyroidism has been a particular interest for you?

I am a board certified psychiatrist in private practice for 16 years. I was trained at Jefferson Medical College in Philadelphia, pa. internship and residency at University of California, San Francisco, and Fellowship in Diagnostic Psychiatry at The Institute of Pennsylvania Hospital in Philadelphia, spanning 9 years (1978-1987). I was a full-time faculty attending at SF General Hospital/UCSF 1987-1990, serving as a volunteer clinical faculty assistant professor after leaving for a full-time private practice. I am in the process of reappointment to UCSF faculty status which lapsed after my departure to private practice. My interest in thyroid dates back to medical school 1981-1982 when I studied endocrinology and acted as co-investigator in a study on chronic pain association with the then newly discovered endorphins. The obvious intertwining of hormones and mood/behavior seemed to be under-appreciated by my colleagues and professors, with a few exceptions.

When I studied at Langley Porter Institute as a major teaching site for UCSF, one of my teachers, Victor Reus, M.D., made a strong impression on me and some of my fellow residents. He has been focusing on thyroiditis and psychiatric disease for decades, publishing important articles and researching this area. The UCSF department of psychiatry is so diversified that Dr. Reus' teaching was not always given the attention it clearly deserved competing with many other approaches to the practice of psychiatric medicine. I became more interested in thyroid evaluation and testing as the technology of laboratory thyroid monitoring improved with ultra-sensitive TSH, antibody detection, etc. Articles were appearing in the journals showing an area of medicine that seemed relevant to psychiatry and endocrinology, with neither field taking the lead in pursuing answers to the complaints of so many patients that were falling through the cracks between medical specialties.

As I started to explore this problem, I was stunned by the incredibly high numbers of undiagnosed thyroid patients. I found when doing routine TSH and antibody testing. At one point, 1-2 newly detected thyroiditis/hypothyroid patients were diagnosed per week in my office practice. I knew then that there had to be many more people suffering with this condition and not getting proper attention. The clincher came some 10 years ago when I was able to diagnose Hashimoto's thyroiditis in my mother from over 2000 miles away. Her own internist had to defer to me for interpretation of the tests (thyroid antibodies) because he couldn't figure out what they meant (I had requested she get a TSH and anti-thyroid autoantibodies). The subject has grown into one of my major subspecialty areas of interest, with research, lectures and papers published on thyroid and psychiatry.

In talking about the relationship of depression to hypothyroidism, in your article, "Treatment of Anergic Depression In Hashimoto's thyroiditis With Fluoxetine and D- Amphetamine," you state that

"When the TSH returns to the normal range most symptoms will resolve. However, it has become apparent in clinical practice that depressive symptoms and anergia may persist despite correction of the hypothyroid state by replacement of thyroid hormone."
I have three questions that relate to this statement. First, have you found that anywhere in the designated "normal range" of TSH levels is sufficient to resolve symptoms, and in particular, depression? Or is there a particular level that seems to be more associated with resolution of symptoms?

Many patients seem to need replacement hormone sufficient to get the TSH down around 1.0 or less, even below .50 (although the lower TSH levels often generate fear, panic, or worse in some MD's who use the TSH values as absolute strict limitations. I've had a few scrapes with MD's who would stop my treatment of patients that were feeling fine for once in many years simply because the #s, TSH levels, were too low (e.g. 0.05) for the Doctors comfort!!) . It would be a good research project to correlate TSH levels with psychiatric symptoms. I haven't done that yet, my impression is that most patients with fatigue, anergia and depression need TSH levels in the lower zone <1.0.

Second, what is your estimate of the number of patients who are still plagued with various symptoms of depression despite optimal TSH levels?

Roughly about half in my practice. Remember, my sampling of patients is different from the generals practitioner's patients group. I will tend to see the patients who weren't successful with their treatment at the GP's office. So, that estimate may not apply to a larger group of patients.

Third, do you find that the addition of T3 drugs can help in some cases?

T3 definitely helps. No question about it! T3 has been used by psychiatrists for decades to augment antidepressant treatments that weren't completely effective (without known hypothyroidism being present).

What are your thoughts about the February 1999 study reported on in the New England Journal that found that the addition of supplemental T3 to the standard regiment of T4 (synthetic levothyroxine, like Synthroid) "improved the quality of life for most [hypothyroid] patients"?

No surprise there. It's been long overdue, but certainly a welcome confirmation for those of us who've been recommending it for years.

