-IBIS-1.7.6-
tx
immune system
chronic fatigue syndrome
Nutrition
dietary guidelines
therapeutic foods:
Many factors underlie and aggravate chronic fatigue and nutritional therapies can be used to address them in treating the syndrome; they include: depression, stress, impaired detoxification, chronic infection, impaired immune function, candidiasis and dysbiosis, food sensitivities, subclinical hypothyroidism, hypoglycemia/dysglycemia, hypotension, low or depleted adrenal function, low self-esteem and/or lack of sense of purpose in life.
eating principles:
elimination/rotation diet, rotation diet, rotation diet expanded
calorie percentages: 70% complex carbohydrates, protein 12-15%, fat 15-18%
high fiber
therapeutic foods:
foods that tonify the Kidney, nourish Xue (Blood)
foods rich in Zinc, Vitamins C and B-complex
garlic, onions
meat, beans
fresh juices:
carrot (Walker, p. 137)
carrot and spinach (Walker, p. 137)
carrot, beet, and cucumber (Walker, p. 137)
carrot and celery (Shefi)
celery and sour apple (Shefi)
avoid:
food intolerances (King DS. Biol Psychiatry. 1981 Jan;16(1):3-19.)
coffee, caffeine, sugar, refined foods, processed foods, sweets and candies, stress
(Christensen L, Somers S. Int J Eat Disord. 1996 Jul;20(1):105-109.)
supplements
High-potency multi-vitamin/mineral formula
Vitamin A: 50,000 IU per day.
Folic Acid: 1-10 mg per day; often best to start with a three month trial; to enhance immune function and decrease fatigue and depression.
Pantothenic acid: 250-500 mg per day, especially valuable for adrenal support
Vitamin B12 2,500-5,000 mcg of vitamin B12 via IM injection, every two to three days, for several weeks, especially if deficiency demonstrated upon testing. Researchers and experienced clinicians have used 6,000-70,000 mcg per day; these higher doses are often for a three week initial trial period. Supplementation intended to improve microcirculation while decreasing fatigue, pain and depression.
(Ellis FR, Nasser S. Br J Nutr 1973;30:277-283; Lawhorne L, Rindgahl D. JAMA 1989;261:1920-1923; Lapp CW, Cheney PR. CFIDS Chronicle Physicians Forum, Fall, 1993, 19-20; Gaby AR. Townsend Letter. Feb/Mar 1997, 27.)
Vitamin C, 500-1000 mg three times daily, up to 6-8 g per day, especially valuable for adrenal support. Researchers and experienced clinicians have used 10-15 g per day. Clinical research indicates benefit in improved immune function, decreased pain, and improved microcirculation.
Vitamin E: 200-400 IU per day.
Germanium: 100 mg per day.
Magnesium, especially in a form bound to citrate or Krebs cycle intermediates 200-300 mg three times daily. Some investigators have reported that individuals with chronic fatigue are more likely to demonstrate low levels of magnesium. Supplementation is particularly indicated with decreased magnesium levels in red blood cells; in such cases, 100 mg via IM injection once weekly for six weeks may be recommended. Often combined with Malic acid; typical ratio of 600 mg Magnesium per day and 2400 mg Malic acid per day. An eight week trial period should demonstrate decreased muscle pain if appropriate.
(Friedlander HS. Curr Ther Res 4;1962:441-449; Hicks JT. Clin Med Jan 1964:85-90; Ahlborg H, et al. Acta Physiologica Scandinavia 74;1968:238-245; Cox IM, et al, Lancet 337;1991:757-760; Shaw DL. Am J Med Sci 243;1962:758-769; Gantz NM. Lancet 1991;338:66; Gullestad L, et al. Magnes Trace Elem 10;1991:11-16; Cox IM, et al. Lancet 1991;337:757-760; Howard JM, et al. Lancet 1992;340:426; Clague IF, et al. Lancet 1992;340:124-125; Jessop C. Fibromyalgia Network Newsletter compendium #2, October 1990-January 1992; Hinds G, et al. Ann Clin Biochem 1994;31(Pt. 5):459-461; Grant JE, et al. J Am Diet Assoc 1996;96:383-386; Murray M, Pizzorno J. 1998, 367-368.)
