CFS

Chronic Fatigue Syndrome Linked to Low T3 Syndrome

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Some people with the condition known as chronic fatigue syndrome (CFS) have low circulating levels of the thyroid hormone triiodothyronine (T3) and normal levels of thyroid-stimulating hormone (TSH), new research shows. The results suggest these patients may be in a hypometabolic state, but one expert thinks the low levels are more likely a consequence, rather than a cause, of CFS.

The findings, based on 98 patients with CFS and 99 age- and sex-matched controls, were published online March 20 in Frontiers in Endocrinology by Begoña Ruiz-Núñez, a PhD student at the University of Groningen, the Netherlands, and colleagues.

Several CFS symptoms resemble those of hypothyroidism but without the marked increase in TSH. This is also the case, the authors point out, in the so-called low T3 syndrome. Low T3 syndrome, also known as euthyroid sick syndrome, is characterized by decreased serum T3 and/or thyroxin (T4) levels, increased reverse T3 (rT3), and no significant increase in TSH.

This low T3 syndrome might be in line with recent metabolomic studies that point to a hypometabolic state (Proc Natl Acad Sci U S A. 2016;113:E5472-E5480), and if confirmed, T3 and iodide supplements may be indicated as treatments, say Núñez and colleagues.

But endocrinologist Willard H Dere, MD, professor of internal medicine at the University of Utah, Salt Lake City, isn’t convinced.

“The limited data are consistent with what is seen in other inflammatory and chronic disease states. There is no current evidence that thyroxine or tri-iodothyronine replacement in those with low T3 syndrome is beneficial. Furthermore, in hypothyroid patients on thyroxine replacement, the use of tri-iodothyronine, along with L-thyroxine, is thought by some experts to be beneficial, but this view is not a consensus,” he told Medscape Medical News.

Differences Seen in Thyroid Hormones, Inflammatory Markers

The patients were recruited from a single clinic in Amsterdam, and all had been diagnosed with CFS based on 1994 criteria. However, those criteria differ in several ways from more recent definitions of what is now termed myalgic encephalomyelitis (ME)/CFS, including those published by the US Institute of Medicine (IOM) in 2015.

Both definitions include disabling fatigue that lasts more than 6 months and does not improve with rest, and cognitive impairment. However, the IOM criteria place post-exertional malaise as central to the diagnosis, whereas it’s not required in older definitions. Moreover, the IOM criteria don’t require that other potentially fatiguing illnesses be ruled out before making the diagnosis, whereas the older definition does.

In the current study, the 21 men and 77 women with CFS had a mean age of 43 years and body mass index (BMI) of 22 kg/m2. The 23 men and 76 women who were control participants had a mean age of 39 years and BMI of 23 kg/m2, which were not significantly different from the CFS group.

Compared with controls, the CFS group had lower levels of free triiodothyronine (FT3), total T4 (TT4), total T3 (TT3), percent TT3, sum activity of peripheral deiodinases (SPINA-GD), and secretory capacity of the thyroid gland (SPINA-GT), as well as lower ratios of TT3/TT4, FT3/FT4, TT3/FT3, and TT4/FT4, and higher percent rT3 and rT3/TT3 ratio.

There were no differences between groups in other thyroid hormone parameters, notably TSH, FT4, rT3, and percent TT4.

FT3 levels below the reference range were more frequent in the CFS group (16/98) compared with controls (7/99; P = .035), with an odds ratio of 2.56 (95% CI, 1.00 – 6.54).

However, Dere commented, “The subset of patients with the low T3 syndrome is relatively small, and their laboratory values don’t vary substantively from that of the control group. Overall, I think the probability of a low T3 syndrome causing ME/CFS is low.”

In measures of metabolic inflammation, no significant differences were found in white blood count, high-sensitivity C-reactive protein (hsCRP), tryptophan/kynurenine ratio, or urinary isoprostanes, but the CFS group did have lower kynurenine and tryptophan levels than controls.

Ferritin was higher and HDL-cholesterol was lower in patients with CFS. Zonulin, a parameter of intestinal permeability, was also lower in patients with CFS compared with controls.

