PROCEDURE PERFORMED AT MEDICAL WELLNESS ASSOCIATES BY EMMA McGOWAN, M.D. AND MARTIN GALLAGHER, M.D.
"Effectiveness and tolerability of acupuncture compared with metoprolol in migraine prophylaxis," Streng A, Linde K, et al, Headache, 2006; 46(10): 1492-502. (Address: Dr. Andrea Streng, Centre for Complimentary Medicine Research, Department of Internal Medicine II, Technische Universitat Munchen, Kaiserstr, 9, 80801, Munich, Germany).
An Open lettr to National Football League Commissioner Roger S. Goodell.
Preeminent Harvard psychiatrist Lester Grinspoon smoked pot with Carl Sagan (a lot), which prompted him to write two books about cannabis, Marihuana Reconsidered (1971) and Marijuana, the Forbidden Medicine (1993). Dr. Grinspoon asked us to consider running an open letter he'd written to the commissioner of the National Football League, Roger S. Goodell, imploring him to actively support research into using cannabis to treat long term head trauma, and we felt his thoughts are worth sharing.
As both a medical doctor and one of millions of fans who enjoy professional football as a spectator sport, I'm becoming increasingly uncomfortable with the growing specter that many of the athletes I cheer from the sidelines will one day pay the steep price of developing Chronic Traumatic Encephalopathy (CTE) due to concussions and other repetitive brain injuries incurred in the course of their profession.
Already the NFL has offered former players $765 million to settle a lawsuit charging your organization with knowingly concealing a link between traumatic brain injury and pro football, an agreement later struck down by a judge who feared that sizable payout could actually prove far too small to adequately cover all current and future cases of CTE. So it's not hard to imagine the NFL's liability eventually growing to well more than a billion dollars, a staggering figure that nonetheless pales in comparison to the human toll paid in terms of pain, suffering, and untimely death among former players.
To your credit, you recently showed a willingness to explore all possible means of alleviating the frequency and severity of CTE cases in the NFL, including the controversial idea that compounds found in marijuana could play a vital role in protecting player's brains. Asked about that very possibility, you said: “I'm not a medical expert, [but] we will follow medicine and if they determine this could be a proper usage in any context, we will consider that."
Given the severity of the problem, however, I think you, and the NFL, must go beyond simply following the medicine, and help lead the way by directly funding research to determine if cannabis—including preparations with no psychoactive effects, such as those with a high-cannabidiol (CBD) to tetrahydrocannabinol (THC) ratio—can indeed provide significant protection against the damage of repetitive concussions.
Already, many doctors and researchers believe that marijuana has incredibly powerful neuroprotective properties, an understanding based on both laboratory and clinical data. But unfortunately, the extensive research required to definitively determine cannabis's ability to prevent CTE will require millions of dollars in upfront investment, and despite the great promise many now see in cannabinopathic medicine, it's hard to imagine who else has both the motive and the means to provide such funding.
Typically, a new medicine reaches the market because a pharmaceutical company pays for research to establish both its efficacy and safety. But it's highly unlikely that a pharmaceutical company will get involved in studying cannabis as a treatment for CTE, because the plant (and its natural components) can't be patented, and would therefore likely fail to provide an adequate return on investment even if developed into a successful treatment.
The only other potential source of funding is the US government, which remains inexcusably resistant to any clinical study designed to examine marijuana's potential benefits.
Fortunately, the NFL's pockets are plenty deep enough to launch a serious, intensive research program designed to determine whether or not some combination of cannabinoids is effective in preventing the consequences of concussions. This would not only be a great public service, it's in the league's own financial self-interest. Especially since so few other promising options exist for alleviating the problem.
Attempts to improve protective equipment can only go so far without seriously diminishing the skills and capacities of the player. The helmet as currently designed is excellent at protecting the skull, but not its contents—the brain. And given the limitations imposed by physics, anatomy and neurophysiology, I question how much more any helmet design can do to limit the frequency or severity of concussions. I also see little potential in further rules changes to adequately address this issue, without altering the game so severely that it no longer resembles football as we know it.
Which means we must explore the potential for internal protection of the brain. This research will not be quick or inexpensive, but it must happen. In the meantime, I implore you to immediately stop subjecting players to drug tests for marijuana, so they no longer face severe penalties for choosing a potentially life-saving medicine that can be used legally in twenty states.
Lester Grinspoon M.D.
This is a case report of a 27-year-old man with ulcerative colitis who had infantile colic, loose stools and frequent vomiting for the first 5 years of his life. He was atopic and had symptoms of eczema, rhinitis and sinusitis from an early age. The patient suffered from different arthralgias in the neck, back and wrist. Transient muscle aches were also noted.
Generalized body itches were present. He was placed on an elimination diet where a different fruit, vegetable, grain and protein was used daily. Water was the only fluid and salt was the only condiment allowed. The colic, flatulence and diarrhea improved rapidly but it took 6 weeks for the mucous and blood to disappear. Offending foods were pineapple, cottage cheese, milk, beef, wheat, maize, sugar among others. His pustular acne cleared up after 4 weeks and remained that way 30 months later. He has also gained weight.