Sodium: Moderate increase in sodium intake has been reported to subjectively reduce symptoms for individuals who have been diagnosed with neurally-mediated hypotension.
(Rowe PC, et al. Lancet 1995;345:623-624.)
Zinc: 30-60 mg per day. Researchers and experienced clinicians have used 135 mg per day; these higher doses are often for a two week initial trial period. Supplementation intended to improve immune function and muscle strength and endurance while decreasing fatigue and pain.
Essential Fatty Acids: 280 mg GLA with 135 EPA daily can faciliuate general improvement. Some researchers have used a combination of 80% evening primrose oil and 20% concentrated fish oil. A three month trial can help determine appropriateness and degree of efficacy.
(Kury PG, et al. Biochem Biophys Res Commun 1974;56:478-483; Rasmussen H, et al. Biochim Biophys Acta 1975;411:63-73; Simpson LO, et al. Proc Univ Otago Med Sch 1984;62:122-123; Kamada T, et al. Diabetes 1986;35:604-611; Behan PO, et al. Acta Neurol Scand 1990;82:209-216; Horrobin DE. Med Hypotheses 1990;32:211-217; Gray JB. Martinovic AM. Med Hypotheses 1994;43:31-42; Warren G, et al. Acta Neurol Scand 1999;99:112-116.)
L-Carnitine: 1-2 g of carnitine taken three times daily may be helpful according to some preliminary research. A three month clinical trial can help determine appropriateness and degree of efficacy. Carnitine is essential for mitochondrial energy production.
(Plioplys AV, Plioplys S. Neuropsycholbiol 1997;35:16-23.)
L-Tryptophan: 100 mg three times daily may be helpful in reduing pain, fatigue and depression, especially in individuals demonstrating symptoms of fibromyalgia. A three month clinical trial can help determine appropriateness and degree of efficacy. Tryptophan is essential for neurotransmitter production.
Coenzyme Q10: 100 mg daily can often provide significant improvement in muscle endurance. A three month trial can help determine appropriateness and degree of efficacy.
DHEA: 5-25 mg twice daily; can be a key therapeutic element when warranted; see DHEA topic in Materia Medica for more information
NADH: In a randomized, double-blind, placebo-controlled crossover study of 26 patients with chronic fatigue syndrome, there was a significant positive response to the use of a reduced form of nicotinamide adenine dinucleotide (NADH) i.e., ENADA the stabilized oral absorbable form.
(Forsyth LM, et al. Ann Allergy Asthma Immunol 1999 Feb;82(2):185-191.)
Adrenal extract: May be especially relevant for individuals with a significant history of severe strses or overwork.
(Tinera, JW. NY State Med J 55;1955:1869-1876; Demitrack, M.A. Ann Med 1994 Feb;26(1):1-5.)
Thymus extract 750 mg crude polypeptide fraction, one to two times daily.
(Murray M, Pizzorno J. 1998, 370)
footnotes
Abraham GE, Flechas ID. Hypothesis: Management of fibromyalgia: rationale for the use of magnesium and malic acid. J Nutr Med 1992;3:49-59.
Ahlborg H, Ekelund LG, Nilsson CG. Effect of Potassium-Magnesium Aspartate on the Capacity for Prolonged Exercise in Man. Acta Physiologica Scandinavia 74;1968:238-245.
Ali M. Ascorbic acid reverses abnormal erythrocyte morphology in chronic fatigue syndrome. Am J Clin Pathol 1990;94:515. Abstract #117.
Ali M. Hypothesis: chronic fatigue is a state of accelerated oxidative molecular injury. J Adv Med 1993;6:83-96.
