By Kerry Bone
(Issue: Nov, 2001)
Editor’s Note: We recommend that you discuss herbal treatments with your physician first to prevent adverse interactions with any prescription drugs you may be taking.
I received the following letter from a long-time patient: “I am writing to tell you that I have fully recovered from chronic fatigue syndrome. After my last consultation with you, I resumed paid employment — initially part-time and then full-time. Recently I commenced a new position working as an accountant — my area of employment prior to my illness! I now enjoy an active social life and exercise in the forms of yoga and ice skating. I have learnt to take time out to relax and rejuvenate myself, so that I don’t reach energy sapping levels of fatigue. The help that I received from professionals (such as yourself), friends and family, enabled me to take control of and rebuild my life. I would like to thank you for your help.”
Fortunately Michelle’s story is not an unusual one. Over the years I have seen herbal treatments cause substantial changes for the better in chronic fatigue syndrome (CFS), with many patients completely recovered and returned to full and productive employment, but it does take time! Often patients with CFS are their own worst enemies, switching from one treatment to the next, following every fad and consequently never allowing the gradual restoration of normal energy that herbs can slowly bring about.
What is CFS?
Although the name might be new, chronic fatigue syndrome (CFS) is not a new disorder. While the affliction described as ‘neurasthenia’ in Victorian times does not necessarily represent an early forerunner, the ‘bed cases’ or ‘sofa cases’ reported among middle-class women in the period from 1860 to 1910 probably were CFS.  By the time of World War I, a syndrome resembling CFS was a common complaint in Europe and North America.  CFS is also known as post-viral fatigue syndrome or myalgic encephalomyelitis (ME).
CFS can occur in epidemics. In the June 1951 edition of the Medical Journal of Australia, Dr Richard Pellew reported an epidemic of 800 cases in South Australia. Patients complained of headaches, joint pain, fatigue, depression, lack of concentration and a general feeling of malaise. He called his paper “A Clinical Description of a Disease Resembling Poliomyelitis,” an association which has more recently been emphasized by British scientists who believe that enteroviruses are involved in CFS.
Although the orthodox medical profession was reluctant at first to recognize CFS as a physical disorder, rather than a variant of depression or neurosis, recent scientific evidence supports a physical etiology. Nonetheless, treatment of CFS as a psychiatric problem is still relatively widespread. The scientific community is now showing a great interest in CFS. More than 1000 papers have been published on this topic, many of these in the last three years. A research journal devoted exclusively to the study of CFS was launched: the Journal of Chronic Fatigue Syndrome. The general impression is that the incidence of CFS is increasing, but this may be due to better diagnosis stemming from increased understanding of the disease.
Medical research has now identified a number of abnormalities in CFS. Such research tends to support some of the naturopathic understanding of the disorder. These two approaches can be combined to provide a rational and effective approach to the phytotherapy of CFS.
CFS was formally defined in 1988 as disabling fatigue of at least six months’ duration of uncertain etiology.  Additional symptoms can include mild fever, sore throat, painful lymph nodes, weight gain, exertional malaise, muscle weakness, muscle and joint pain, headaches, depression, light-headedness, anxiety, visual and cognitive impairment and disturbed sleep patterns. It usually has a relatively definite onset which resembles influenza. Six of these additional symptoms must be present, plus two or more of the following signs: low-grade fever, nonexudative pharyngitis, and palpable or tender lymph nodes. 
This clinical definition of CFS has a number of weaknesses, particularly the six months ‘qualifying period’, but currently there is no accepted biochemical test for the condition. Another problem is that the definition is somewhat restrictive. Many patients with chronic, unexplained fatigue and typical symptoms of CFS may not exactly fulfill the above definition.
What Causes CFS?
The fact that CFS can occur in epidemics has always pointed to an infectious origin. However, despite the fact that various researchers have implicated a number of viruses, a clear association with a single viral infection has not been established. Originally Epstein-Barr Virus (EBV) was thought to be the cause, since CFS can follow mononucleosis. More recently, associations with Human Herpes Virus 6 (HHV-6) and Coxsackie B viruses have been studied.
