Located in the third ventricle of the brain, the pineal gland secretes melatonin, a potent antioxidant and modulatory hormone that mediates the body's response to light/dark cycles, immune dysfunction, stress, and a variety of other physiological and emotional factors. Recently, pineal gland dysfunction has been strongly implicated in the pathogenesis and clinical course of MS. Interestingly, independent research has cited both abnormally high and abnormally low levels as possible triggers for the disease.

MS is more prevalent in northern regions of the globe. One possible explanation is that reduced exposure to sunlight in higher latitudes results in chronic oversecretion of melatonin by the pineal gland. This in turn promotes hypertrophy of the thymus, eventually resulting in the inability of the thymus to entrain T-lymphocytes to distinguish between foreign antigens and cells normally found in the body. Indeed, experimental models show that constant darkness exacerbates the symptoms of autoimmune disease. Based on these findings, one researcher proposed that "intercurrent virus infection and higher melatonin levels in winter could be interactive or synergistic risk factors for the development of MS."1

Another model for the etiology of MS focuses on the potential immune vulnerability posed by a melatonin deficiency. MS rarely strikes an individual before age 15--and one researcher has suggested that this age of onset corresponds with rapidly declining levels of melatonin just before puberty--producing heightened immunological susceptibility. A small study of MS patients with onset of the disease immediately before or after puberty revealed significantly lowered nocturnal levels of melatonin.2

One possible explanation for the apparent discrepancy in these opposing models is that disruptions of melatonin circadian rhythm, involving both unhealthy "highs" and "lows" could be involved in this process.

However melatonin imbalances may be involved in the initial development of the disease, it is deficiencies that seem to correlate with a poorer general prognosis once the disease process is triggered. This may be because remission effects in MS are possibly modulated by the stimulatory influence of melatonin on the immune system. Clinical findings show that when melatonin levels decline, an exacerbation of MS symptoms is often seen.3,4

In one study, 32 MS patients were randomly selected from patients consecutively admitted to a neurology service in a hospital for exacerbations of their symptoms. Nocturnal levels of melatonin and the activity of the pineal gland were monitored over the course of each patient's illness. The study revealed a progressive decline in melatonin levels over the duration of the illness. Since patients with chronic progressive MS had a lower mean melatonin level compared to those with a relapsing-remitting course of the disease, an analysis of melatonin levels may be crucial for understanding the patho-physiology of MS, and specifically, the course of its progression.5

Melatonin is also a metabolite of the important brain neurotransmitter, serotonin. Serotonin depletion is postulated as a possible explanation for some of the relapse symptoms, such as migraine and depression, that often affect MS patients. These disruptions of normal serotonergic mechanisms may act to weaken the blood brain barrier, increasing autoimmune damage to the brain.6

Serotonergic disorders, along with a disrupted patterns of melatonin secretion (normally peak levels of melatonin are released at night and taper off during the day, in what is known as "circadian rhythm"), are also believed to play a role in increased depression among MS patients.7 Restoring the healthy circadian rhythm of melatonin through electromagnetic field treatment has been shown to elicit remarkable symptoms of improvement in some MS patients.7,8

The Melatonin Profile is a noninvasive saliva assessment that analyzes the body's circadian secretion pattern of melatonin, revealing crucial imbalances that could have far-reaching effects on the body's natural immune mechanisms.

References
1 Hutter CD, Laing P. Multiple sclerosis: sunlight, diet, immunology, and aetiology. Med Hypotheses 1996;46(2):67-74.
2 Sandyk R, Awerbuch GI. Multiple sclerosis: the role of the pineal gland in its timing of onset and risk of psychiatric illness. Int J Neurosci 1993;72(1-2):95-106.
3 Sandyk R. Multiple sclerosis: the role of puberty and the pineal gland in its pathogenesis. Int J Neurosci 1993;68:209-25.
4 Sandyk R. The pineal gland and the clinical course of multiple sclerosis. Int J Neurosci 1992;62:65-74.
5 Sandyk R, Awerbuch GI. Relationship of nocturnal melatonin levels to duration and course of multiple sclerosis. Int J Neurosci 1994;75:229-237.
6 Sandyk R, Awerbuch GI. The co-occurrence of multiple sclerosis and migraine headache: the serotoninergic link. Int J Neruosci 1994;76(3-4):249-257.
7 Sandyk R. Suicidal behavior is attenuated in patients with multiple sclerosis by treatment with electromagnetic fields. Int J Neruosci 1996;87(1-2):5-15.
8 Sandyk R. Successful treatment of multiple sclerosis with magnetic fields. Int J Neurosci 1992;66(3-4):237-250.

Call to set up a nutritional consultation so that tests can be performed and a comprehensive strategy of lifestyle, dietary modification and nutrient supplementation can be implemented to aid you in reversing this disorder.

For an appointment, contact our office at: 800-956-7083 and visit our web site www.completehealthinstitute.com go to lab tests and click on appropriate test for information.

Dr. Rispoli, Ph.D., L Ac. has had a clinical practice for over 20 years. Her programs work because she is so thorough in testing and providing a nutritional approach. Remember that the body can heal itself if given the proper nutrients.

The information herein is not intended as diagnosis, treatment or a cure. Should you have a medical condition please seek the advice of your medical doctor.