by Martin Joynes, April, Toronto, Ontario
A slew of recent evidence and rare U.S. and international patents have accelerated research on one of the body's chief defences against illness, the essential, yet little-known protein, glutathione (GSH). Medical patents for natural health interventions are few and far between in the world of chemically-based drugs.
"In the next five or six years, people are going to be using the word glutathione as commonly as they use the word vitamin C or antioxidant, says Dr. Jimmy Gutman, a Montreal-based physician and author of "GSH, Your Body's Most Powerful Protector, Glutathione."
Because GSH plays so many roles in cell metabolism, overwhelming research now supports its application in scores of diseases, including cancer, heart disease, stroke, Alzheimer's, chronic fatigue syndrome and fibromyalgia. But that's just the tip of the medical iceberg.
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BACKGROUND: Disabling fatigue is the main illness related reason for prolonged absence from school. Although there are accepted criteria for diagnosing chronic fatigue in adults, it remains uncertain as to how best to define disabling fatigue and Chronic Fatigue Syndrome (CFS) in children and adolescents.
In this population-based study, the aim was to identify children who had experienced an episode of disabling fatigue and examine the clinical and demographic differences between those individuals who fulfilled a narrow definition of disabling fatigue and those who fulfilled broader definitions of disabling fatigue.
METHODS: Participants (aged 8-17 years) were identified from a population-based twin register. Parent report was used to identify children who had ever experienced a period of disabling fatigue.
Standardised telephone interviews were then conducted with the parents of these affected children. Data on clinical and demographic characteristics, including age of onset, gender, days per week affected, hours per day spent resting, absence from school, comorbidity with depression and a global measure of impairment due to the fatigue, were examined. A narrow definition was defined as a minimum of 6 months disabling fatigue plus at least 4 associated symptoms, which is comparable to the operational criteria for CFS in adults.
Broader definitions included those with at least 3 months of disabling fatigue and 4 or more of the associated symptoms and those with simply a minimum of 3 months of disabling fatigue. Groups were mutually exclusive.
RESULTS: Questionnaires were returned by 1468 families (65% response rate) and telephone interviews were completed on 99 of the 129 participants (77%) who had experienced fatigue. There were no significant differences in demographic and clinical characteristics or levels of impairment between those who fulfilled the narrower definition and those who fulfilled the broader definitions. The only exception was the reported number of days per week that the child was affected by the fatigue. All groups demonstrated evidence of substantial impairment associated with the fatigue.
CONCLUSIONS: Children and adolescents who do not fulfil the current narrow definition of CFS but do suffer from disabling fatigue show comparable and substantial impairment. In primary care settings, a broader definition of disabling fatigue would improve the identification of impaired children and adolescents who require support.
Abstract: The definition of disabling fatigue in children and adolescents
(08-15-2005)
Fowler T, Duthie P, Thapar A, Farmer A.
BMC Fam Pract. 2005 Aug 9;6(1):33 [Epub ahead of print]; PMID: 16091130
[PubMed - as supplied by publisher]. To view this abstract online, just go to www.pubmed.gov and search on PMID: 16091130
Rowan Hooper, 21 July 2005; NewScientist.com news service
AT LONG last, we are beginning to get to grips with chronic fatigue syndrome. Differences in gene expression have been found in the immune cells of people with the disease, a discovery that could lead to a blood test for the disorder and perhaps even to drugs for treating it.
The symptoms of chronic fatigue syndrome have been compared to those of a really bad hangover: extreme weakness, inability to think straight, disrupted sleep and headache. But unlike a hangover, the symptoms linger for years, devastating people's lives.
While nobody doubts CFS exists, just about every aspect of it is controversial. Some say it is the same as myalgic encephalomyelitis, or ME; others disagree. Many specialists are convinced it does have a biological basis, but pinning down physical abnormalities common to all patients has proved tough. People with CFS have often received little sympathy from doctors who dismiss it as "all in the mind".
Now Jonathan Kerr's team, which is moving to St George's University of London, has compared levels of gene expression in the white blood cells of 25 healthy individuals with those in 25 patients diagnosed as having CFS according to strict criteria. The researchers found differences in 35 of the 9522 genes they analysed using DNA chip technology.
The few similar studies done in the past have produced conflicting results, so the team double-checked their results using a more accurate method called real-time PCR. That confirmed that 15 of the genes were up to four times as active in people with CFS, while one gene was less active. The results will appear in the Journal of Clinical Pathology next month.
Kerr is repeating the study in 1000 CFS patients and healthy controls, this time looking at 47,000 gene products. So far, the larger study backs up the earlier results, he told New Scientist.
If Kerr really has succeeded where many have failed, and identified clear physical changes in people with CFS, the lingering opinion that it is "all in the mind" could finally be laid to rest. "This exciting new work shows that some aspects of this complex illness may be understandable in molecular terms, and that CFS is not a 'made up' illness," says Russell Lane, a neurologist at Charing Cross Hospital in London.
It should also be possible to develop a blood test for CFS. The team has already discovered differences in blood proteins related to the changes in gene expression.
Kerr hopes the work might even lead to treatments. "We have shown that a significant part of the pathogenesis resides in the white blood cells and in their activity," he says. "It will open the door to development of pharmacological interventions."
Several of the genes identified by the team in CFS play important roles in mitochondria, the power factories of our cells. "The involvement of such genes does seem to fit with the fact that these patients lack energy and suffer from fatigue," Kerr says.
One of these gene products, EIF4G1, is involved in protein production in mitochondria. It is hijacked by some viruses, so cells may compensate by ramping up gene expression. "I am excited by the paper," says Basant Puri, a CFS expert at Hammersmith Hospital in London. "The group's finding of upregulation of EIF4G1 is consistent with subclinical persistent viral infection."
This fits in with the idea that CFS is sometimes triggered by viruses such as Epstein-Barr, Q fever, enteroviruses and parvovirus B19. "CFS often begins with a flu-like illness which never goes away," Kerr says.
Of the other genes whose expression varies in CFS patients, some are involved in regulating the activity of the immune system. Others play important roles in nerve cells, including a gene called NTE, which codes for an enzyme affected by organophosphates and nerve gases.
Journal reference: Journal of Clinical Pathology (vol 58, p 823, 860)
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