Alan (not his real name) is a 25 year old software engineer who presented with a history of depression over many years dating back to childhood. He was diagnosed with bipolar disorder two years earlier when an unknown SSRI (he couldn’t recall the name) caused him to be excitable, nervous, sweaty, talking too fast, excessive energy, sleeping too little, aggressiveness, excessive spending, and racing thoughts; then cycling into lethargy, difficulty getting out of bed, isolating himself, becoming socially withdrawn, and not eating. The hypomanic episodes would last for 3-5 hours and the depressive episodes would last for a couple of days.
He had been taken off the SSRI, which was later determined to be Lexapro, and placed on Tegretol, which resulted in an allergic reaction characterized by hives. He then was placed on Depakote, which caused severe cognitive problems, and Wellbutrin was added to try to improve his cognition. He was still unable to function, and lithium was added. The Wellbutrin and the Depakote were then discontinued and he was placed on lithium alone, resulting in stable moods with no evidence of mania, yet he had pronounced anxiety and depression, would only sleep 4-6 hours per night, and had a lot of negative thinking at the time he presented to see me.
He reported that moderate depressive symptoms began in his freshman year of college. He gradually became even more depressed and skipped a number of his classes, and started psychiatric treatment after his first year of graduate school. He had enrolled in a very prestigious East Coast University that was highly competitive, and sought treatment as he was afraid that otherwise he would fail out of the program.
He denied any history of mood swings prior to starting the SSRI. There was a family history of “mental instability”. Alan denied any history of hallucinations or delusions. There was no history of concussions or seizures, and no history of significant medical problems. He was diagnosed with depressive disorder, not otherwise specified, and a bipolar disorder secondary to SSRI-induced mood changes. We then ordered a series of laboratory tests and began him on Latuda 20 mg in the evening.
Laboratory tests included mildly elevated white blood count attributed to the lithium, mild anemia, normal chemistries, normal serum magnesium, negative Lyme screening, normal folic acid level, normal C-reactive protein level, T3, T4, TSH and vitamin B12 were all normal, and vitamin D was low.
One month into treatment, he had not improved at all on Latuda 40 mg a day and lithium 900 mg a day. Episodic anxiety, panic attacks, negative thinking, trouble paying attention, reduced memory, irritability, loss of appetite, and social withdrawal continued to be disabling. His irregular sleep patterns had improved 20 to 30%, and excitability and lethargy had improved 10%. We added vitamin D 2000 international units per day, and began him on Lamictal, and also increased Latuda to 60 mg a day.
As he was not doing well despite this regimen, we then performed Genomind genetic testing, and found the following genetic variations: The SLC6A4 was heterozygous, the 5-HT2C was homozygous, the ANK3 was abnormal, the COMT was the VAL/VAL variant, the MTHFR was homozygous, and the CYP2D6 revealed an ultra-rapid metabolizer variation. Because of these abnormalities, we began him on Wellbutrin (addressing the COMT variant) 150 mg a day for the first week, then increased him up to 300 mg a day. We increased the Lamictal (addressing the ANK3 variant) over the next month up to 200 mg a day. We also added Deplin (addressing the MTHFR variant) 15 mg daily.
He was seen one month later and reported “I am doing much better.” “I am getting things done.” “I am sleeping well and feeling more accomplished.” He reported that he was able to return to work part-time, and play music daily for a number of hours each day. Music was now an important emotional outlet that was previously unavailable to him as he had been so profoundly depressed. He began once again to take care of his health and hygiene, and had arranged for three appointments coming up with therapy centers that accepted his health insurance plan. He reported that the panic attacks were gone completely.
One month later, negative thinking was still quite prominent. Irregular sleep was reported by him as 60 to 70% better, trouble paying attention was no better, decreased memory was reported as 20% better, irritability was no better, excitability was unimproved, lethargy was reported as 20% better, loss of appetite was unimproved, and social withdrawal was the same. We increased Lamictal up to 175 mg daily for a week and then 200 mg a day.
He was seen 2 weeks later, and had some increase in negative thoughts, cognitive impairment, a couple of panic attacks, some increased irritability and feeling a bit overly sensitive. His sleep was reported as “fine.” Since Latuda and Lamictal both helped with negative thinking, we increased the Latuda to 80 mg in the evening, and reduced the Lamictal to 175 mg, then down to 150 mg as it was causing some cognitive impairment at the higher doses. He was then seen 2 weeks later. He was feeling a lot less irritable than the last time he had been seen, and overall was feeling better. Work productivity had improved. His cognitive symptoms were enhanced with the addition of the Wellbutrin and a reduction of the Lamictal. His medications at this time were Lamictal 100 mg a day, Latuda 60 mg a day, Deplin 15 mg. daily, lithium 900 mg a day, and Wellbutrin 300 mg XL daily. We agreed to initiate phosphatidylserine 100 mg 3 times a day and green tea, to address his VAL/VAL COMT variation (both of these supplements increase brain dopamine levels).
After another three months on this regimen, he reported that his mood and cognitive functioning were the best that they had been in over five years.