Measures of nutritional factors influencing thyroid function and inflammation that differed between the groups included 24-hour urinary iodine output, a proxy of iodine status, which was lower in patients with CFS. Plasma selenium was similar, but intracellular selenium was higher in patients with CFS. Vitamin D [25(OH)D] status of patients with CFS was higher, but 59% of patients with CFS and 83% of controls presented with 25(OH)D levels below the optimal cutoff of 80 nmol/L, Ruiz-Núñez and colleagues report.

In two sensitivity analyses that excluded patients with the highest levels of inflammatory markers, all the prior findings remained significant except FT3, which was no longer significantly lower in the CFS group.

Markers of Inflammation: Cause or Consequence?

Overall in both groups, FT3, TT3, TT4, and rT3 were positively related with hsCRP.

“The limited data from this study correlates other markers of inflammation with the presence of low T3 and high reverse T3, and are consistent with what is seen with other inflammatory and chronic disease states,” Dere noted.

He added that the low T3 state “seems to be the result, not the cause, of a systemic or localized inflammatory or chronic disease state. During caloric deprivation, the fall in T3 is believed to be an adaptive response directed to saving energy and protein for enduring this acute stress. Thus one can speculate that with some chronic disorders, the diminished plasma T3 helps to preserve caloric expenditure.”

Overall, Dere said he wouldn’t change clinical practice based on these findings. “A serum TSH is a good screening test to rule out primary thyroidal disorders.”

Words prompt us to notice what our subconscious sees.

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It’s a case of hear no object, see no object. Hearing the name of an object appears to influence whether or not we see it, suggesting that hearing and vision might be even more intertwined than previously thought.

Studies of how the brain files away concepts suggest that words and images are tightly coupled. What is not clear, says Gary Lupyan of the University of Wisconsin in Madison, is whether language and vision work together to help you interpret what you’re seeing, or whether words can actually change what you see.

Lupyan and Emily Ward of Yale University used a technique called continuous flash suppression (CFS) on 20 volunteers to test whether a spoken prompt could make them detect an image that they were not consciously aware they were seeing.

CFS works by displaying different images to the right and left eyes: one eye might be shown a simple shape or an animal, for example, while the other is shown visual “noise” in the form of bright, randomly flickering shapes. The noise monopolises the brain, leaving so little processing power for the other image that the person does not consciously register it, making it effectively invisible.

Wheels of perception

In a series of CFS experiments, the researchers asked volunteers whether or not they could see a specific object, such as a dog. Sometimes it was displayed, sometimes not. When it was not displayed or when the image was of another animal such as a zebra or kangaroo, the volunteers typically reported seeing nothing. But when a dog was displayed and the question mentioned a dog, the volunteers were significantly more likely to become aware of it. “If you hear a word, that greases the wheels of perception,” says Lupyan: the visual system becomes primed for anything to do with dogs.

In a similar experiment, the team found that volunteers were more likely to detect specific shapes if asked about them. For example, asking “Do you see a square?” made it more likely than that they would see a hidden square but not a hidden circle.

James McClelland of Stanford University in California, who was not involved in the work, thinks it is an important study. It suggests that sight and language are intertwined, he says.

Lupyan now wants to study how the language we speak influences the ability of certain terms to help us spot images. For instance, breeds might be categorised differently in different languages and might not all become visible when volunteers hear their language’s word for “dog”. He also thinks textures or smells linked to an image might have a similar effect on whether we perceive it as words.

Source: http://www.newscientist.com

Chronic fatigue syndrome scientist finds a temporary home.

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Judy Mikovits is taking her work on the road. The embattled chronic fatigue syndrome (CFS) researcher will conduct her arm of a study sponsored by the US National Institute for Allergy and Infectious Disease (NIAID) on the condition’s link to certain retroviruses at another US government laboratory, the scientist overseeing the study told Nature today.

W. Ian Lipkin, director of the Center for Infection & Immunity at Columbia University in New York, says that Mikovits will team up with her former mentor Frank Ruscetti at his laboratory at the US National Cancer Institute (NCI) in Frederick, Maryland. They are one of three groups testing dozens of blinded blood samples from CFS patients and healthy controls for XMRV and related retroviruses.