Anderson R, Oosthuizen R, Maritz R, et al. The effects of increasing weekly doses of ascorbate on certain cellular and humoral immune functions in normal volunteers. Am J Clin Nutr 1980;33:71-76.
Anderson R. Ascorbate-mediated stimulation of neutrophil motility and lymphocyte transformation by inhibition of the peroxidase/H2O2/ halide system in vitro and in vivo. Am J Clin Nutr 1981;34:1906-1911.
Anderson SA, Talbot JM. A Review Of Folate Intake, Methodology And Status. Bethesda, MD: Federation of American Societies for Experimental Biology; 1981.
Anonymous. A follow-up on malic acid. CFIDS Buyers Club, Health Watch Spring 1993.
Bakan P. Confusion, lethargy and leukonychia. J Orthomol Med 1990;5:198-202.
Behan PO, Behan WM, Horrobin D. Effect of high doses of essential fatty acids on the postviral fatigue syndrome. Acta Neurol Scand 1990;82:209-216.
Bell IR, Markley EJ, King DS, Asher S, Marby D, Kayne H, Greenwald M, Ogar DA, Margen S. Polysymptomatic syndromes and autonomic reactivity to nonfood stressors in individuals with self-reported adverse food reactions. J Am Coll Nutr. 1993 Jun;12(3):227-38.
Abstract: This study compared symptom reports and cardiovascular reactivity of a group of 24 individuals recruited from the community who reported a cognitive or emotional symptom caused by at least one food (food-sensitivity reporters, FSR) vs those of 15 controls (C) without a history of food, chemical, drug, or inhalant sensitivities. The main findings were: 1) FSR indicated sensitivities not only to foods, but also to environmental chemicals, drugs, and natural inhalants, as well as significantly more symptoms than C in multiple systems; 2) more FSR than C noted recent state depression and anxiety, as well as higher trait anxiety on the Bendig form of the Taylor Manifest Anxiety Scale; 3) however, on multiple regression analysis, not only depression, but also the number of sensitivities (foods, chemicals, drugs, inhalants), accounted for part of the variance in total number of symptoms (38 and 17%, respectively), whereas none of the affective measures accounted for any of the variance in total number of sensitivities over all subjects; 4) after controlling for depression and anxiety, FSR still showed a trend toward poorer performance on a timed mental arithmetic task (p = 0.16); and 5) FSR and C showed opposite patterns of heart rate change to two different stressful tasks (mental arithmetic and isometric exercise) (group by task interaction, p < 0.05). The data are discussed in terms of a time-dependent sensitization (TDS) process that predicts a cross-sensitizing and cross-reactive role for xenobiotic agents (e.g., foods, chemicals, drugs, and inhalants) and for salient psychological stress in the expression of psychophysiological dysfunctions of FSR. As in other chronically ill populations, negative affect in food-sensitive individuals may explain greater symptom reporting, but not necessarily account for the illness itself. For either a food or a psychological stimulus to begin to elicit sensitized responses, e.g., marked physiological differences from C, FSR may require multiple, intermittent exposures spaced over 5-28 days rather than on only 1 day.
Botez MI, Botez T, Leveille J, et al. Neuropsychological correlates of folic acid deficiency: facts and hypotheses. In: Botez MI, Reynolds EH, eds. Folic Acid in Neurology Psychiatry, and Internal Medicine. New York: Raven Press; 1979:435-461.
Bou-Holaigah I, Rowe PC, Kan J, Calkins H. The relationship between neurally mediated hypotension and the chronic fatigue syndrome. JAMA 1995;274:961-967.
Bralley JA, Lord RS. Treatment of chronic fatigue syndrome with specific amino acid supplementation. J Appl Nutr 1994;46:74-78.
Buist R. Elevated xenobiotics, lactate and pyruvate in C.F.S. patients. J Orthomol Med 1989;4:170-172.
