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From the Townsend Letter
November 2016

Letter from the Publisher
by Jonathan Collin, MD
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Multiple Sclerosis Support with High-Dose Biotin
Progressive multiple sclerosis is a disease that is frustrating to patients and physicians, with treatments that appear to only slow debility and disability, not offer any prospect of remission. Fréderic Sédel, MD, PhD, of Pitié-Salpêtrière Hospital in Paris, France, does not think that any drug is effective in slowing the progressive symptomatic debility of MS. Sedel and colleagues studied the effect of high-dose biotin (100–300 mg) on a group of 23 MS patients for nearly 2 years. The results revealed qualitative and quantitative improvement in 21 of the 23 patients. In 2015 a placebo-controlled study was presented at the American Academy of Neurology on the use of biotin in progressive multiple sclerosis. Compared with placebo-treated patients, the biotin-treated patients demonstrated statistically significant improvement at 12 months. In 2016 a follow-up report of the aforementioned biotin-treated patients, lead research neurologist Ayman Tourbah, MD, reported that the reversal of disease progression seen with 12 months of biotin treatment was sustained over the ensuing 12 months. According to Tourbah, this is the first "drug" that has "reversed the progression of the disease in a statistically significant proportion of patients." Tourbah noted that the incidence of relapse in the biotin-treated patients was markedly lower than those treated with placebo.
What is the mechanism for biotin's effectiveness in slowing progression in multiple sclerosis? In this issue of the
Townsend Letter, Todd Born, ND, and Stephen Levine, PhD, review the hypothesized etiologies of MS and how biotin can counter the pathologic mechanisms. While high-dose biotin does not appear to have adverse effects, it may work more effectively in combination with high-dose vitamin B1 (thiamine). Born and Levine's review suggests that in MS, neuron demyelination may develop following severe mitochondrial dysfunctioning. Inadequate oxygenation – ineffective utilization of oxygen –appears to accelerate failure of mitochondrial functioning. The authors write that biotin reverses impaired oxygenation of the neuron mitochondria. For that reason Born and Levine suspect that high-dose biotin may play an important role in other neurologic degenerative diseases. One caveat: high-dose biotin will interfere with unrelated laboratory tests, especially thyroid testing, and it would need to be discontinued for 1 to 2 weeks to get accurate lab tests.
Is Smell the Key to Pain Control?
I hardly need to say anything about the terrible state of affairs that we face in the US on managing pain. The recent generic snail-mail that I received from the Surgeon General asking me to sign a pledge to strictly limit my prescribing of opioids speaks volumes about the crisis. For those "truly" dealing with chronic pain who are dependent on oxycodone, refilling their prescription with their physician is bound to be as tense as a game of poker when each patient is suspected of bluffing. Undoubtedly, not a few will be forced to seek their pain medication on the streets, or worse, forced into heroin use. Obviously, alternatives are needed for managing pain, but it is far easier to tell the patient that they need to use other options than finding one(s) that are effective. While various non-opioid drug therapies are touted to manage pain effectively, they usually are costly, dysphoria-inducing, and not nearly so pain relieving. Psychological approaches are helpful but generally insufficient. Acupuncture, physical therapy, massage, and injection therapies are helpful but do not suffice. Vitamins, nutraceuticals, herbals, and homeopathics offer some solace but also fail to manage pain adequately. Could administration of essential oils be the key to managing pain?
Sarah Lobisco, ND, makes the case this issue, in the first part of a two-part article, that one can sniff out pain. How could a smell play any role in experiencing pain? The science of olfaction is not simple physiologically. Lobisco reviews the complex neuroanatomic relationships that exist in processing smells. What is the key brain structure involved in interpreting smell? The amygdala. But the amygdala is also vitally involved in processing emotions and pain. The fact that the amygdala is receiving smell and pain sensory input while processing emotional response provides the connection necessary for smell to be integrated with pain and vice versa. In this first part, Lobisco reviews a number of rodent and human experiments that establish the connection between smell, emotional response, and pain. Lobisco conjectures if one can draw this smell-to-pain relationship with chemical scents, what would be the therapeutic value of using patient-specific essential oils for addressing chronic pain? She explores this possibility in part 2 in the December 2016 issue.

Jonathan Collin MD

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1. Ali M. Oxygen and Aging. Denville, NJ: Canary 21 Press; 2003.
2. Shea butter [online article]. Wikipedia.
3. 21 reasons to use shea butter [online article]. America Shea Butter Institute.

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