Mikovits had been slated to perform the study while at the Whittemore-Peterson Institute for Neuro-Immune Disorders (WPI) in Reno, Nevada. But she was fired from her job in September for not sharing a cell line with another scientist there. She was arrested in California last month and charged in Nevada with possessing stolen lab notebooks and other materials that belonged to the WPI. She also faces a civil suit in connection to the materials, some of which have since been returned to the WPI (read ‘Embattled scientist in theft probe’ for more details).

Mikovits and Ruscetti collaborated on a 2009 Science paper that suggested that CFS patients were far more likely to be infected with XMRV than healthy people.

After numerous labs failed to find the virus, the NIAID tapped Lipkin last year to lead a multi-centre study examining the link. The ‘Lipkin study’ involves Mikovits and Ruscetti, researchers at the National Institutes of Health and the US Food and Drug Administration who identified sequences of viruses related to XMRV in CFS patients, and a team at the US Centers for Disease Control and Prevention that has been unable to find any trace of XMRV (for a run-down of the entire episode see our story ‘Fighting for a cause‘).

“[The WPI is] no longer involved because the whole point was to have Mikovits try to reproduce her work, and having someone else at the institute do so wouldn’t address the questions,” Lipkin says. “It’s critical that she do the work. She doesn’t have a lab at present, so it’s going to be done at NCI.”

Lipkin had initially hoped to have the study done by the end of this year, but he now says that only about half of the samples are ready to send to researchers. He plans to meet with Ruscetti and Mikovits tomorrow to hear their plans for conducting the study. “We’re going to get through this as rapidly as we can, but make certain what we present to people is going to be complete,” Lipkin says.

Lipkin says that he is convinced by work from John Coffin’s team at the NCI, showing that XMRV emerged in the 1990s as a lab contaminant and is unlikely to underlie CFS (see Science raises questions about XMRV). But he says those findings do not rule out the possibility that CFS patients are infected with related retroviruses that, for some reason, only Mikovits has been able to detect.

Lipkin came to Mikovits’s defence in her latest troubles. He says that she should be entitled to keep a copy of her laboratory records and lamented her arrest. “It’s very, very ugly and the sooner we put all this behind us the better off we’re all going to be,” he says.

Neither Mikovits nor Ruscetti could be reached for comment, but we will update this post if they get back to us.

Hat tip to CFS: A novel blog, which reported today that Mikovits and Ruscetti were looking for a site to conduct their portion of the Lipkin study.

Source:Nature.

 

Chronic fatigue syndrome scientist finds a temporary home.

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0


Judy Mikovits is taking her work on the road. The embattled chronic fatigue syndrome (CFS) researcher will conduct her arm of a study sponsored by the US National Institute for Allergy and Infectious Disease (NIAID) on the condition’s link to certain retroviruses at another US government laboratory, the scientist overseeing the study told Nature today.

W. Ian Lipkin, director of the Center for Infection & Immunity at Columbia University in New York, says that Mikovits will team up with her former mentor Frank Ruscetti at his laboratory at the US National Cancer Institute (NCI) in Frederick, Maryland. They are one of three groups testing dozens of blinded blood samples from CFS patients and healthy controls for XMRV and related retroviruses.

Mikovits had been slated to perform the study while at the Whittemore-Peterson Institute for Neuro-Immune Disorders (WPI) in Reno, Nevada. But she was fired from her job in September for not sharing a cell line with another scientist there. She was arrested in California last month and charged in Nevada with possessing stolen lab notebooks and other materials that belonged to the WPI. She also faces a civil suit in connection to the materials, some of which have since been returned to the WPI (read ‘Embattled scientist in theft probe’ for more details).

Mikovits and Ruscetti collaborated on a 2009 Science paper that suggested that CFS patients were far more likely to be infected with XMRV than healthy people.

After numerous labs failed to find the virus, the NIAID tapped Lipkin last year to lead a multi-centre study examining the link. The ‘Lipkin study’ involves Mikovits and Ruscetti, researchers at the National Institutes of Health and the US Food and Drug Administration who identified sequences of viruses related to XMRV in CFS patients, and a team at the US Centers for Disease Control and Prevention that has been unable to find any trace of XMRV (for a run-down of the entire episode see our story ‘Fighting for a cause‘).