Calkins H, Shyr Y, Frumin H, et al. The value of the clinical history in the differentiation of syncope due to ventricular tachycardia, atrioventricular block, and neurocardiogenic syncope. Am J Med 1995;98:365-373.
Campos Y, Huertas R, Lorenzo G, et al. Plasma carnitine insufficiency and effectiveness of L-camitine therapy in patients with mitochondrial myopathy. Muscle Nerve 1993;16:150-153.
Carmel R. Approach to a low vitamin B 12 level. JAMA 1994;272:1233.
Caruso I, Sarzi Puttini P, Cazzola M, Azzolini V. Double-blind study of 5-hydroxytryptophan versus placebo in the treatment of primary fibromyalgia syndrome. J Int Med Res 1990; 18:201-209.
Christensen L, Somers S. Comparison of nutrient intake among depressed and nondepressed individuals. Int J Eat Disord. 1996 Jul;20(1):105-109.
Abstract: OBJECTIVE: The study investigated the nutrient intake of depressed and nondepressed subjects. METHOD: Twenty-nine depressed subjects and a matched group of nondepressed subjects completed a 3-day food record. RESULTS: Results revealed that depressed and nondepressed groups consume similar amounts of all nutrients except protein and carbohydrates. Nondepressed subjects consume more protein and depressed subjects consume more carbohydrates. The increase in carbohydrate consumption comes primarily from an increase in sucrose consumption. DISCUSSION: The increased carbohydrate consumption is consistent with the carbohydrate cravings characteristic of the depressed and may relate to the development or maintenance of depression.
Christensen L, Bourgeois A, Cockroft R. Dietary alteration of somatic symptoms and regional brain electrical activity. Biol Psychiatry. 1991 Apr 1;29(7):679-682.
Clague JE, Edwards RH, Jackson MJ. Intravenous magnesium loading in chronic fatigue syndrome. Lancet 1992;340:124-125.
Coppen A, Wood K. Tryptophan and depressive illness. Psychol Med 1978;8:49-57.
Cordova A, Alvarez-Mon M. Behaviour of zinc in physical exercise: a special reference to immunity and fatigue. Neurosci Biobehav Rev 1995;19:439-445.
Cox IM, Campbell MJ, Dowson D. Red blood cell magnesium and chronic fatigue syndrome. Lancet 1991;337:757-760.
Creagan ET, Moertel CG, OFallon JR, et al. Failure of high-dose vitamin C (ascorbic acid) therapy to benefit patients with advanced cancer. N Engl J Med 1979;301:687-690.
De Lorenzo F, Hargreaves J, Kakkar VV. Pathogenesis and management of delayed orthostatic hypotension in patients with chronic fatigue syndrome. Clin Auton Res 1997;7:185-190.
De Simone C, Famularo G, Tzantzoglou S, et al. Carnitine depletion in peripheral blood mononuclear cells from patients with AIDS: effect of oral L-carnitine. AIDS 1994;8:655-660.
Delgado PL, Charney DS, Price LH, et al. Serotonin function and the mechanism of antidepressant action. Reversal of antidepressant-induced remission by rapid depletion of plasma tryptophan. Arch Gen Psychiatry 1990;47:411-418.