A review of some of the research demonstrates the confused state of our understanding of the role of viruses in CFS. For example a Canadian study found no difference in EBV antibody titers (levels) between CFS patients and controls,  but a US study found antibody evidence of active EBV infection in some patients with CFS.  A majority of a group of US Army reservists who developed CFS after active duty in Saudi Arabia tested positive for either acute or reactivated EBV infection.  However, positive EBV antibody profiles found in many CFS patients are not necessarily indicative of active infection.  Association between CFS and HHV-6 is no clearer, with some studies finding a positive association, [7-9] and as many other studies finding no evidence of HHV-6 involvement in CFS. [9-12]
The announcement of a strong link between CFS and a retrovirus might have been a major breakthrough,  but subsequent investigations have found that retroviruses are not involved in CFS.[14-10] Borna disease virus could be involved,  but a Swedish study found no evidence for such a connection. 
The link between CFS and some kind of enterovirus, possibly a Coxsackie B Virus, was particularly interesting. Coxsackie B viruses are related to the polio virus, which can infect and weaken muscle tissue. There was evidence from British research that enteroviral RNA occurs in the muscle tissue of CFS patients  and this may lead to mitochondrial injury.  However, a Spanish investigation found only minor changes in muscle tissue which did not support the hypothesis that viral infection is a cause of muscle fatigue.  Also the British research group appears to have abandoned their stance on enteroviruses, concluding that it was unlikely that a persistent enterovirus plays a pathogenic role in CFS.  However, an effect in initiating the disease process should not be excluded. 
The only sense which can be made of this research is that:
1. either a number of viruses are capable of triggering CFS, in which case CFS is not an infection in the strict meaning of the term because there is no single causative agent.
2. or that CFS may involve the reactivation of the immune response to previous viral infections. In other words, the immune system may be fighting the ghosts of past viral infections.
It is worthwhile to examine the implications of CFS epidemics. The Royal Free epidemic in London was a famous epidemic where a polio-like illness struck down many people. The illness also affected cranial nerves, which is not a feature of CFS. The majority recovered in a matter of weeks to months, but a significant number went on to develop CFS. These susceptible people among the staff at the Royal Free Hospital were left with CFS, but the original epidemic was probably a Coxsackie viral infection and therefore was not actually CFS.  Hence the CFS was caused by a viral trigger. The fact that the viral infection occurred in an epidemic created a related epidemic of CFS.  It is likely that the same conclusions can be drawn from studying other CFS epidemics. 
Other microorganisms have also been linked to the incidence of CFS. Polymerase chain reaction (PCR) techniques have established a connection between possible mycoplasmal blood infections and CFS in 50 to 60% of patients. [24-26] However, until these organisms are isolated and cultured from the blood of CFS sufferers, such a link must be regarded as tenuous.
Another indirect connection to infection with coagulase negative Staphylococcus, has been described. The pattern of muscle catabolism seen in CFS corresponds to that produced by this organism.  Also CFS and fibromyalgia patients treated with staphylococcus toxoid vaccine do show clinical improvement. 
Infection with yeast, possibly Candida albicans has been hypothesized.  Since there is a high prevalence in CFS sufferers of nonallergic sinusitis and this condition is associated with fungal infection and fungal allergy, it was recently suggested that the upper respiratory tract could harbor a chronic yeast infection in CFS. 
