Chronic Fatigue Syndrome (CFS) -- Part I
G. Douglas Andersen, DC
There are very few diseases that don't sap a person's energy. When a patient comes in complaining of fatigue, we must take a good history and rule out serious illnesses such as cancer, anemia, viral or bacteria infection, blood sugar abnormalities, sleep disorders, lifestyle problems, and depression, to name a few. For a complete list, please see Holmes, et al.1 When you have ruled out all of these conditions, there is a good chance you have a chronic fatigue patient on your hands.
Many times the chiropractor is not the first professional a chronic fatigue (CF) patient has seen, often coming to us as a last resort. Also, many CF patients will enter our offices not for treatment of CF, but for relief of the musculoskeletal complaints that often accompany it. It is no secret that the allopathic practitioners who believe in CF have a difficult problem treating this condition. There are also many doctors who incorrectly call chronic fatigue patients depressed. Depression certainly can cause fatigue, and many fatigued patients are depressed, but we must find out which came first. Obviously, if every doctor in town tells you that you don't have a problem, it would be hard not to get depressed.
Chronic Fatigue Syndrome (CFS) seems to be a postviral dysfunction of the body's energy production system. It can affect the liver, central nervous system, gastrointestinal system, and immune system. Transport proteins and enzymes involved in metabolism of food components for energy utilization have a decreased ability or inability to penetrate cellular membranes, especially those of the mitochondria. Stationary ergometric testing at UCLA revealed low oxygen consumption in CFS patients. ATP levels are also reduced by both decreased production and increased breakdown.2,3
Diagnosis The diagnosis of CFS includes the following:
1. Sudden onset. Patients can often pinpoint the origin of their problems to specific dates or even a specific hour.
2. Musculoskeletal complaints including headaches, migratory muscle and joint pain, and weakness without inflammation.
3. Neuropsychiatric complaints including loss of concentration, memory, and learning ability. Less common but also seen are visual disturbances, irritability, depression, and sleep disorders.
4. Fatigue exacerbated by activity.
5. Canker sores in the mouth.
6. Crimson crescent pattern and cobblestoning of the pharynx.
7. Indistinct fingerprints.
8. Increased frequency and/or development of allergies to food or environment.
9. Low grade fever.
10. Three to five times more frequent in women than men.1,4,5
If they have the signs and symptoms of CF for six months prior to diagnosis, many people will seek care well before the 26 week mark. Unfortunately, there are no specific tests for CFS. Gerow et al., have a nice review of laboratory, imaging, and biopsy findings that may help confirm or deny CFS.6
Treatment Considerations
As with diagnosis, there is no magic bullet for the treatment of CFS. Nutritional support for CFS can be very complicated. This is not a condition for the nutritional novice. Those of you comfortable with complex nutritional medicine should consider the following when treating CFS patients:
1. Food allergy or subclinical hypersensitivity. Have the patient keep a dietary record and remove whatever foods they consume a lot of for a period of at least three weeks and monitor their symptoms. If there is no change in the most often consumed food, remove the second most often consumed food and repeat. Usually, if a person is unknowingly hypersensitive to a food, it will be one of the top half dozen foods they consume. Food elimination is not easy and requires a patient who is highly motivated, which is not hard to find with patients who truly suffer from this condition. Possible drug and inhalant allergies should also be worked up.
2. Detoxification. A program using nutrient-enriched oligoantigenic proteins is the preferred method of detoxification (professional companies put out such products; check with your representative). Like food elimination, detoxification patients must be highly motivated and when you have completed the detoxification phase of the program, foods are then reintroduced slowly and monitored closely.
3. Dietary modification. Decrease fats, simple carbohydrates, caffeine, and other stressors such as excessive use of over-the- counter medication, alcohol, tobacco, etc. No surprises here. Most people just feel better on a low-fat, low-stressor diet that is high in whole grains, fruits, and vegetables. Fresh fruits and vegetables should be emphasized. Fluid intake should be increased to a minimum of eight servings of water per day with four servings of fresh juice.
References
1.Holmes, Kaplan, Gantz, et al. Chronic fatigue syndrome; A working case definition. Annals of Internal Medicine. 1988, 108:387-389.
2.Cheney, Paul. Preventive Medicine Update. Gig Harbor, WA: Healthcom and Associates. January 1994.