Demitrack MA. Chronic fatigue syndrome and fibromyalgia. Dilemmas in diagnosis and clinical management. Psychiatr Clin North Am. 1998 Sep;21(3):671-92, viii. (Review)
Demitrack, M.A. Chronic Fatigue Syndrome: A Disease of the Hypothalamic-Pituitary-Adrenal Axis? Ann Med 1994 Feb;26(1):1-5. (Review)
Demitrack MA, Crofford LJ. Evidence for and pathophysiologic implications of hypothalamic-pituitary-adrenal axis dysregulation in fibromyalgia and chronic fatigue syndrome. Ann N Y Acad Sci. 1998 May 1;840:684-97. (Review)
Abstract: Chronic fatigue syndrome (CFS) is characterized by profound fatigue and an array of diffuse somatic symptoms. Our group has established that impaired activation of the hypothalamic-pituitary-adrenal (HPA) axis is an essential neuroendocrine feature of this condition. The relevance of this finding to the pathophysiology of CFS is supported by the observation that the onset and course of this illness is excerbated by physical and emotional stressors. It is also notable that this HPA dysregulation differs from that seen in melancholic depression, but shares features with other clinical syndromes (e.g., fibromyalgia). How the HPA axis dysfunction develops is unclear, though recent work suggests disturbances in serotonergic neurotransmission and alterations in the activity of AVP, an important co-secretagogue that, along with CRH, influences HPA axis function. In order to provide a more refined view of the nature of the HPA dusturbance in patients with CFS, we have studied the detailed, pulsatile characteristics of the HPA axis in a group of patients meeting the 1994 CDC case criteria for CFS. Results of that work are consistent with the view that patients with CFS have a reduction of HPA axis activity due, in part, to impaired central nervous system drive. These observations provide an important clue to the development of more effective treatment to this disabling condition.
Demitrack MA. Neuroendocrine aspects of chronic fatigue syndrome: a commentary. Am J Med. 1998 Sep 28;105(3A):11S-14S. (Review)
Dettori AG, Ponari O. Antalgic effect of cobamamide in the course of peripheral neuropathies of different etiopathogenesis. Minerva Med 1973;64:1077-1082. [Article in Italian]
Deulofeu R, Gascon J, Gimenez N, Corachan M. Magnesium and chronic fatigue syndrome. Lancet 1991;338:641. (Letter)
Ellis FR, Nasser S. A pilot study of vitamin B12 in the treatment of tiredness. Br J Nutr 1973 Sep;30(2):277-283.
Famularo G, De Simone C. A new era for carnitine? Immunol Today 1995;16:211-213.
Forsyth LM, MacDowell-Carneiro AL, Birkmayer GD, et al. The measurement of 5-HIAA urinary concentrations as a predictive marker of efficacy of NADH in chronic fatigue syndrome. Paper presented at the Bi-Annual Research Conference of the American Association for Chronic Fatigue Syndrome (AACFS), Cambridge, MA, October 10-11, 1998.
Forsyth LM, Preuss HG, MacDowell AL, Chiazze L Jr, Birkmayer GD, Bellanti JA. Therapeutic effects of oral NADH on the symptoms of patients with chronic fatigue syndrome. Ann Allergy Asthma Immunol 1999 Feb;82(2):185-191.
Abstract: BACKGROUND: Chronic fatigue syndrome (CFS) is a disorder of unknown etiology, consisting of prolonged, debilitating fatigue, and a multitude of symptoms including neurocognitive dysfunction, flu-like symptoms, myalgia, weakness, arthralgia, low-grade fever, sore throat, headache, sleep disturbances, and swelling and tenderness of lymph nodes. No effective treatment for CFS is known. OBJECTIVE: The purpose of the study was to evaluate the efficacy of the reduced form of nicotinamide adenine dinucleotide (NADH) i.e., ENADA the stabilized oral absorbable form, in a randomized, double-blind, placebo-controlled crossover study in patients with CFS. Nicotinamide adenine dinucleotide is known to trigger energy production through ATP generation which may form the basis of its potential effects. METHODS: Twenty-six eligible patients who fulfilled the Center for Disease Control and Prevention criteria for CFS completed the study. Medical history, physical examination, laboratory studies, and questionnaire were obtained at baseline, 4, 8, and 12 weeks. Subjects were randomly assigned to receive either 10 mg of NADH or placebo for a 4-week period. Following a 4-week washout period, subjects were crossed to the alternate regimen for a final 4-week period. RESULTS: No severe adverse effects were observed related to the study drug. Within this cohort of 26 patients, 8 of 26 (31%) responded favorably to NADH in contrast to 2 of 26 (8%) to placebo. Based upon these encouraging results we have decided to conduct an open-label study in a larger cohort of patients. CONCLUSION: Collectively, the results of this pilot study indicate that NADH may be a valuable adjunctive therapy in the management of the chronic fatigue syndrome and suggest that further clinical trials be performed to establish its efficacy in this clinically perplexing disorder.
