This is a partially-completed, preliminary draft of an article that I wrote in the summer of 2009, with occasional additions thereafter. Additions to the article are based primarily upon subsequent literature review.
In 2014, when I emailed an earlier draft of this article to Professor Guiles Guillemin--who was and continues to be the Head of the Neuroinflammation Group at Macquarie University, the Co-Director of the Motor Neuron Disease Research Center at Macquarie University, the Co-Director of the Neurodegenerative Diseases Research Centre at Macquarie University, and the Editor-in-Chief of The International Journal of Tryptophan Research--he sent me an enthusiastic reply, offering to co-author a revised and finalized version of the article for publication in The International Journal of Tryptophan Research. I had no background whatsoever in life sciences or medicine, and had immersed myself in the medical literature review for about eight months before writing the draft. Having such a highly-regarded co-author would have been an enormous benefit.
At that point in time, the draft provided an overview of the role of the kynurenine pathway as a cause of pathogenesis in Lyme neuroborreliosis and quite a few other chronic infections. The article explained how chronic activation of a hyperinflammatory immune response results in excitotoxicity, oxidative stress, impairment of antioxidant defenses, and devastating deactivation of the immune response against both intracellular and extracellular infections, such as Lyme neuroborreliosis, if those infections are the cause of the chronic, hyperinflammatory immune response that results in overactivation of the kynurenine pathway. Because aggressive antibiotic treatment of advance Borrelia burgdorferi infection results in exacerbation of the inflammatory immune response, the article provides a well-researched hypothesis that in cases of prolonged infection with B. burgdorferi, such as my own 30 year history of infection with both B. burgdorferi and Babesia microti, aggressive antimicrobial treatment can damage such patients far more in a less than a year than the underlying, untreated infections had damaged such a patient over the prior 30 years. Such was the case with me, when I was treated with two intravenous antibiotics simultaneously, along with oral antimicrobials, for both Lyme neuroborreliosis and infection with Babesia microti.
The article also provided a thoroughly-researched hypothesis concerning the mechanisms of action of ketamine as an antidepressant. And it provided my hypothesis that ketamine taken with buprenorphine would synergistically reduce depression. I had developed tolerance to such a high dose of ketamine that 300 mg intramuscular ketamine daily could not control my depression. Nor could buprenorphine any longer control my depression. But when I found a psychiatrist who was willing to prescribe both drugs together, my hypothesis turned out to be correct (sample size: one). Moreover, buprenorphine prevented me from developing any additional tolerance to ketamine. I was able to take 300 mg IM ketamine daily (10 injections @ 30 mg each daily) and 8 mg buprenorphine twice daily for six years--from August 2011 to early 2017--which reduced my depression from the severe-to-extreme range to the lower moderate range.
I was unable to accept Professor Guillemin's offer of co-authorship in 2014 because during the two years before I mailed him the draft, I had been diagnosed with additional medical disorders that have high fatality rates and were supposedly incurable. I had managed to cure those medical conditions after another round of intensive medical literature review, but I felt it was more important to continue my research and to find an even better treatment for depression.
Specifically, I had developed complex regional pain syndrome from the left elbow, along the left forearm, and into the left hand after falling out of bed in 2012 and landing on my left elbow on a hard wood floor. Immediately, I began experiencing peripheral neuropathy from the left elbow, down the left forearm, and throughout the left hand. Over a period of seven months, the tingling and numbness became an intense burning sensation. And at that point, I suddenly began experiencing identical symptoms simultaneously in my right arm. At the eight month point, I discovered a case report of cure of CRPS using the exact model of near-infrared laser I already owned: a 7.5 watt, 980 nanometer Avicenna laser that emitted a divergent beam with a spot size of 1 square centimeter at 0 mm distance. After traveling three centimeters, the beam became 56% wider, and therefore 56% less powerful. I treated my left arm from the elbow to the end of the left hand with an output of 7.5 watts, holding the lens very close to the skin while moving the hand piece back and forth for 15 minutes, three days in-a-row. After the third daily treatment in 2012, I was completely cured , and have never experienced any recurrence of CRPS.