“[The WPI is] no longer involved because the whole point was to have Mikovits try to reproduce her work, and having someone else at the institute do so wouldn’t address the questions,” Lipkin says. “It’s critical that she do the work. She doesn’t have a lab at present, so it’s going to be done at NCI.”

Lipkin had initially hoped to have the study done by the end of this year, but he now says that only about half of the samples are ready to send to researchers. He plans to meet with Ruscetti and Mikovits tomorrow to hear their plans for conducting the study. “We’re going to get through this as rapidly as we can, but make certain what we present to people is going to be complete,” Lipkin says.

Lipkin says that he is convinced by work from John Coffin’s team at the NCI, showing that XMRV emerged in the 1990s as a lab contaminant and is unlikely to underlie CFS (see Science raises questions about XMRV). But he says those findings do not rule out the possibility that CFS patients are infected with related retroviruses that, for some reason, only Mikovits has been able to detect.

Lipkin came to Mikovits’s defence in her latest troubles. He says that she should be entitled to keep a copy of her laboratory records and lamented her arrest. “It’s very, very ugly and the sooner we put all this behind us the better off we’re all going to be,” he says.

Neither Mikovits nor Ruscetti could be reached for comment, but we will update this post if they get back to us.

Hat tip to CFS: A novel blog, which reported today that Mikovits and Ruscetti were looking for a site to conduct their portion of the Lipkin study.

Source:Nature.

 

What is CFS?

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Chronic fatigue syndrome (CFS) is characterised by prolonged fatigue associated with a wide range of accompanying symptoms. It has also been called post-viral fatigue syndrome, myalgic encephalomyelitis (ME) or chronic fatigue.

CFS can affect people of any age. However, it’s most common between the ages of 25 and 45. It’s estimated that about 150,000 people in the UK have CFS, with women affected more often than men.

CFS symptoms

To be diagnosed with CFS an adult must have severe chronic fatigue for at least four months with no other medical condition identified as the cause. They must also have one or more of the following symptoms:

  • Substantial impairment in short-term memory or concentration
  • Sore throat
  • Tender lymph nodes
  • Muscle pain
  • Multi-joint pain without swelling or redness
  • Headaches of a new type, pattern or severity
  • Unrefreshing sleep
  • Post-exertional malaise lasting more than 24 hours

Other symptoms that may occur include:

  • Abdominal pain
  • Alcohol intolerance
  • Bloating
  • Chest pain
  • Chronic cough
  • Diarrhoea
  • Dizziness
  • Dry eyes or mouth
  • Earaches
  • Irregular heartbeat
  • Jaw pain
  • Morning stiffness
  • Nausea
  • Night sweats
  • Psychological problems, such as depression, irritability, anxiety, panic attacks
  • Shortness of breath
  • Skin sensations
  • Tingling sensations
  • Weight loss

In general, the symptoms of CFS aren’t improved by bed rest and may be worsened by physical or mental activity.

Preventing CFS

Since it’s not known what causes CFS, it’s difficult to prevent. There’s no evidence to support the view that CFS is a contagious disease and there’s no precise identified cause.

It’s believed that a person’s genes may make them more susceptible, and that viral infection, stress, depression, or a major life event (for example bereavement, job loss) may act as triggers for CFS to develop in susceptible individuals.

In some cases a specific disease, such as an underactive thryoid gland or a head injury, can be identified as the underlying cause of the sort of symptoms typically found in CFS. A range of tests and investigations are done when a person first consults their doctor with symptoms, in order to check for these diagnoses and rule out them out as a cause. So CFS remains a diagnosis of exclusion (where all other identifiable medical causes for symptoms have been ruled out).

CFS treatments

There’s no specific treatment for CFS either. However, medicines can be prescribed to relieve the symptoms: for example, painkillers may be given for muscle pains and headaches, and antidepressants for depression.

Behaviour therapy, physiotherapy, occupational therapy, counselling, relaxation therapy, and graded exercise may help. Reducing stress, eating a healthy diet, rest periods, pacing and support groups also help many people with CFS.

Source:BBC Health News.