Friedlander, HS. Fatigue as a Presenting Symptom: Management in General Practice. Curr Ther Res 4;1962:441-449.
Fuchs D, Weiss G, Wachter H. Pathogenesis of chronic fatigue syndrome. J Clin Psychiatry 1992;53:296. (Letter)
Fukuda K, Straus SE, Hickie I, et at. The chronic fatigue syndrome: a comprehensive approach to its definition and study. International Chronic Fatigue Syndrome Study Group. Ann Intern Med 1994;121:953-959.
Gaby AR. Literature Review and Commentary. Townsend Letter for Doctors and Patients. Feb/Mar 1997, 27. (Review)
Gantz NM. Magnesium and chronic fatigue. Lancet 1991;338:66. (Letter)
Gerster H. The role of vitamin C in athletic performance. JAm CoIl Nutr 1989;8:636-643.
Godfrey PS, Toone BK, Carney MW, et al. Enhancement of recovery from psychiatric illness by methylfolate. Lancet 1990;336:392-395.
Goldberg A. No article title available. CFIDS Chronicle, Summer/Fall 1989.
Goodman KI, Salt WB 2nd. Vitamin B12 deficiency. Important new concepts in recognition. Postgrad Med 1990;88:147-150,153-158.
Grant JE, Veldee MS, Buchwald D. Analysis of dietary intake and selected nutrient concentrations in patients with chronic fatigue syndrome. JAm Diet Assoc 1996;96:383-386.
Grau JM, Casademont I, Pedrol E, et al. Chronic fatigue syndrome: studies on skeletal muscle. Clin Neuropathol 1992;11:329-332.
Gray JB, Martinovic AM. Eicosanoids and essential fatty acid modulation in chronic disease and the chronic fatigue syndrome. Med Hypotheses 1994;43:31-42.
Gullestad L, Oystein Dolva L, Birkeland K, Falch D, Fagertun H, Kjekshus J. Oral versus intravenous magnesium supplementation in patients with magnesium deficiency. Magnes Trace Elem. 1991-92;10(1):11-16.
Abstract: The efficacy of oral magnesium supplementation in correcting magnesium deficiency was examined in a group of 40 elderly patients with suspected magnesium deficiency. The patients were randomized in a double-blind, placebo-controlled fashion to oral magnesium-lactate-citrate for 6 weeks. Magnesium status was assessed by an intravenous magnesium-loading test at baseline and after treatment. For comparison, another group of 23 patients received 30 mmol magnesium sulfate intravenously daily for 7 days. A group of 30 patients without known predisposition to magnesium deficiency and a group of 27 young healthy subjects served as controls. The initial magnesium-loading test in the placebo group reduced magnesium retention from a mean 41% (95% confidence intervals 34-49) to 22% (15-29) (p less than 0.01). In the group receiving oral magnesium supplementation for 6 weeks, magnesium retention decreased from 39% (31-47) to 10% (2-18) (p less than 0.01), which was significantly better than with placebo treatment (p less than 0.01). The magnesium retention after oral magnesium supplementation was comparable to that observed after parenteral administration of magnesium for 7 days, 6% (-4 to 16), and to that in the reference groups of patients 4% (-2 to 10) and healthy control subjects 3% (-2 to 8). The study suggests that the bioavailability of orally given magnesium-lactate-citrate is satisfactory, and that oral administration of magnesium for 6 weeks may restore magnesium depots in patients with magnesium deficiency.