Because I had already developed tolerance to a very high dose of ketamine before discovering that buprenorphine prevented additional tolerance, I had to take 300 mg intramuscular ketamine daily combined with buprenorphine. After about 16 months, I developed excruciating ketamine-induced interstitial cystitis. A major hospital in Seattle was able to do nothing to alleviate my symptoms. It appeared that I would either have to stop taking ketamine, which would result in a relapse of extreme depression that I could not survive, or that I would destroy my bladder over the next month, leading to the same outcome as well as a destroyed bladder. So I began treating the ureters and the bladder with my 7.5 watt laser. I had to treat each ureter for 30 minutes daily with that laser, from the top of the ureters down to the bladder. But within three days, the interstitial cystitis was under control. A week after I began treating myself with the laser, I went back to the hospital for a scope of my ureters and bladder. The doctors were astounded that they could find no damage. Among other things, the laser activates mesenchymal stem cells, which travel from the bone marrow to locations throughout the body that are damaged, and repair the damage. Over the next five years, I upgraded to more powerful lasers and a more effective wavelength. First, I upgraded to a 10 watt, 980 nm Diowave laser that emitted a divergent beam with a spot size of 3 square centimeters at 0 mm distance. I was able to treat myself less often than I had with the outdated 7.5 watt, 980 nm Avicenna laser. Then I upgraded to a hand piece that emits a collimated beam, which I used with the 10 watt laser. Immediately, I was able to treat myself 12 times less often to achieve the same result that I had achieved using a divergent beam. I was then able to significantly reduce the treatment time when I upgraded to a 15 watt, 810 nm Diowave laser that emits a collimated beam. And finally, when I upgraded to a 30 watt, 810 nm Aspen laser that emits a collimated beam, I was able to treat each ureter down to the bladder for five minute each month (10 minutes of treatment per month) to achieve the same results I had achieved with four hours of treatment weekly using the 7.5 watt, 980 nm Avicenna laser. I continued taking 300 mg ketamine and 8 mg buprenorphine BID that entire time. A with a wavelength of 810 nanometers penetrates into any part of the human body, including the brain, about three times more effectively than a 980 nm beam with the same power density.
In 2015, I a pilot study demonstrating that lasers at least 30 times less powerful than my 30 watt laser (effectively at least 30 times less powerful, because they emitted divergent beams) cured about 90% of patients with severe, suicidal depression caused by traumatic brain injury within two months after starting treatment, when treated twice per week for 20 minutes for those two months. But lasers with the power output in those pilot trials had no effect on my depression. I have never seen depression as extreme as mine described in any medical literature. Here is a one minute and eight second video of me that was taken in April 2011, almost four months before I found a psychiatrist who was willing to prescribe 300 mg IM ketamine and 8 mg buprenorphine BID. When this video was taken, I was taking only buprenorphine.
https://www.dropbox.com/s/qsbza9huy2zb8w4/2011%2005-22%20Video%20of%20Anthony%20severely%20depressed%20%287%20on%20scale%20of%200%20to%2010%29.mp4?dl=0In 2017, I continued to increase the treatment time when treating the temporal regions and frontal lobes using my 30 watt, 810 nm Aspen laser that emits a collimated beam. I treated for 10 minutes, and took a one minute break, and treated for another ten minutes. Finally, when I reached 50 minutes of treatment per day, I began experiencing dramatic antidepressant effects, enabling me to reduce my dose of ketamine from 300 mg daily to nothing at all in a period of six weeks. And I have been able to reduce the dose of buprenorphine by half.
I added information about near-infrared laser to this draft article, but not nearly to the extent that I would like to do so. I plan on turning this into two separate articles: one about ketamine and buprenorphine, and the other about high-power, near-infrared laser therapy.
