An Innovative New Treatment for MigraineSeptember 2004
By Dr. Sergey A. Dzugan
|LE Magazine September 2004|
| An Innovative New Treatment for Migraine
By Dr. Sergey A. Dzugan
The following article details a groundbreaking treatment program that achieved a 100% success rate for the cessation of migraine headaches during the study period. The cause and relief of migraine is an extremely complex issue involving hormonal balance, neurochemicals, and metabolic integrity. While this article may appear somewhat complicated, it summarizes years of research that can now deliver relief from migraine. If you or someone you know suffers from migraine, we encourage you to read the following article very carefully and to share it with your physician.
While recent advances in treatment have reduced the symptoms of suffering for millions of migraine patients, the underlying causes of migraine continue to be a focus of debate. In this article, we will present an innovative treatment that cured all patients treated for migraine in a recent study. This study was initially conducted at the North Central Mississippi Regional Cancer Center in Greenwood, MS, in association with Dr. Arnold Smith, and was continued at the Life Extension Foundation.
The Continuing Mystery of Migraine
Migraine affects about 10-15% of the population in various countries.2-4 Migraine may occur at any age, but its prevalence increases from childhood up to 40 years of age.5 Migraine is more common in women than in men. According to the American Migraine Study, 17.6% of females and 6% of males in the US currently suffer from severe migraine.6
The numerous theories and hypotheses that have been advanced concerning the causes of migraine are a subject of dispute among experts on the disorder.7 For example, the theory of migraine as a result of dilated blood vessels in the brain was suggested in the early 1850s by Brown-Sequard and Claude Bernard. Their theory was rebutted, however, when Du Bois-Reymond proposed constriction of the brain’s blood vessels as the cause of migraine in 1860.8
Today, no single hypothesis readily explains the mechanism underlying migraine.9 Because of this, new hypotheses continue to emerge but defy acceptance,10 as shown in the accompanying sidebar. While sufficient scientific data exist to support many disparate hypotheses, scientists have yet to promulgate a single hypothesis that explains all the laboratory findings and clinical observations.
Current Treatment Approaches
As one might expect, each hypothesis is accompanied by its own recommended treatment regimen and no single treatment is effective for everyone, or even for a given person with every migrainous attack.
As a result, it is not surprising that so many migraine sufferers (migraineurs) express dissatisfaction with their treatment and discontinue treatment despite continued debilitating migraine. Indeed, 44.5% of patients surveyed reported adverse events after using various drugs for migraine, and these side effects were considered serious in 1.7% of those treated.28 The adverse events, including dizziness, nausea, headache, tingling of the fingers or toes, difficulty in thinking, and fatigue, are evidence of the need for safer, more effective medications for the treatment of migraine.29,30 While behavioral management and relaxation training are important complements to pharmacological therapy, drugs remain the mainstay of migraine therapy.31-37
In reviewing the medical literature in an effort to determine the cause of migraine, one repeatedly encounters several consistently documented abnormalities:
Several studies performed since the 1960s have demonstrated that migraine is caused by a primary biochemical disorder of the central nervous system involving neurotransmitters, and serotonin in particular. Serotonin has long been implicated as a key neurotransmitter in migraine.39 The body’s serotonin level falls during a migraine attack.40 Among its other actions, the release of serotonin results in blood vessel constriction in the brain and impaired neural transmission.
The pineal gland, a primary source of serotonin and melatonin, is also known to contribute significantly to migraine attacks.41,42 Research has found that the pineal hormone melatonin is low in migraine patients,43 suggesting impaired pineal function.44 Additionally, several studies have demonstrated that the administration of melatonin to migraine sufferers relieved pain and decreased headache recurrence in some cases.43,45 It has been suggested that the pineal gland could act as the intermediate causative factor of migraine, via a derangement of melatonin.42 The melatonin precursor serotonin showed diurnal variations with opposite phases to melatonin synthesis.46 What this indicates is that serotonin levels rise during the daytime and fall at night. Melatonin levels rise at night and decrease during the day. Stress and dietary habits lead to deficiencies of both serotonin and melatonin. A diminished ratio of melatonin to serotonin leads to a decline in adaptive processes.47 Also, abnormal circadian rhythms of cortisol may occur in states of decreased melatonin.48 Our research supports the hypothesis that migraine is a response to a pineal circadian irregularity, and that the administration of melatonin normalizes this circadian cycle;45 that is, melatonin may play a role in resynchronizing biological rhythm to lifestyle, and may subsequently relieve migraine.
During the last 15 years, many researchers have proposed that migraine is generated by a hyperexcitable brain. A migraine attack can be triggered at any time, depending on the threshold of brain excitability, and in fact, the frequency of migraines is proportional to the excitability level. According to classic theory, a migraine attack is initiated by a cerebrovascular spasm followed by extracranial vasodilatation. This change may be caused by an imbalance in brain biochemistry. Decreased cellular oxygen can cause an increase in the flow of calcium from the extracellular fluid to the intracellular space, resulting in a calcium overload and cellular dysfunction.49 Disturbances in mitochondrial oxidation reactions, magnesium deficiency, or abnormalities of cellular calcium channels may be responsible for the neuronal hyperexcitability between attacks.50 We believe that the restoration of calcium-magnesium balance is one of the critical issues in migraine therapy.