Tag: press release

Chronic Fatigue Patients Show Lower Response To Placebos

Contrary to conventional wisdom, patients with chronic fatigue syndrome respond to placebos at a lower rate than people with many other illnesses, according to the first systematic review of the topic.

According to the new analysis by Dr. Hyong Jin Cho of King’s College London and colleagues, 19.6 percent of patients with chronic fatigue syndrome improved after receiving inactive treatments, compared with a widely accepted figure of about 30 percent for other conditions.

Because the placebo effect seems to be strongest in diseases with highly subjective symptoms, some medical professionals believed it could be as high as 50 percent among CFS patients.

The review, reported in the current issue of Psychosomatic Medicine, pooled data from 29 studies in which 1,016 people with CFS received various placebos.

CFS is a complex illness that has no known cause or cure. Myriad symptoms include severe malaise, muscle and joint pain, sleep and mood disturbances and headache. The symptoms continue for at least six months and cannot be explained by any other medical conditions. The Centers for Disease Control and Prevention estimate that as many as 500,000 Americans may have CFS or related conditions.

With so many mysteries surrounding CFS, a great deal of controversy exists among both doctors and patients as to whether its origins are primarily psychological or physiological. Current evidence suggests that emotional or social stresses such as bereavement or problems at work, combined with other triggers such as common viral infections, contribute to the disorder. Additional factors, such as avoidance of physical activity, may cause the symptoms to become chronic, says Cho.

The authors propose several possible explanations for the surprisingly low placebo response revealed in the analysis. Perhaps patients have low expectations due to the reality that CFS is very difficult to treat and often persists for many years. Alternatively, disconnects between how patients and doctors view the illness “may impede development of a collaborative therapeutic relationship,” reviewers suggest.

The study also showed that the placebo response is 24 percent for medical interventions but only 14 percent for psychiatric/psychological treatments. The authors say the reason may be that many CFS sufferers seen in specialist settings or self-help groups “have a firm conviction that their illness is of physical origin” and thus would have little faith in psychiatric/psychological treatments. This finding supports the idea that the placebo response is greatly influenced by patients’ expectations of improvement.

According to the review, behavioral therapy and graded exercise therapy have benefits, and if patients were more aware of them, says Cho, they might be “more open, more optimistic, and more collaborative with the professionals, and the overall outcome of the treatments could be enhanced.”

Dr. Lucinda Bateman, an internist who specializes in CFS and fibromyalgia and serves on the board of the American Association for Chronic Fatigue Syndrome, has worked with about 500 CFS patients over the past 15 years.

“In my clinical experience, I have found that CFS is among the most difficult conditions to improve at all, with either physical or psychological interventions.” This is true in part, she says, because there is a great deal of variation among patients diagnosed with CFS, and Bateman believes that ultimately CFS may be found to involve more than one disease.

In the absence of a cure, Bateman has found that the most effective treatment for CFS combines improving symptoms with medication, helping patients retain physical conditioning when possible and using psychological and psychiatric interventions to help patients adapt to living with chronic illness.

She doesn’t discount the placebo effect, however. “When you say to people, ‘I believe you, I will help you manage your symptoms, I will advocate for you,’ that hope and feeling of control over their disease could be considered placebo effect, but it’s an important part of delivering medical care.”‘

 

Source: Center For The Advancement Of Health. “Chronic Fatigue Patients Show Lower Response To Placebos.” ScienceDaily. ScienceDaily, 22 March 2005. https://www.sciencedaily.com/releases/2005/03/050322120639.htm

 

Hit-and-run Injury To The Brain: New Evidence On Chronic Fatigue Causation

Press Release: A seven-year tracking study has prompted scientists to suggest that chronic fatigue syndrome could be the result of brain injuries inflicted during the early stages of glandular fever.

Australian researchers have put the suggestion in this week’s Journal of Infectious Diseases, which reveals new findings from the ‘Dubbo Infection Outcomes Study’. Since 1999, a team led by UNSW Professor Andrew Lloyd have been tracking the long-term health of individuals infected with Epstein-Barr virus (EBV), Ross River virus (RRV) or Q fever infection. Their goal is to discover whether the post-infection fatigue syndrome that may affect up to 100,000 Australians is caused by the persistence of EBV, a weakened immune system, psychological vulnerability, or some combination of these.

Glandular fever — sometimes called ‘the kissing disease’ — is caused by Epstein-Barr virus (EBV). Transmitted via saliva, its acute symptoms include fever, sore throat, tiredness, and swollen lymph glands. Most patients recover within several weeks but one in ten young people will suffer prolonged symptoms, marked by fatigue. When these symptoms persist in disabling degree for six months or more, the illness may be diagnosed as chronic fatigue syndrome (CFS).