3.Cheney, Paul. Chronic fatigue syndrome as a metabolic disorder. The CFIDS Chronicle. Summer 1993.
4.Rigdon, Scott. Preventive Medicine Update. Gig Harbor, WA: Healthcom and Associates. January 1994.
5.Tobi & Strauss. Chronic mononucleosis -- a legitimate diagnosis. Postgraduate Medicine. 1988, 83: 69-78.
6.Gerow, Poierier, & Alt. Chronic fatigue syndrome. JMPT. October 1992, 15,8: 529-534.
G. Douglas Andersen, DC
Brea, California
Chronic Fatigue Syndrome -- Part II
Last month we reviewed diagnostic criteria of chronic fatigue syndrome (CFS), along with dietary and detoxification considerations. This month our focus will be on the micronutrients that should be considered for the treatment of CFS.
1. Immune system stimulation
Stimulating the immune system can be done with a variety of products such as vitamin A, vitamin C, bioflavonoids, vitamin E, beta carotene, vitamin B6, zinc, copper, manganese, arginine, Echinacea, and thymus, just to name a few. There are many fine immune formulas available to the chiropractic doctor.
2. Mitochondrial support
CFS patients have mitochondrial dysfunction in the form of (1) increased oxidant exposure and damage; (2) decreased oxidative phosphorylation; and (3) membrane permeability changes. The mitochondria is the main user of oxygen in the cell and generates reactive by-products during the production of ATP. Because of its compromised condition in CFS, the requirements for antioxidants are increased both to quench the by-products being produced and to fight the effects of the spreading oxidative damage originally initiated by the causative factors. In addition to the many antioxidants mentioned in #4 for immune function, glutathione and coenzyme Q10 should also be considered. Adequate amounts of the full B complex will help normalize mitochondrial metabolism.1 Normalizing and/or restoring normal mitochondrial membrane function and permeability can be helped with the addition of omega-3 fatty acid supplementation.2
3. Minerals such as chromium, magnesium, and potassium magnesium aspartate.
Chromium is obviously for those CFS patients who also are displaying symptoms of blood sugar abnormalities. Many CFS patients also seem to have decreased intracellular magnesium levels, and magnesium supplementation can often help. Aspartic acid is a carrier molecule that helps deliver potassium and magnesium into the cell. It is also a substrate in the Krebs cycle. Of all the supplements that are touted to decrease fatigue, potassium and magnesium aspartates probably have more positive scientific studies behind them than anything else on the market.3
4. Branch chain amino acids may help CFS patients.
If the tryptophan to BCAA ratio is too high, neurotransmitters made from tryptophan increase, causing physical and mental fatigue.4 When patients first contract CF, the body activates a metabolic pathway that increases the rate of conversion of ATP to cyclic AMP, which is used for immune system stimulation. It seems that CF patients have difficulty turning this pathway off when it is no longer required. The inability to properly regulate this pathway leads to losses of ATP in times of inadequate production. Branch chain amino acids can down-regulate this ATP to cyclic AMP process.5
5. Deficiencies of certain B vitamins, such as folic acid, pantothenic acid, and vitamin B12 have also been the causes and the cures of fatigue, and thus when treating CFS patients, the status of these nutrients should be looked at closely.3
6. The monoester of the fatty acid lauric acid has been shown to have significant antiviral properties.
This is especially important for patients who come in with the symptoms of CF, but who have not waited six months to seek care. Thus, it is likely that the virus is still active in their body and a lauric acid monoester should be considered.
Tough Cases
In cases with inadequate results, make sure your patient is fully complying with the treatment plan. Changing diets, taking supplements, and eliminating bad habits is not easy for a healthy person to accomplish, let alone a sick one. But difficult conditions often have difficult treatment plans.
If your patient has complied, find out if you are the first doctor to treat this condition. If you are, consider a second opinion if you have had no improvement in the symptom complex after eight weeks or if symptoms have been deteriorating after four weeks. If the patient has already been treated by numerous professionals for CFS, and the above scenario of no change in eight weeks or symptom exacerbation after four weeks occurs, re-review all prior records to insure you do in fact have a CFS patient. Next, change all brands of supplements that contain herbs, amino acids, or glandular products. Raw materials, manufacturing, packaging, shipping, and storing are just a few of the many variables that can affect product potency. Substitute multiple vitamin and mineral formulas with individual nutrients or groups of nutrients such as B-complex, macro and microminerals, and antioxidant formulas. Give all accessory nutrients individually. Your professional representatives can help you with this. Needless to say, changing brands and individualizing supplements requires greater patient compliance. However, it is sometimes a necessary step for patients who have fallen through the cracks to get to your office and have continued to tumble through your first line of treatment.
