Get FREE U.S. Shipping on $75 Orders*

A Descriptive Questionnaire-Based Study on the Use of Biobran (MGN3), in Chronic Fatigue Syndrome

1 Star2 Stars3 Stars4 Stars5 Stars (75) votes, average: 3.11 out of 5

Author: Dr. Julian Kenyon

(Issue: Nov, 2001)


Biobran (MGN3, an Arabinoxylan compound), is a glyco-protein derived from rice bran and is produced by the partial hydrolysis of the water-soluble hemi cellulose fraction of rice bran by carbohydrases derived from lentius edodes mycelia. This preparation has been shown to enhance human natural killer cell activity (Ghoneum, 1998).

Chronic fatigue syndrome is characterised by deficiency of natural killer cell activity (Caligiuri M, Murray C, Buchwaldd, et al, 1987). We therefore decided to try the use of Biobran on 10 patients with chronic fatigue syndrome for a 2-month period, assessing their progress by the use of a visual analogue scale, and a Likert scale of fatigue (See Appendix I), (Guyatt G.H., Townsend M, Berman L.B., Keller J.L., 1987). We also used a fatigue scale (Chalder T, Berelowitz G, Pawlikowska T, et al, 1993). (See Appendix II).

Chronic fatigue syndrome (CFS) is a debilitating disease of increasing social and economic importance. Although women are statistically more susceptible than men, the disease has been diagnosed in children, adults and wide range of ethnic groups (Jordan et al. 1998). Current observation suggests a prevalence of between 10 and 100 cases per 100,000 in the USA. (Levine, 1997). CFS is characterised by persistent relapsing fatigue of greater than six month’s duration that is not alleviated by rest and is exacerbated by moderate exercise (Fukuda et al., 1994, Krupp et al., 1991).

Against this background of fatigue, a range of other manifestations are common, but vary greatly amongst sufferers. These include muscle and joint pain, sore throat and swollen lymph nodes. A further range of symptoms relates to brain dysfunction such as poor concentration, light sensitivity, sleep disturbance and migraine attacks. Case definition requires the presence of four symptoms in addition to chronic fatigue, and the exclusion of other medical conditions which may present a similar picture (Komaroff et al., 1996).

The diversity of the clinical picture of chronic fatigue suggests a multi-factorial disease with perhaps a common underlying mechanism. Many models of the illness have been studied, but causation remains obscure. The evidence for the involvement of a pathogenic agent, such as a virus or a toxin or a variety of toxins, in at least a proportion of CFS sufferers seems likely. Most noticeably, on several occasions where the disease has produced localized epidemics suggestive of a transmissible agent (Jenkins, 1991).

The majority of sporadic cases, are characterized by acute onsets and often described as post-viral syndromes (Behan, 1997, Chalder et al.1995). Attempts to identify a specific pathogen has been inconclusive although several agents remain under suspicion, including the Epstein Barr virus and cytomegalovirus (Diluca et al., 1995, Koo 1989, Martin 1997, Patnaik et al. 1995). The most convincing evidence points to an involvement of an enterovirus in some cases (Archard et al., 1998, Behan et al., 1991, B owies et al. 1993, Cunningham et al., 1990, Galbraith et al 1997, Nairn et al. 1995, Swanink et al., 1994).

Perhaps the most contentious model for CFS is that it is a neurological and psychiatric illness. The extensive neurological symptoms, supported by objective measurements certainly demonstrate that brain function is impaired (Dopino and Kane 1996, Tiersky et al., 1997). At the molecular level, measurements of neurotransmitters indicate that brain disturbances are related to, but distinct from, depressive conditions (De Luca et al., 1997, Gorbach and Bartlett, 1996). Cognitive behavioural therapy has been offered to patients with varying degrees of success, but these studies shed little light on the initial cause of the illness (Deale et al. 1997).

Materials and Methods

Ten patients were recruited from the author’s clinical practice. These were ten consecutive chronic fatigue patients who came to see the author following the delivery of sufficient Biobran (supplied by Daiwa Pharmaceuticals, Tokyo, Japan), to carry out this study. The patients were given an Informed Consent and asked whether they wished to take part in the study. They were then issued enough Biobran (supplied in sachets of powder, taken three times a day, each sachet mixed with a glass of water and taken by mouth half an hour after each meal), to last two months. They were asked to fill out a fatigue scale (Chalder et al., 1993), and a visual analogue scale, and a Likert scale of fatigue (Guyatt et al., 1987). They were asked to fill out the same questionnaire and visual analogue scale and Likert scale of fatigue at the end of two months.