The researchers followed the course of illness among 39 people diagnosed with acute glandular fever. Eight patients developed a ‘post-infective fatigue syndrome’ lasting six months or longer, while the remaining 31 recovered uneventfully. Detailed studies of the activity of the Epstein-Barr virus in the blood and the immune response against the virus were conducted on blood samples collected from each individual over 12 months.

Commenting on the findings, Professor Lloyd says: “Our findings reveal that neither the virus nor an abnormal immune response explain the post-infective fatigue syndrome. We now suspect it’s more like a hit and run injury to the brain.

“We believe that the parts of the brain that control perception of fatigue and pain get damaged during the acute infection phase of glandular fever. If you’re still sick several weeks after infection, it seems that the symptoms aren’t being driven by the activity of the virus in body, it’s happening in the brain.”

The research team comprising scientists from the University of New South Wales, the University of Sydney and the Queensland Institute of Medical Research plan to test their ‘brain injury’ hypothesis by doing neurological tests on the study participants.

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About the Dubbo Infection Outcomes Study: this is a major prospective cohort study following individuals from the time of onset of documented infection with Epstein-Barr virus (the cause of glandular fever), Ross River virus (the mosquito-borne infection which causes rash and joint pain) and Q fever (an infection common in meatworkers and those exposed to livestock).

Research Paper:
‘Prolonged illness after infectious mononucleosis is associated with altered immunity but not with increased viral load’, The Journal of Infectious Diseases, vol. 193 (2006), pp 664-671. Authors: Barbara Cameron, Mandvi Bharadwaj, Jacqueline Burrows, Chrysa Fazou, Denis Wakefield, Ian Hickie, Rosemary French, Rajiv Khanna, Andrew Lloyd.

Funding: The Dubbo Infection Outcomes Study is 82 per cent funded by the US Centers for Disease Control. It also receives funding from the National Health and Medical Research Council of Australia.

 

Source: University of New South Wales. “Hit-and-run Injury To The Brain: New Evidence On Chronic Fatigue Causation.” ScienceDaily. ScienceDaily, 1 March 2006. https://www.sciencedaily.com/releases/2006/03/060301092926.htm

 

New Hypothesis Proposed For Cause Of Chronic Fatigue Syndrome

Press Release: COLUMBUS, Ohio — Researchers here have proposed a new theory for the cause of chronic fatigue syndrome (CFS) — one that blames the illness both on a low-level viral infection and on the body’s own immune response to that virus.

If true, it would offer an explanation for why virologists so far haven’t found evidence of a common virus when looking at a population of CFS patients. The hypothesis was included in a paper published in the current issue of the American Journal of Medicine.

The new theory, proposed by Ronald Glaser, professor of medical microbiology and immunology, and Janice Kiecolt-Glaser, professor of psychology and psychiatry at Ohio State University, is the latest work in more than two decades of their research on the effects of stress on the human immune system.

“Our data suggests that stress may be causing the expression of certain viral proteins and that these proteins may be modulating the body’s immune response, turning it on or off,”Glaser said.

CFS was first characterized by researchers in the mid-1980s who described it as a combination of symptoms including low-grade fevers, body aches, malaise, and depression among other signs. The condition seems more prevalent among young adult women. Those diagnosed with CFS often experience stress and depression.

Symptoms routinely linger for six months or more and may continue for years. The federal Centers for Disease Control and Prevention estimate that CFS may affect anywhere from four to 10 of every 100,000 people in the United States.

Other researchers have reported higher-than-normal titers of antibodies to various latent viruses — Epstein-Barr virus, cytomegalovirus, human herpes virus 6, for example — in the blood of patients diagnosed as having CFS. But no one viral infection was present in all patients — evidence that would be needed to prove a viral cause of the illness.

The Ohio State researchers’ new theory poses several mechanisms that might be linked to CFS.

Once a person is infected, these viruses can remain latent in the body for long periods of time. Glaser proposes that the viruses could be partially reactivated, that is, viral proteins could be produced at levels high enough to cause a low-grade infection but too low to be seen using current laboratory assays.

Glaser and Kiecolt-Glaser suggest that CFS patients may experience an ongoing, low-grade viral infection — more like a smoldering fire rather than a three-alarm blaze — which could stimulate parts of the immune response without raising antibody titers to typically high levels.

That low-grade infection would be enough to increase production of various cytokines — chemical mediators for the immune system — and begin the immune response.