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Heap LC, Peters TJ, Wessely S. Vitamin B status in patients with chronic fatigue syndrome. JR Soc Med 1999;92:183-185.
Heseker H, Kubler W, Pudel V. Westenhoffer J. Psychological disorders as early symptoms of a mild-to-moderate vitamin deficiency. Ann N YAcad Sci 1992;669:352-357.
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Hinds G, Bell NP, McMaster D, McCluskey DR. Normal red cell magnesium concentrations and magnesium loading tests in patients with chronic fatigue syndrome. Ann Clin Biochem 1994;31(Pt. 5):459-461.
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Horrobin DE. Post-viral fatigue syndrome, viral infections in atopic eczema, and essential fatty acids. Med Hypotheses 1990;32:211-217.
Howard JM, Davies S, Hunnisett A. Magnesium and chronic fatigue syndrome. Lancet 1992;340:426. (Letter)
Jacobson W, Saich T, Borysiewicz LK, et al. Serum folate and chronic fatigue syndrome. Neurology 1993;43:2645-2647.
Jessop C. Fibromyalgia Network Newsletter compendium #2, October 1990-January 1992.
Johnston CS, Collison R. Capillary fragility as a functional measure of vitamin C status. J Am Coll Nutr 1996;15:536.
Judy W. Southeastern Institute of Biomedical Research, Bradenton, Florida. Presentation to the 37th Annual Meeting, American College of Nutrition, October 13, 1996.
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Kaminski M, Boal R. An effect of ascorbic acid on delayed-onset muscle soreness. Pain 1992;50:317-321.
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King DS. Can allergic exposure provoke psychological symptoms? A double-blind test. Biol Psychiatry. 1981 Jan;16(1):3-19.
Abstract: Clinical ecologists report that exposure to allergens can induce cognitive and emotional symptoms as well as somatic symptoms in susceptible individuals, but controlled tests are meager. In a test of the hypothesis that sublingual exposure to allergens would produce cognitive-emotional symptoms in allergy patients, double-blind provocative testing was conducted at an allergy clinic; 30 allergy patients complaining of at least one psychological symptom were selected. Self-report, heart-rate, and several mood and psychological performance measures were obtained. MMPI scores indicated a pathological sample. Reported cognitive-emotional symptoms were greater for allergens than for placebos (p = 0.001), while placebo symptoms were equal to base rate. Greater variability of heart rate change was found for allergens than for placebos (p = 0.008). Severe reactions occurred more frequently to allergens (p = 0.008). Severe reactions occurred more frequently to allergens (p = 0.02). Other dependent measures were not affected by the allergens or the placebos. It is concluded that allergens may contribute to psychopathology in some individuals.
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Kinsman RA, Hood J. Some behavioral effects of ascorbic acid deficiency. Am J Clin Nutr 1971;24:455-464.
Krotkiewski M, Gudmundsson M, Backstrom P, Mandroukas K. Zinc and muscle strength and endurance. Acta Physiol Scand 1982;116:309-311.
Kuratsune H, Yamaguti K, Takahashi M, Misaki H, Tagawa S, Kitani T. Acylcarnitine deficiency in chronic fatigue syndrome. Clin Infect Dis 1994 Jan;18 Suppl 1:S62-67.
Kuratsune H, Yamaguti K, Lindh G, Evengard B, Takahashi M, Machii T, Matsumura K, Takaishi J, Kawata S, Langstrom B, Kanakura Y, Kitani T, Watanabe Y. Low levels of serum acylcarnitine in chronic fatigue syndrome and chronic hepatitis type C, but not seen in other diseases. Int J Mol Med. 1998 Jul;2(1):51-56.