The immune abnormalities which occur in CFS are also inconsistent, perhaps because different viral triggers may cause different malfunctions. One important US study published in The Lancet found no difference between CFS patients and controls for any white blood cell counts, save the CD8 T lymphocytes.  These cells were activated, similar to that which occurs in a viral infection, and the cytotoxic cell subset was increased. These differences were significant (p=0.0l) in patients with major symptoms of CFS. The study was noteworthy because of the large number of patients involved, and also because the degree of these changes corresponded to the severity of the CFS. The authors concluded that immune activation in CFS leads to increased secretion of cytokines which causes the observed symptoms. Their findings were consistent with chronic stimulation of the immune system, perhaps by a virus. If this is correct, the feeling of malaise experienced in the early stages of influenza, when cytokine output is incre ased, is similar to the way CFS sufferers feel most of the time. Cancer patients treated with the cytokine interleukin-2 to boost immunity, experience side effects remarkably similar to CFS. However, the above results were not supported by a study which found evidence of CD4 T lymphocyte activation in CFS patients.  In support of this theory it has recently been shown that levels of TNF-alpha are significantly increased in patients with CFS compared to controls. 
The above research found no indication of reduced natural killer (NK) cell activity, however this finding has been reported in several studies. For example, a correlation between low levels of NK cell activity and severity of CFS was found in 20 CFS patients.  Also a marked decrease in NK cell activity was found in almost all patients with CFS, as compared with healthy individuals.  However, a Danish study found that NK cell activity in CFS patients was no different from healthy controls.  Another relatively common but inconsistent finding is the reduced response of lymphocytes to stimulation by mitogens. [32,37]
An increased occurrence of autoantibodies such as antinuclear antibodies (ANA), [38,39] thyroid antibodies,  and rheumatoid factor  have been found in CFS patients. This, together with an observed high incidence of circulating immune complexes, led a German research team to conclude that CFS is associated with or is the beginning of manifest autoimmune disease.  These findings were supported by a large study on 579 patients from Boston and Seattle which found that levels of immune complexes were abnormal in 35% of CFS patients compared to 2% of controls (p=0.000l), and ANA was abnormally high in 15% of CFS patients compared to 0% of controls (p=0.003).  The same study found that serum cholesterol and IgG levels were also significantly raised in CFS.
Serum levels of some cytokines are often raised in CFS. For example, levels of interleukin-1 alpha,  tumor necrosis factor (TNF) alpha [38,42] and TNF-beta  were significantly more often increased in CFS patients.
Nickel allergy is more prevalent in CFS patients, especially women with CFS, and it was suggested that smoking or diet could be sources of the nickel exposure.  Other workers who found a high incidence of mercury and nickel allergy in CFS sufferers proposed a connection with dental amalgam. 
A study of 24 CFS patients who were 50 years or younger found that 100% had slightly abnormal ECG readings, compared to only 22.4% of controls (p<0.0l).  Mild left ventricular dysfunction was found in 8 of 60 patients with CFS, and gross dysfunction occurred with increasing workloads. 
Simpson and coworkers found that subjects complaining of chronic fatigue were more likely to have abnormally-shaped (nondiscocytic) red blood cells.  They concluded that this association of increased nondiscocytes and impaired muscle function could indicate a cause and effect relationship, which would be in agreement with the physiological concept of fatigue as resulting from inadequate oxygen delivery.  Simpson advocates the use of evening primrose oil and fish oil to decrease nondiscocytes, and given the favorable influence of Ginkgo biloba on red blood cell fragility and blood rheology, it might also be indicated.
Regional cerebral blood flows to the cortex and basal ganglia were significantly reduced in a majority of CFS patients.  This finding of reduced regional cerebral blood flow in CFS is supported by a study in older patients which found that the abnormal blood flow in CFS was different from that observed in depression. 
Delayed orthostatic hypotension caused by excessive venous pooling (and also linked to a subnormal circulating erythrocyte volume) is a frequent finding in CFS, which appears to be linked to fatigue. [50-53]
Magnetic resonance imaging (MRI) scans of the brains of CFS sufferers found a high incidence of inflammation (edema and demyelination) in association with serological evidence of active HHV-6 infection.  This controversial finding of brain abnormalities in CFS has been somewhat supported by a study which observed that CFS patients had significantly more abnormal scans than controls: 27% vs. 2%.  However, the authors felt that this might instead indicate that some patients labelled with CFS could actually be suffering from other medical conditions. Abnormal MRI and single-photon emission computed tomography (SPECT) scans were found with greater frequency in CFS patients compared to normal controls.  SPECT abnormalities were present in 81% of CFS patients versus 21% of control subjects (P[less than]0.01).  The presence of brain abnormalities in CFS, as assessed by MRI, were related to subjective reports of poor physical function. 