“A lot of the symptoms that you find in chronic fatigue syndrome are the same ones induced by cytokines during our normal immune response,” Glaser said.

He admits that studies of patients have yet to show a pattern of abnormal cytokine behavior that would substantiate their theory but he has an explanation for that.

“We haven’t discovered all the cytokines involved in immunity. We may not have found the right one, yet,” he said, adding that new cytokines are steadily being identified.

Stress and depression may be playing a related role as well, Kiecolt-Glaser said. Earlier research has repeatedly shown that increased stress and depression can reactivate latent viruses, decrease the body’s immune response, and stimulate the production of certain cytokines linked to some CFS-like symptoms.

“Part of this is a chicken-and-egg problem,” Kiecolt-Glaser said. “People diagnosed with CFS often are depressed since they’re unable to carry out normal, daily activities. What we don’t know is whether the depression followed the diagnosis of CFS or if CFS contributed to it.

“We do know, however, that this kind of depression can weaken our immune response.”

Glaser said researchers need to reconsider past work on CFS.

“We need to look for immune system changes that are much more subtle and specific than those we’ve been using as benchmarks,” he said.

 

Source: Ohio State University. “New Hypothesis Proposed For Cause Of Chronic Fatigue Syndrome.” ScienceDaily. ScienceDaily, 3 November 1998. https://www.sciencedaily.com/releases/1998/10/981031180910.htm

Chronic Fatigue Syndrome Impairs A Person’s Slow Wave Activity During Sleep

Press Release: Chronic fatigue syndrome (CFS) has been associated with altered amounts of slow wave sleep, which could reflect reduced electroencephalograph (EEG) activity and impaired sleep regulation. A study published in the journal SLEEP finds that CFS is also associated with a blunted slow wave activity (SWA) response to sleep challenge, suggesting an impairment of the basic sleep drive and homeostatic response.

The study, authored by Roseanna Armitage, PhD, and colleagues at the University of Michigan, focused on 13 pairs of identical twins discordant for CFS. Analyses, which were restricted to the first four non-REM periods each night in order to show comparability, revealed that SWA, or other sleep EEG measures, did not differ between the CFS and healthy twins during a regular night’s sleep. According to Armitage, it was only after a “challenge” to sleep regulation was introduced (keeping them awake an extra four hours) that the CFS twins exhibited significantly less SWA power in the first non-REM period of recovery sleep and accumulated a smaller percentage of SWA in the first non-REM period than their twin counterparts.

“CFS shares symptoms with depression, and some experts have suggested that it is not a distinctly different disorder,” said Armitage. “We have also conducted studies of SWA response to sleep challenge in depression, and the results are very different. Depressed women did not show a blunted SWA response to sleep challenge. The present CFS study included only women, and none had current depression. Therefore, our results cannot be explained on the basis of depression.”

Experts recommend that adults get between seven and eight hours of sleep each night to maintain good health and optimum performance. Persons who think they might have a sleep disorder are urged to consult with their primary care physician, who will refer them to a sleep specialist.

Article: “The Impact of a Four-Hour Sleep Delay on Slow Wave Activity in Twins Discordant for Chronic Fatigue Syndrome”, Sleep, May 1, 2007.

 

Source: American Academy of Sleep Medicine. “Chronic Fatigue Syndrome Impairs A Person’s Slow Wave Activity During Sleep.” ScienceDaily. ScienceDaily, 7 May 2007. www.sciencedaily.com/releases/2007/05/070501075253.htm

Research Provides More Evidence That Chronic Fatigue Syndrome Is A Legitimate Medical Condition

Press Release: Researchers at Georgetown University Medical Center have found that chronic fatigue syndrome (CFS) may be rooted in distinct neurological abnormalities that can be medically tested. Although the sample studied was small, this research provides objective, physiological evidence that the controversial disorder can be considered a legitimate medical condition.

Chronic fatigue syndrome defines a range of illnesses including fibromyalgia and Gulf War syndrome, all of which have fatigue as a major symptom. Even among medical professionals, there is a disagreement about the causes, diagnosis and treatment of CFS because so much about the disorder remains unknown. One reason CFS is difficult to diagnose is because it shares symptoms with many other diseases, including multiple sclerosis and lupus. Even when other illnesses are ruled out and a CFS diagnosis is given, there is not a standardized course of treatment and it’s difficult for doctors to measure patient improvement. Estimates are that two to four times as many women as men are diagnosed with CFS.

The Georgetown study, published in the November edition of the BMC Neurology Journal, an online publication, reveals that patients diagnosed with CFS and its family of illnesses have a set of proteins in their spinal cord fluid that were not detected in healthy individuals. These proteins might give insight into the causes of CFS and could someday be used as markers to diagnose patients with the disorder.