Conclusion
Chronic fatigue syndrome is a complex problem manifesting biochemical individuality in those who suffer from it. It is this author's opinion that a complementary approach including optimal diet, micronutrient support, stress control, and support from family and friends are all necessary components of a successful treatment program.7 Manipulation, modalities, and soft tissue therapy should be utilized as symptoms dictate, taking care not to overtreat. Prescription medication should be reserved for short-term symptom control in acute situations. To round out the optimal treatment team,the inclusion of an MD familiar with or open to nutritional medicine, along with psychological support and professional management (preferably RPT) of an individualized exercise program should be included.
References
1. Bland JS. Advancement in Clinical Nutrition. Healthcom Seminars 1993-94. Gig Harbor, WA: Healthcom and Associates.
2. Behan and Horrobin. Effects of high doses of essential fatty acids on postviral fatigue syndrome. ACTA Neurol. Scand. 1990, 82:209-216
3. Werbach M. Nutritional Influence on Illness (2nd ed.). Tarzana, California: Third Line Press.
4. Newsholme, et al. (1991) Physical and mental fatigue; Do changes in plasma amino acids play a roll? Biochemical Society Transactions. 19: 358-362.
5. Cheney P. Chronic fatigue syndrome as a metabolic disorder. The CFIDS Chronicle. 1993.
6. Gaby A, Wright J. Nutritional Therapy for the '90s. Gaby-Wright Nutritional Institute, Baltimore, MD. September1991.
7. Atkins R. Super Energy in a World of Chronic Fatigue. Wellness Communications, Inc., Alexandria, VA. 1994.
G. Douglas Andersen, DC
Brea, California
S.A.M. G. Douglas Andersen, DC, DACBSP, CCN
Last month, we discussed S-adenosyl-l-methionine (a.k.a. SAM) and focused on the studies where it has been used to treat patients with osteoarthritis. To review, SAM is a naturally occurring intermediate of methionine metabolism. It is a methyl donor and considered a sulfhydryl amino acid.
This month, our discussion will shift to a possible connection between SAM and homocysteine, along with two areas where SAM therapy has shown promise: fibromyalgia and depression. In an interesting Swedish study,1 researchers compared 18 healthy women to 12 women with chronic fatigue syndrome and/or fibromyalgia. They measured homocysteine in both groups. In the serum they did not find any differences, but when researchers looked at cerebrospinal fluid levels, they found that chronic fatigue syndrome patients and fibromyalgia patients had mean values of homocysteine that were triple that of controls.
Excessive homocysteine in the serum is metabolized in two ways:
1.methylation -- folic acid and vitamin B12 facilitate the donation and transfer of their methyl groups to homocysteine to reform methionine. The majority of homocysteine is metabolized this way.
2.transulfuration -- vitamin B6 helps convert homocysteine to cysteine.
Homocysteine History Revisited
Elevated serum homocysteine was linked to the atherosclerotic process 30 years ago by Kilmer McCully, MD. Unfortunately, for decades Dr. McCully's findings were ignored by mainstream medicine. It was only recently that the medical community has acknowledged that Dr. McCully was not misguided, but in fact decades ahead of the rest of the world. In addition to atherosclerosis, homocysteine may be involved in neural tube defects, Down's syndrome and declining brain function.3 Now, we may be adding fibromyalgia and depression to this list.
The SAM Connection
So what role does S-adenosyl-methionine play in cerebrospinal fluid homocysteine levels? Researchers are not yet sure. When SAM donates methyl groups, it is converted to S-adenosyl-homocysteine would appear that more SAM would mean more homocysteine, a situation we want to avoid. However, in the Swedish paper, the authors felt there may be a link in the SAM to ASH ratio, and when SAM levels are low, homocysteine may build up. The SAM to ASH ratio theory was proposed because the authors were aware of studies showing that administration of SAM helps patients with fibromyalgia and depression.