It should be stressed that modern techniques of brain imaging are highly sensitive, and these findings do not necessarily indicate gross organic brain defects. They are probably more indicative of a chronic encephalitis which is either viral or immunological in origin.
Pituitary and hypothalamic abnormalities
Patients with CFS have a mild central adrenal insufficiency secondary to either a deficiency of corticotropin-releasing hormone (CRH) or some other central stimulus to the pituitary-adrenal axis.  This leads to a decreased response of the adrenal cortex. The literature on this aspect of CFS was recently reviewed.  It has been suggested that, since cytokines potently influence the hypothalamic-pituitary-adrenal (HPA) axis, their activation may underlie many of the features found in CFS and depression.  Urinary free cortisol was found to be decreased in one study on CFS patients, which suggests hypoactivity of the HPA axis.  However, another study found that salivary cortisol levels were slightly increased in a CFS cohort. 
Arginine-vasopressin secretion was found to be erratic in patients with CFS and also total body water content was increased.  The investigators suggested that these findings might indicate hypothalamic dysfunction in CFS, perhaps triggered by a persistent viral infection.
Further evidence of hypothalamic dysfunction, particularly involving serotonin metabolism, has also been uncovered. Challenge with the drug buspirone, which is a serotonin reuptake inhibitor, causes stimulation of prolactin release. However, after buspirone challenge in CFS patients, the increase in prolactin was greater compared to depressed patients and healthy controls.  This suggests a hypersensitivity of hypothalamic serotonin receptors in CFS patients.
Abnormalities in memory and cognitive function
A number of objective tests have revealed memory deterioration in CFS patients compared to healthy controls, but findings between studies have not been consistent. Short-term memory,  general memory,  retrieval from semantic memory  and memory requiring cognitive effort  have been found to be impaired. However, other studies have found that memory was not impaired,  or was only mildly impaired.  It has bee suggested that impaired information processing, rather than primary memory dysfunction, may underlie the cognitive problem that afflict so many patients with CFS. 
CFS and multiple sclerosis (MS) patients have some similar cognitive abnormalities,  but the impairment is greater in MS.  CFS patients show impaired concentration  and speed of information processing. 
Raised serum ACE levels
Increased serum concentration of angiotensin-converting enzyme (ACE) is a marker for sarcoidosis and diseases involving the blood vessels. Serum ACE levels were also elevated in 80% of patients with CFS as compared with only 9.4% of control subjects. 
Metabolites of various monoamine neurotransmitters were examined in the cerebrospinal fluid (CSF) and plasma of CFS patients.  No differences were found in CFS samples, however basal plasma levels of a noradrenaline metabolite were lower and levels of a serotonin metabolite were higher in patients than in controls.  These findings are not consistent with neurotransmitter patterns seen in depression and could indicate increased sympathetic nervous activity. The investigators felt that these results are compatible with a syndrome marked by chronic lethargy; fatigue and persistent immune stimulation.
Most patients with CFS were found to have sleep disorders which are likely to contribute to the daytime fatigue and may also be important in the etiology of the syndrome. [76,77] CFS patients had significant elevations in fatigue, subjective sleep disturbance and objective sleep disorders compared to MS patients and a healthy control group. 