Abstract: Recently, we found a serum acylcarnitine (ACR) deficiency in Japanese patients with chronic fatigue syndrome (CFS). To clarify whether this ACR abnormality is a characteristic of CFS or not, we also studied the levels of serum carnitine in Swedish subjects. Both serum ACR and free carnitine (FCR) levels in normal healthy subjects were quite different between Japanese (n=131) and Swedish people (n=46) (p<0.001). However, it is confirmed that Swedish patients with CFS (n=57) also had serum ACR deficiency (p<0.001). When we studied the levels of serum ACR and FCR in Japanese patients with various kinds of diseases (CFS, hematological malignancies, chronic pancreatitis, hypertension, diabetes mellitus, chronic hepatitis type C, psychiatric diseases), a significant decrease in the levels of serum ACR was only found in patients with CFS and chronic hepatitis type C (p<0.001). Therefore, we concluded that ACR deficiency in serum might be a characteristic abnormality in only certain types of diseases.
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Lapp CW, Cheney PR. The rationale for using high-dose cobalamin (Vitamin B 12). The CF1DS Chronicle Physicians Forum Fall 1993;19-20.
Lapp CW. Chronic fatigue syndrome is a real disease. North Carolina Family Physician 1992;43:6-11.
Lapp CW. Q: Given the complexities and diversity of symptoms of CFIDS, how do you approach the treatment of CEIDS patients? The CFIDS Chronicle PhysiciansForum March 1991;1(1).
Lawhorne L, Rindgahl D. Cyanocobalamin injections for patients without documented deficiency. Reasons for administration and patient responses to proposed discontinuation. JAMA. 1989 Apr 7;261(13):1920-23.
Abstract: We reviewed the records of 1222 patients who attended a newly acquired rural satellite clinic and found that 120 (10%) had been receiving regular cyanocobalamin injections, but that only 4 (3%) met accepted criteria for its administration. Open-ended interviews with 48 of these patients revealed that they had been receiving cyanocobalamin injections for a mean of 9.9 years for 3.3 symptoms each and with a mean effectiveness rating of 2.9 (scale, 0 to 4). After receiving education regarding the appropriate indications for cyanocobalamin injections, 25 (52%) of the patients were willing to stop receiving them at least temporarily. However, 18 patients (38%) who were younger and who reported greater symptom relief would actively seek a physician who would continue to administer cyanocobalamin. Our findings suggest that some patients who have been receiving cyanocobalamin injections but who do not have a documented deficiency will stop receiving the injections when presented with reasonable alternatives.
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Abstract: Carnitine is essential for mitochondrial energy production. Disturbance in mitochondrial function may contribute to or cause the fatigue seen in Chronic Fatigue Syndrome (CFS) patients. Previous investigations have reported decreased carnitine levels in CFS. Orally administered L-carnitine is an effective medicine in treating the fatigue seen in a number of chronic neurologic diseases. Amantadine is one of the most effective medicines for treating the fatigue seen in multiple sclerosis patients. Isolated reports suggest that it may also be effective in treating CFS patients. Formal investigations of the use of L-carnitine and amantadine for treating CFS have not been previously reported. We treated 30 CFS patients in a crossover design comparing L-carnitine and amantadine. Each medicine was given for 2 months, with a 2-week washout period between medicines. L-Carnitine or amantadine was alternately assigned as fist medicine. Amantadine was poorly tolerated by the CFS patients. Only 15 were able to complete 8 weeks of treatment, the others had to stop taking the medicine due to side effects. In those individuals who completed 8 weeks of treatment, there was no statistically significant difference in any of the clinical parameters that were followed. However, with L-carnitine we found statistically significant clinical improvement in 12 of the 18 studied parameters after 8 weeks of treatment. None of the clinical parameters showed any deterioration. The greatest improvement took place between 4 and 8 weeks of L-carnitine treatment. Only 1 patient was unable to complete 8 weeks of treatment due to diarrhea. L-Carnitine is a safe and very well tolerated medicine which improves the clinical status of CFS patients. In this study we also analyzed clinical and laboratory correlates of CFS symptomatology and improvement parameters.
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