In 1991 Jacobsen, in a double-blind, placebo-controlled study, gave 800 mg of SAM orally to 44 fibromyalgia patients for six weeks. The results of the study showed that SAM administration produced mood elevations along with decreases in pain and fatigue.4
In a 1994 study, Grassetto and Varotto5 gave 800 mg of oral SAM along with a 200 mg intramuscular injection to 47 fibromyalgia patients over a six week period. At the end of the study, the authors used rating scales that showed a 40% reduction of tender point scores and a 35% reduction of depression scores. Measuring depression was included in both fibromyalgia studies, due to the fact that it often accompanies fibromyalgia.
In a study focusing on depression only, 80 postmenopausal women were given 600 mg of SAM in a double-blind, placebo-controlled, randomized trial with a washout. The results of the study showed that when SAM was given for 30 days, the level of depression decreased after 10 days of supplementation.6
Side Effects
SAM is generally very well tolerated in the vast majority of patients who use it. The most common side effects are nausea and other gastrointestinal symptoms. SAM is not recommended for people who suffer from bipolar disorders.
Conclusion
Having another weapon to use for both fibromyalgia and depression is exciting. I will be closely following the literature to see if there are any applications with SAM for chronic fatigue syndrome as well. I expect that with the renewed interest in SAM, scientists will figure out exactly how it works with patients who have fibromyalgia and depression, as well as how it affects homocysteine.
In the meantime, clinicians should make sure that fibromyalgia/chronic fatigue patients are receiving adequate amounts of the B complex, especially vitamin B12, folic acid, and vitamin B6.
Recommendations
The reason SAM has not been available was due to the high cost of manufacturing a stable, bioavailable product. Although SAM can now Hayward, California, the cost is still prohibitive. Based on the studies I have reviewed, I plan to try SAM in the following ways:
1. osteoarthritis patients who are not helped by glucosamine; 2. osteoarthritis patients who cannot tolerate glucosamine;
3. osteoarthritis patients who cannot tolerate nonsteroidal anti-inflammatories; 4. osteoarthritis patients who are concerned about long-term, nonsteroidal anti-inflammatory side effects; and 5. patients with fibromyalgia who are not responding well to their current regimens.
The dosing schedule I will attempt is as follows: For patients over 200 pounds I will dose 1200 mg per day in divided doses. For patients 150-175 pounds, the dose will be 1000 mg. For patients under 150 pounds, the dose will be 800 mg. I will try these amounts for a two-week period, since the literature indicates that people should notice the effects of SAM after one to two weeks of ingestion.
For those patients who feel better after two weeks, I will then reduce their daily dose of SAM by 200 mg and each week reduce SAM by 200 mg per day until the lowest dose that continues to give a benefit is achieved. I anticipate this number will probably be in the range of 400 to 800 mg per day. If a patient does not feel a difference after two weeks of therapy, I will discontinue SAM supplementation due to its high cost. I encourage clinicians who try SAM to share their results (positive or negative) with me.
References
1.Regland. Increased concentrations of homocysteine in the cerebrospinal fluid in patients with fibromyalgia and chronic fatigue syndrome. Scandinavian Journal of Rheumatology 1997;26:301.
2.Andersen GD. Homocysteine. Dynamic Chiropractic March 23, 1998, p. 28.
3.Whitaker. Health and Healing August 1997;7(8):3.
4.Jacobsen, et al. Oral s-adenosyl-methionine in primary fibromyalgia. Double-blind clinical evaluation. Scandinavian Journal of Rheumatology 1991;20:294-302.
5.Grassetto and Varotto. Primary fibromyalgia is responsive to s-adenosyl-l-methionine. Current Therapeutic Research 1994;55:797-806.
6.Salmaggi, Bressa, et al. Double-blind, placebo-controlled study of s-adenosyl-l-methionine in depressed postmenopausal women. Psychotherapy and Psychosomatics 1993;59(1):34-40.
G. Douglas Andersen, DC, DACBSP, CCN
Brought to you by courtesy of:
HURST CHIROPRACTIC CENTER
Dr. Rickey W. Hurst, D.C.
Chiropractic Holistic Physician; Nutritional Analyst
330 Towles Ave.
McMinnville, TN. 37110
(931) 473-7805 [email protected]