The fatigue questionnaire was scored with the first box (See Appendix II) scored as one, the second as two, the third as three and the fourth as four. The scores are represented in Figure 1.

From these results, four patients clearly improved (Patients 1, 2, 8 & 10). One patient withdrew (Patient 3, because following three weeks’ course of Biobran she developed mouth ulcers and facial spots appeared; it was unclear as to whether these symptoms were related to the Biobran; she decided at that point to withdraw from the study.) Two patients, (4 & 9), got worse, and three patients (5,6 & 7), showed no change.

Of this group of chronic fatigue syndrome patients, Patients 1, 2, 8 and 10 had clear viral etiologies. Patient 3, who withdrew, also had a clear viral etiology but withdrew from the study. Patients 4 and 9 had unclear initial causation. They both experienced significant stress in their business and personal lives during the time of the study so there is a possibility of these external factors being responsible for the deterioration seen over the two-month period in these patients.

Patients 5, 6 and 7, had clear toxic causations to their chronic fatigue syndrome. Patient 5 had had longterm exposure to poisonous laboratory chemicals, which brought on the slow onset of chronic fatigue syndrome. Patients 6 and 7 had long continued exposure to organophosphate pesticides used in cultivation of mushrooms commercially. Following this, chronic fatigue syndrome developed in both of them.


The only patients to show significant improvement, have clear viral etiologies. It is in this group of patients that decreased natural killer cell activity has been noted, (Caligieuri M, et al., 1987). Chronic fatigue syndrome has been commonly noted after toxic exposure, particularly to organophosphates. In these patients no abnormalities in natural killer cell activity has been observed. Two of the patients with unclear etiologies, are difficult to comment on.

Two side effects were noted in Patient 3 and Patient 10. The side effects in Patient 3 have been noted and resulted in this patient withdrawing from the study. In Patient 10, marked cervical lymphadenopathy developed after two weeks of taking Biobran, and continued throughout the whole time the patient was on Biobran. This was taken as indicating immune system activation. This was Patient 10, who obtained an improvement.


In those patients with a clear viral etiology of chronic fatigue syndrome, Biobran produced significant improvement. This improvement persisted for approximately six weeks following stopping the Biobran, (an effect noted by Ghoneum, 1998).

This study shows that Biobran is effective in patients with chronic fatigue syndrome who have a clear viral etiology. It does not appear to benefit patients with alternative causations of chronic fatigue syndrome. It would be wise to measure natural killer cell activity of patients with chronic fatigue syndrome before commencing Biobran treatment, and to reserve treatment only for those patients with depressed natural killer cell activity. This paper would support such an approach.


Archard LC, Bowles NE, Behan PO, Bell EJ, & Doyle D (1988). Post-Viral Fatigue Syndrome – Persistence of Enterovirus RNA in Muscle and Elevated Creatine-Kinase. Journal of the Royal Society of Medicine 81, 326-329.

Behan PO (1997). Chronic Fatigue Syndrome after Viral Infections. Sports, Exercise and Injury 3, 31-36.

Behan WMH, Gow J, Clements GD, More IAR & Behan PO (1991). Enteroviral Sequences and Mitochondrial Lesions in Muscle Biopsies of Patients with Post-Viral Fatigue Syndrome. Journal of Pathology 163,A 154A-154.

Bowles NE, Bayston TA, Zhang HY, Doyle D, Lane RJM, Cunningham L, Archard LC (1993). Persistence of Enterovirus RNA in muscle biopsy samples suggest that some cases of chronic fatigue syndrome result from a previous inflammatory viral myopathy. Journal of Medicine 24, 145-160.

Caliguri M, Murray C, Buchwald et al., Phenotypic and functional deficiency of natural killer cells in patients with chronic fatigue syndrome. J Immunol 139, 3306-3313, 1987.

Chalder T, Berelowitz G, Powlikowska T, et al. Development of the fatigue scale. J. Psychosom. Res. 1983;37:147;153.

J. Chron, Dis, 1987, 40:1129-1133.

Chronic Fatigue Syndrome in Children and Adolescents: A Review. Journal of Adolescent Health 22, 4-18.

Chalder T, Wessely S, Wallace P, Hirsch S, and Wright D, (1995). Viral Illness and Chronic Fatigue (Syndrome). Lancet 346, 449-449.