“For years, patients with chronic fatigue syndrome have suffered from painful symptoms for which there is no blood test, diagnosable physical condition or any method for doctors to measure improvement,” said James Baraniuk, MD, assistant professor of medicine at Georgetown University Medical Center and first author on the study. “Our research provides initial evidence that chronic fatigue syndrome and its family of illnesses may be legitimate, neurological diseases and that at least part of the pathology involves the central nervous system.”

The disorder is characterized by profound fatigue that is not improved by bed rest and that may get worse with physical or mental activity, according to the Centers for Disease Control and Prevention. Persons with CFS usually function at a lower level of activity than they were capable of before the onset of illness, feeling too tired to perform normal activities or easily exhausted with no apparent reason. Patients also report various nonspecific symptoms, including weakness, muscle pain, impaired memory and/or mental concentration, insomnia and post-exertional fatigue lasting more than 24 hours.

The study looked at 50 individuals suffering from at least two disorders related to CFS, including fibromyalgia and Gulf War syndrome. By examining spinal cord fluid in patients with CFS and in healthy individuals, the researchers found that CFS patients have 16 proteins that healthy individuals do not. Five of these 16 proteins are found in all patients with the illnesses but in none of the controls. The results indicate that those 16 proteins could possibly serve as a “biosignature” for the disease and could someday be used to diagnose CFS.

“Although this is a small study and more research on the subject is necessary, these results indicate it might be possible to develop a simple laboratory test to diagnose these disorders in the future,” Baraniuk said.

Other co-authors on the paper include Begona Casada, PhD, and Hilda Maibach, MS, of Georgetown University Medical Center; Daniel J. Clauw, MD, of the University of Michigan; and Lewis K. Pannell, PhD, of the University of South Carolina; and Sonya Hess, PhD, of the National Institute of Diabetes and Digestive and Kidney Diseases.

 

Source: Georgetown University Medical Center. “Research Provides More Evidence That Chronic Fatigue Syndrome Is A Legitimate Medical Condition.” ScienceDaily. ScienceDaily, 10 January 2006. www.sciencedaily.com/releases/2006/01/060110013424.htm

Chronic Fatigue: Clues In The Blood

Press Release: University of New South Wales, July 8, 2007. Researchers at UNSW believe that blood may hold vital insights into what is happening in the brain of patients with chronic fatigue syndrome (CFS).

In a study unparalleled in its scope, a team led by UNSW Professor Andrew Lloyd of the Centre for Infection and Inflammation Research, has studied the differences in gene expression patterns in the blood of people who either recover promptly after acute glandular fever or develop the prolonged illness called post-infective syndrome.

The researchers examined six million pieces of gene expression information for analysis in the project, known as the Dubbo Infection Outcomes Study. The study is named after the NSW town in which the work was conducted. The team studied the expression of 30,000 genes in the blood, testing each of the 15 individuals between four and five times over a 12-month period.

The team was able to narrow its findings to the expression of just 35 genes whose pattern of expression correlated closely with the key symptoms of the illness when examined from onset through to recovery. Gene expression is significant because it is the process by which a gene’s DNA sequence is converted into the proteins which ultimately determine the manifestations of disease.

Since 1999, the team has been tracking the long-term health of individuals infected with Ross River virus (RRV), Q fever infection and Epstein-Barr virus, which causes glandular fever.

“These [35] genes might point to the nature of the disease process that underlies CFS, which is currently unknown,” said Professor Lloyd, who is based in the School of Medical Sciences at UNSW. “None of them are ones that I would have predicted, except for those relating to neurotransmitters,” he concedes. “Some of them relate to transport of zinc and other metal ions within the cell, which may suggest a fundamental disturbance in cellular function.”

The researchers now hope to narrow the focus of research onto the expression of these 35 genes in the blood of a much larger group of subjects from the Dubbo Infection Outcomes Study, with varied patterns of illness and recovery.

“There are very few complex diseases which have been comprehensively analysed, with large scale and longitudinal studies, like this,” said Professor Lloyd. “It sets a standard for highly sophisticated, comprehensive gene expression studies in the blood of all sorts of human diseases from rheumatoid arthritis and multiple sclerosis through to schizophrenia.”

The research paper has been published in the Journal of Infectious Diseases.

 

Source: University of New South Wales. “Chronic Fatigue: Clues In The Blood.” ScienceDaily. ScienceDaily, 8 July 2007. https://www.sciencedaily.com/releases/2007/07/070706090020.htm