Muscle and metabolic abnormalities
Behan and coworkers have observed mitochondrial abnormalities in the skeletal muscle tissue of CFS patients.  In support of this finding another research team using exercise tests found a defect of oxidative metabolism, with resultant acceleration of glycolysis in muscle tissue.  This means that muscle cells are quickly depleted of ATP and exhaustion is reached more rapidly. Behan has subsequently shown that levels of the enzyme calcium ATPase, which allows calcium ions to move into the cell to help produce ATP, are abnormally raised in CFS.  He found that CFS patients who exercise have a low rate of oxygen consumption, but at the same time the lactic acid produced in their muscles is significantly increased, which also suggests that oxygen utilization is reduced.
However, other research groups have not supported these findings. Biopsies of muscle tissue from CFS patients did not show consistent abnormalities,  and studies of skeletal muscle physiology in CFS did not reveal any specific metabolic abnormality.  A component of the muscle fatigue in CFS may arise from an inability of the nervous system to fully activate skeletal muscle during intense, sustained exercise.  In other words, the cause of the fatigue may stem from the central nervous system.
Japanese scientists have found lower levels of serum acylcarnitine in CFS, which they proposed might explain the fatigue and muscle weakness.  Also, the concentration of serum acylcarnitine tended to increase to normal with recovery from fatigue in CFS.  However, an open clinical study in 20 CFS patients found no improvement after 3 months of L-carnitine therapy. 
Studies on the magnesium status of CFS patients have not resolved this issue. A study on one patient found considerable improvement after 6 weeks of therapy with intravenous magnesium sulfate,  but a study of 89 patients with CFS found no evidence of magnesium deficiency in any patient. 
When serum folate levels of 60 patients with CFS were assayed it was found that 50% had values below 3.0 mcg/L.  The authors concluded that some CFS patients are deficient in folic acid.
It has been hypothesized that the imbalances in immune function, the HPA axis and the sympathetic nervous system in CFS can be explained by changes in essential fatty acid (EFA) metabolism.  Dietary EFA modulation afforded substantial improvement in a majority of cases.  A Japanese study did find that serum concentrations of EFA’s were depleted in CFS sufferers,  and a controlled clinical trial of evening primrose oil and fish oil demonstrated significant symptom reduction.  However a recent trial did not demonstrate any benefit from EFA supplementation. 
Despite the large number of published studies on CFS, there have been very few clinical trials. In particular, the evening primrose and fish oil study cited above has only been repeated once, with negative results, even though it was conducted 11 years ago.  A Japanese herbal formula was used to successfully treat CFS in an open clinical trial.  This complex tonifying formula included Panax, Rehmannia, licorice, cinnamon, Astragalus, dong quai and Schisandra.
Trials on conventional medical treatments for CFS are also scarce. A clinical trial on the new biological response modifier Ampligen (poly(I).poly (C12U)) has shown promise.  Ampligen is an immunomodulatory drug which is thought to heighten the response to viral infections, but it may have other activities. The disadvantages of Ampligen are that it is very expensive, needs to be administered by injection and is only available in the USA for research use.
The Naturopathic Viewpoint
Like the scientists, most naturopaths cannot agree about CFS. Hence the views expressed here are subjective and based on my own reading and experience.
CFS is a subtle immune dysfunction which might be caused by a complex interaction between emotional, infectious and environmental stressors. This immune dysfunction leads to a state of autotoxicity which can be further exacerbated by previous or current exposure to environmental toxins. For each patient the particular factors which may be contributing to this interaction need to be identified and dealt with through the therapeutic regime. In addition, the abnormalities which are now known to occur in CFS should be countered or corrected.
Because it is geared to the treatment of individual patients, the naturopathic approach is ideally suited to the management of CFS. As the medical research shows, CFS patients differ greatly in their disease expression and a single cause cannot be found. It is a multifactorial disorder, and the factors will vary from patient to patient, although the basic pattern will be the same.