Can you tell us a little about the progression of recommendations you'd typically recommend for a hypothyroid patient suffering from depression? (I.e. first treat thyroid, then antidepressant like X or Y, then add d-amphetamine, etc.) Would some doctors consider the use of d-amphetamine in these sorts of cases controversial, and if so, why? What are the contraindications, side effects, or dangers to long-term use of these drugs? Can people easily become addicted?

There are lots of issues here. First, unless I'm doing a research study, every patient gets unique treatment. No cookie cutter approaches form me. That said, once the TSH is adequately lowered to 1.0 or 0.50, I assess the mood disorder symptoms such as low energy, fatigue, apathy, leaden feeling in the limbs, etc. I might try an activating antidepressant as an add-on or switch over, and again re-assess the symptoms. This may go on for 1-2 months, if possible. On occasion, there just isn't time {such as when a patient must be functional now! or risk dire consequences, E.G. case of twins mother putting her babies at risk for physical injury!} In those cases rapid action is imperative. Once a patient has gotten symptom relief with an antidepressant, and still has residual fatigue, or anergia, then a psychostimulant trial is offered as an additional treatment. I haven't seen addiction develop in the many dozens of patients treated over the years. If a patient did misuse the drug, it would quickly become apparent due to controlled-drug Rx regulations. But what is typical in my practice is that my patients tend to limit these drugs themselves, often cutting back as soon as they feel they can. The controversy is related to the use of a class of drug that has the potential for abuse in some vulnerable populations. Some MD's simply refuse to ever Rx such drugs. patent selection and screening is very important. Stimulants are really very safe, compared to many non-controlled drugs. I believe they are underutilized as a therapeutic class, although the trend is slowly changing [especially as more treatment of ADD has brought the usage of stimulants into greater acceptance].

In your article, you frequently mention binge eating of carbohydrates. Is this a behavior typically associated with depression, hypothyroidism, or both, and can you explain more about this phenomenon?

Carbohydrate binging is associated with some depressive syndromes. One explanation derives from the early work of Wurtman and Wurtman out of Boston who studied diet and mood / behavior. They saw a direct link between the intake of certain foods preferentially by some patients with depression. Subsequent studies revealed that carbo-binging (selective ingestion of starches, sugars, etc. ) results in enhanced absorption of l-tryptophan from the gut. This is because sugars fuel a selective absorption pump in the lining of the gut that preferentially takes in more tryptophan leaving other amino acids behind. L-tryptophan is the precursor to serotonin, known to us now as a major neurotransmitter in the brain, particularly in regards to mood and sleep functions. Studies on patients prone to depression but currently in remission relapsed into clinical depression when fed a diet free of all tryptophan. I know of no work connecting thyroid to this phenomenon, although the idea deserves further study.

What do you feel the relationship is between hypothyroidism, depression, and obesity or being overweight? Do you find that weight loss becomes easier in patients for whom the depression is fully treated?

This is too complex a topic for this format today. There is an inter-relationship of all three factors on many different levels. I will say that although it seems intuitive that weight loss would be easier once depression lifts, the reality isn't always such. The antidepressants used these days, although worlds better than their predecessors, cause some side effects. Weight gain is one commonly seen with a number of the antidepressants prescribed currently.

In your article you state: "After the depressive symptoms were resolved, fatigue states persisted. Only after the addition of a psychostimulant did the fatigue resolve. "Can you explain in basic terms why the fatigue still remains for some patients, and how a psychostimulant liked-Amphetamine might help?

The idea behind residual symptoms of fatigue in euthymic and "euthyroid" patients (normal numbers on labs or rating scales) is that the autoimmune process, independent of thyroid hormone levels, causes a malaise on a chronic, waxing and waning, course. This is due to the toll on the body that is taken through antibody production, antibody/antigen interaction, destruction of complexes from interactions of these factors, etc. Thus, the autoimmune illness runs a separate course on a chronic basis, depleting patients of energy and leading to fatigue. The amphetamines seem uniquely suited for this condition because they are helpful in treatment of pathological fatigue states, in general, and provide stimulation in a way that thyroid patients seem "deficient" in . Thyroid disease appears to "numb up" the post-synaptic receptors for adrenalin, dopamine, and other neurotransmitters. This is in part why hypothyroidism causes delayed reflexes(doctor's hammer to the knee doesn't cause kick to the .... of the doctor). The nerve signals aren't getting in very well. The stimulants shower the nerve receptors with lots of adrenalin, dopamine, etc. This overcomes the numb receptor getting more signal through to enhance motor/sensory response, reduce fatigue, improve mood and sharpen cognition.

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