"Ulcerative Colitis - A Patient Report," Borok, G., South African Family Practice, 1989;10:468-474.
Insomnia, Sleep Disorder - Acupuncture, Traditional Chinese Medicine, Traditional East Asian
Medicine, Electroacupuncture, Electrical Stimulation
In a sham-controlled study involving 60 adult subjects reporting insomnia for 3 or more nights per week for a period of at least 3 months, treatment with acupuncture (electroacupuncture), 3 times per week for a period of 3 weeks, was found to improve sleep. Subjects were divided into 2 groups. One group received real acupuncture (electroacupuncture at points: Yin Tang, DU-20, bilateral ear Shen Men, Sishencong, Anmian), while the other group received a sham treatment (“placebo acupuncture” at the same acupuncture points with Streitberger needles that do not pierce through the skin). As compared to pre-treatment, subjects in both groups reported significant improvements in sleep. Improvements were measured according to sleep diaries, 3-day actigraphy, self-reported questionnaires, and scores on the Insomnia Severity Index. Subjects who received real acupuncture were found to have significantly greater improvement, assessed via sleep diary and actigraphy. Moreover, a significantly greater percentage of subjects in the real acupuncture group were found to have sleep efficiency of 85% or greater, and a significantly greater percentage were found to have less than 30 minutes of wake after onset of sleep. These results suggest that acupuncture may be a safe and effective treatment for patients with primary insomnia - a debilitating disorder that has wide-ranging adverse implications. The authors conclude, “Because of some limitations of the current study, further studies are necessary to verify the effectiveness of acupuncture for insomnia.”
"Electroacupuncture for primary insomnia: a randomized controlled trial," Yeung WF, Chung KF, et al, Sleep, 2009; 32(8): 1039-47. (Address: Department of Psychiatry, University of Hong Kong, Hong Kong SAR, China).
Homocysteinemia, or elevated plasma homocysteine, is a major factor that can influence poor cardiovascular health. High plasma levels of homocysteine appear to have negative effects on the vasculature, impairing the functional abilities of endothelial and smooth muscle cells. Suboptimal intake of several B vitamins, renal failure, environment, diet, stress, and genetic defects in homocysteine metabolism can all contribute to abnormal homocysteine levels.
Homocysteine is a sulfur containing amino acid that is created in the body from methionine, an essential amino acid derived solely from dietary intake. Methionine is metabolized into homocysteine via an intermediate, S-adenosylmethionine. Homocysteine can be metabolized to produce cysteine, a nonessential sulfur-containing amino acid, or it can be remethylated to methionine. Whether the body needs cysteine or methionine will dictate which path homocysteine metabolism will take.
Production of cysteine from homocysteine requires two specific enzymes for which vitamin B-6 is an essential coenzyme. Without adequate vitamin B-6, homocysteine cannot be metabolized into cysteine. The body can also metabolize homocysteine by remethylating it to methionine. The primary route by which homocysteine is remethylated to methionine requires folate in the form of methyltetrahydrofolate as a methyl donor and vitamin B-12 (methylcobalamin) as a coenzyme. Methyltetrahydrofolate, or L-methylfolate, is synthesized in the body from dietary folic acid. However, L-methylfolate can be used directly by the body, without the need for folic acid conversion via the enzyme 5,10-methylenetetrahydrofolate reductase (MTHFR). In certain populations, the body’s ability to convert folic acid to 5-MTHF by use of this enzyme may be compromised due to genetic differences.
B vitamins, in particular folate, methylcobalamin, and vitamin B-6 are necessary for the body to metabolize homocysteine. A deficiency or suboptimal levels of any of these essential vitamins may cause plasma homocysteine levels to rise. Dietary surveys and epidemiological studies indicate that suboptimal levels of folate, vitamin B-12, and vitamin B-6 are common in many population groups. Elderly individuals, smokers, alcoholics, and medications users, including estrogens and popular medications for cholesterol and blood glucose control, are at risk for subclinical deficiencies of one or more of these B vitamins.
TMG, trimethylglycine, also known as betaine anhydrous, acts as a methyl donor in the methionine/homocysteine cycle. One route of homocysteine metabolism is by methylation to form methionine, using a methyl group from methylcobalamin or from trimethylglycine. Methionine is then converted to S-adenosylmethione (SAMe). Trimethylglycine is absorbed rapidly and has a high volume of distribution due to extensive distribution to tissues, including the kidneys and liver. When taken orally, trimethylglycine can support normal homocysteine levels.† Improvement in plasma homocysteine may be seen within a week, and steady state could be reached within a month.
Choline, also considered a B vitamin, can be oxidized to betaine which serves as a methyl donor to convert homocysteine to methionine. Dietary intake of choline might also support healthy homocysteine level.† The effect of dietary choline intake may be greatest on those with lower folate levels.