What might this pattern be? In my experience the majority of CFS patients were devitalized before they contracted the disorder. This might have been due to emotional pressures, work pressures, family pressures, ambition, toxins, pregnancy, or even a bad diet, but the end result is the same. This observation is supported by the finding that stress is a significant predisposing factor in CFS.  Any stressor, be it chemical, physical, biological or emotional then acts to aggravate this condition. This reduced capacity to cope with stress is a key factor in creating the vicious cycle which perpetuates the syndrome.
The devitalization then leads to weakened immunity and finally to an abnormal immune response to a viral infection. A stalemate is reached where the resultant hyperimmune state causes autotoxicity, but is not sufficiently focussed to resolve a viral presence, or any other cause, and restore health. It is a curious state where some compartments of the immune system are overactive, but other compartments are deficient.
Other causative factors might either add to the immune dysfunction or to the autotoxicity, or act as stressors to increase devitalization. These include:
* intestinal dysbiosis, endotoxemia or similar syndromes, allergies or food intolerances,
* toxins e.g. dental amalgam, hair dyes, pesticides,
* chronic inflammation or infection.
These additional factors will not apply in every patient; it is a matter of individualization and appropriate treatment.
Herbs for CFS
In general only six to eight herbs should be used at one time, so a judicious selection of the herbs mentioned below should be made on the basis of the individual case history. There is nothing wrong with trying different herbs at different times so that those most suited to the individual patient can be found.
Tonic and adaptogenic herbs
Tonics help revitalize the patient, and adaptogens improve the response to stress. Tonics can also correct immune function. Although the claims made below for individual herbs are generally based on pharmacological or clinical studies, they will not be referenced here. Further details are available in the scientific literature.
Major herbs in this group are:
* Panax ginseng – tonic, adaptogenic, stimulates hypothalamic output and ACTH and hence adrenal cortex function, increases stamina, spares muscle use of carbohydrate.
* Eleutherococeus senticosus — adaptogenic, stimulates Tlymphocyte function.
* Astragalus membranaceus — tonic and immune-enhancing, increases NK cell activity.
* Withania somnifera — is a tonic herb which is not stimulating.
Adrenal restorative herbs
Although the immune-boosting function of these herbs might seem unwise, they do help CFS, often dramatically. For example, an English doctor has reported the successful use of Eleutherococcus for CFS in Russia. 
The main herbs for this purpose are licorice (Glycyrrhiza glabra) and Rehmannia glutinosa. A case study from Japan observed that a CFS patient went into remission when she developed hyperaldosteronism due to an adrenal tumor. When the adrenal tumor was removed the CFS returned.  Licorice in high doses can cause pseudoaldosteronism due to its aldosteronelike action. A high potassium low sodium diet, as in the Gerson therapy, can raise plasma aldosterone. Obviously licorice should not be used in such high doses that it causes pseudoaldosteronism.
These may seem contraindicated, but CFS will stabilize and gradually improve if the immune system can be properly focussed. In addition, immune-enhancing herbs are often needed to help prevent the recurrent viral infections which can plague patients with CFS. Echinacea angustifolia or Echinacea purpurea are safe to use since, on current knowledge, they mainly enhance phagocytic activity. This can improve antigen recognition which leads to better immune responsiveness.
There are a few nontoxic herbs which can depress immune function and may be useful at some stages of treatment. The safest to use is the Indian herb Hemidesmus indicas (Indian sarsaparilla).
Although the viral association is not always clear, these herbs can be useful in many cases. Hypericum perforatum (St John’s wort) has the advantage that it is antiviral and antidepressant, since depression is often a feature of CFS. Hypericum is active against enveloped viruses such as EBV and HHV-6. Thuja occidentalis is also active against enveloped viruses as well as naked viruses such as the wart virus and enteroviruses.
In addition, research found that Hypericum improves cognitive function. It also raises mental capacity in depressed patients.
Other corrective herbs
Ginkgo biloba, Salvia miltiorrhiza and Zanthoxylum clava-herculis (prickly ash) will improve blood flow. Ginkgo decreases erythrocyte fragility, improves blood rheology and improves short-term memory. Valeriana officinalis (valerian), Passiflora incarnata (passionflower), Piper methysticum (kava) and other such herbs will help the disordered sleep pattern. Crataegus (hawthorn) may help any cardiac and circulatory abnormalities. EFA therapy with evening primrose oil and fish oil is recommended.