Cunningham L, Bowles NE, Lane RJM, Dubowitz V, Archard LC (1990). Persistence of Enterovirus RNA in chronic fatigue syndrome is associated with the abnormal production of equal amounts of positive and negative strands of enteroviral RNA. Journal of General Virology 71, 1399-1402.

Deale A, Chalder T, Marks L, Wessely S (1997). Cognitive Behaviour Therapy for Chronic Fatigue Syndrome: A Randomised Controlled Trial. American Journal of Psychiatry 154, 408-414.

De Luca D, Zorzenon M, Mirandola P, Colle R, Botta GA, Cassai E (1995). Human Herpes Virus – 6 and Human Herpes Virus – 7 in Chronic Fatigue Syndrome. Journal of Clinical Microbiology 33, 1660-1661.

De Luca J, Johnson SK, Ellis SF and Natelson BH (1997). Cognitive Functioning is impaired in patients with chronic fatigue syndrome devoid of psychiatric disease. Journal of Neurology, Neurosurgery and Psychiatry 62, 161-155.

Dipino RK, Kane RK (1996). Neurocognitive Functioning in Chronic Fatigue Syndrome, Neuropsychology Review 6, 47-60.

Fukuda K, et al. (1994). The chronic Fatigue Syndrome – a comprehensive approach to its definition and study. Annals of Internal Medicine 121, 953-959.

Galbraith DN, Nairn C and Clements GB (1997). Evidence for Enteroviral Persistence in Humans. Journal of General Virology 78, 307-312.

Gorbach SL, Bartlett JG (1996).Depression and Chronic Fatigue Syndrome. Infectious Disease in Clinical Practice 5, 461-461.

Ghoneum M. Advancement of natural killer cell activity by modified arabinoxylane from rice bran (MGN-3). Int. J Immuno Therapy XIV (2) 89-99 (1998).

Guyatt GH, Townsend M, Berman LB, Keller JL. A comparison of Likert and visual analogue scales for measuring change in function. Jenkins R (1991). Epidemiology – Lessons from the Past. British Medical Bulletin 47, 952-965.

Jordan KM, Landis DA, Downe MC, Osterman SK, Thurm AE and Jason LA (1998).

Komaroff AL, Fagioli LR, Geiger AM, Doolittle TH, Lee J, Kornish J, Gleit MA and Guerriero RT (1996). An Examination of the Working Case Definition of Chronic Fatigue Syndrome. American Journal of Medicine 100, 56-64.

Koo D (1989). Chronic Fatigue Syndrome – A Critical Appraisal of the Role of Epstein Barr Virus. Western Journal of Medicine 150, 590-596.

Krupp LB, Mendelson WB, and Friedman R (1991). An Overview of Chronic Fatigue Syndrome. Journal of Clinical Psychiatry 52, 403-410.

Levine PH (1997). Epidemiologic Advances in Chronic Fatigue Syndrome. Journal of Psychiatric Research 31, 7-18.

Martin WJ (1997). Detection of RNA Sequence and Cultures of a Stealth Virus isolated from the cerebrospinal fluid of a health care worker with chronic fatigue syndrome – Case Report. Pathobiology 65, 57-60.

Nairn C, Galbraith GDN & Clements GB (1995). Comparison of Coxsackie-B Neutralisation and Enteroviral PCR in Chronic Fatigue Patients. Journal of Medical Virology 46, 310-313.

Patnaik M, Komaroff AL, Conley E, Ojoamaize EA, Peter JB (1995). Prevalence of Igm antibodies to Human Herpes Virus – 6 Early Antigen (P41/38) in Patients with Chronic Fatigue Syndrome. Journal of Infectious Disease 172, 1364-1367.

Swanink CMA, Vercoulen J, Galama JMD, Roos MTL, Meyaard L, Vandervenjongekrijg J, Denijs R, Bleijenberg G, Fennis JFM, Miedema F, Vandermeer JM (1996). Lymphocyte sub-sets apoptois and cytokines in patients with Chronic Fatigue Syndrome. Journal of infectious Disease 173, 460-463.

Tiersky LA, Johnson SK, Lange G, Natelson BH, De Luca J (1997). Neuropsychology of Chronic Fatigue Syndrome: A Critical Review. Journal of Clinical and Experimental Neuropsychology 19, 560-568.

COPYRIGHT 2001 The Townsend Letter Group

COPYRIGHT 2001 Gale Group

ProHealth CBD Store


1 Star2 Stars3 Stars4 Stars5 Stars (75) votes, average: 3.11 out of 5

Leave a Reply