Notes about treatment
Devitalization is a major part of CFS, so results must be measured in months not weeks. If results are slow to come the patient should be encouraged, since improvement usually does occur with consistent use of herbs. Patients must be instructed not to overexert themselves when they begin to feel improvement as this can cause a relapse. They should only partake in mild exercise and should not exercise beyond the point of fatigue. Sleep helps to restore the immune system and CFS patients will not improve unless they have adequate sleep, which maybe more than they needed previously. They must avoid stress and emotional crises as much as possible. The importance of stress as a cause and sustaining factor of CFS should not be underestimated and appropriate lifestyle measures must be incorporated into the treatment plan.
Some patients with CFS can easily catch infections. If this occurs, the tonic herbs should be discontinued and diaphoretic and immune-enhancing herbs should be administered until the acute stage is over. CFS patients can usually take relatively large amounts of tonics without feeling overstimulated.
Panax and Echinacea can often be of poor quality due to substitutions or poor processing. Hence do not accept the statement from patients that, “I tried Ginseng and it did not work,” until you are sure that they used high quality, authentic preparations.
Case History 1
‘Kylie’ aged 17 had glandular fever six years previously. Suffered from fatigue ever since, but after beginning year 12 fatigue was particularly severe. Often catching colds and influenza, her attendance was less than 50%. Even on ‘well’ days she often did not have the energy to attend school. Herbal treatment consisted of the following basic formula (written for 1 week):
Astragalus membranaceus 1:2 30 mL
Panax ginseng 1:2 15 mL
Ginkgo biloba standardized 20 mL
Echinacea angustifolia 1:2 35 mL
Dose 5 mL with water t.d.s. 100 mL
In addition, Withania 1:2 5 mL once a day was prescribed.
If a cold came on, the above treatment was stopped for three to four days and the following formula was taken:
Zingiber officinale 1:2 10 mL
Echinacea angustifolia 1:2 40 mL
Euphrasia officinalis 1:2 20 mL
Achillea millefolium 1:2 30 mL
Dose 5 mL with warm water up to five times a day. 100 mL
‘Kylie’ had difficulty taking the herbal formula because it was too stimulating. So the dose was reduced to half and gradually increased. There was only slight improvement in her condition for three months, but then gradual and steady progress was made. While she still receives herbal treatment from time to time, she has been free of CFS for several years.
Case History 2
‘John’ was 35 and had not worked for three years. By the time he sought herbal treatment he complained that he was getting sicker and sicker. He had constant headaches, and had chronic sinusitis for about ten years. His history showed a previous high exposure to insecticides and years of overwork due to family pressures. His wife could not cope with his not working and his marriage was strained. Various formulas were given but the treatment settled at the following (for one week):
Panax ginseng 1:2 l5 mL
Astragalus membranaceus 1:2 30 mL
Crataegus spp folia 1:2 20 mL
Ginkgo biloba standardized 20 mL
Picrorrhiza kurroa 1:2 15 mL
Glycyrrhiza glabra 1:1 20 mL
Scutellaria baicalensis 1:2 30 mL
Dose 8 mL with water t.d.s. 150 mL
In addition Echinacea angustifolia 1:2 5 mL once a day was prescribed from time to time. Also an ‘acute formula’ similar to the one above was taken during colds and influenza instead of the basic formula. The Crataegus was for the headaches and circulation and the Baical Skullcap for the sinusitis. ‘John’ actually worsened in the first three months of treatment, probably because of the natural progression of the disorder. However after five months he thanked the friend who recommended herbal treatment, because it was “the best thing I could have done” (in the context of his CFS). He has gradually improved, but still needs to improve further before he can return to full-time employment.
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