 

 

Understanding anger

It’s important to realise several things about anger before you start tackling it. First, anger is a normal process that has allowed humans to evolve and adapt. It isn’t a bad thing in itself, but problems occur if it isn’t managed in the right way.

Anger is also a mixture of both emotional and physical changes. A big surge of energy goes through your body as chemicals, such as adrenaline, are released.

Once the cause of the anger is resolved, you may still have to deal with the physical effects – all that energy has to go somewhere. This can be taken out on another person, such as a partner, or an object – by punching a wall, for example. This last option can lead down the road to self-harm.

The other alternative is to suppress the energy until the next time you’re angry. This may mean you release so much pent-up emotion that you overreact to the situation. Realising this can lead to feelings of shame or frustration when you reflect on your actions, and to further repression of your feelings.

On the other hand, just letting your anger go in an uncontrolled fashion can lead to a move from verbal aggression to physical abuse – don’t forget, the other person is probably feeling angry with you too.

But there is a flip side to anger. Because of the surge of energy it creates, it can be pleasurable. This feeling is reinforced if becoming angry allows the release of feelings of frustration, or if a person’s response to your anger gives you a sense of power.

It’s important to acknowledge and keep an eye on this side of the problem – it can have an almost addictive element.

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Recognising why you get angry

It’s important to be aware of the positive feelings you get from anger as well as the negative ones.

By recognising the positive and negative feelings associated with your anger, it’s important to find other means of achieving and concentrating on the positives ones.

Each person’s positives are different, so there will be different solutions for everyone, but some strategies might include:

  • Trying a non-contact competitive sport.
  • Learning relaxation or meditation.
  • Shouting and screaming in a private, quiet place.
  • Banging your fists into a pillow.
  • Going running.

Any of these may help to vent your frustration and burn off any feelings you’re bottling up.

Anger management techniques

However, this still leaves the problem of dealing differently with those situations that make you angry. This takes practice.

The first thing to do is list the situations that make you angry. Note down exactly what it is about them that makes you angry – it may be the immediate situation, or it could be that it represents a build-up of issues you haven’t resolved.

Now ask yourself four questions about your interpretation of these situations:

  • What evidence is there to show this is accurate?
  • Is there another equally believable interpretation of what’s going on here?
  • What action can I take to have some control of the situation?
  • If my best friend were in this situation, what advice would I give to them?

This won’t dispel the anger for every situation, but when you’re angry it can be difficult to assess a situation accurately. If a situation arises unexpectedly and you feel your temper rising, walk away and complete this exercise if you can.

If your anger isn’t resolved by this, make sure you’ve given enough thought to what exactly you’re angry about. You need to be sure exactly before you can resolve it. It will usually involve a person, but not necessarily the one who’s the target of your anger in the situation and this is the person you need to work the situation out with.

To do this, find a time to raise the problem when you feel more in control of your temper. It may be a good idea to agree a time in advance.

CUDSAIR

It may feel like a tall order to discuss the issue without getting angry, but following a plan may help. Professor Richard Nelson-Jones has developed a good structure to use, called CUDSAIR. This stands for:

  • Confront.
  • Understand.
  • Define.
  • Search.
  • Agree.
  • Implement.
  • Review.

First, it’s important that you confront the problem and not the person. State the nature of the problem and how it makes you feel. Be clear that it’s the problem – not the person – that makes you feel like this. This way you’ll develop a joint definition and ownership of what’s going on.

Next, it’s important to understand each other’s view of the situation. It may help to agree that each person should be able to say what they think about the problem without being interrupted by the other. After this, identify areas where you disagree. Don’t discuss the disagreements yet, just agree that you disagree. This is how you define the problem.

The next step is to search for solutions. Here, be as outrageous as you like – but again, don’t make personal attacks. Generate as many possible solutions as you can – at the moment, it doesn’t matter how unrealistic they seem.

Finally, you have to agree on a solution. This is probably the most delicate part of the whole process. It’s important that you both make concessions and acknowledge those that the other person has made. It’s also important not to have unrealistic expectations – it’s likely that the final solution won’t be ideal for either of you, but the resulting compromise will probably be better than the problems the anger generated.

It’s important that you both keep to the agreement. It’s also important not to overreact to any breaches. Point them out, but there’s no need to get angry. You have the agreement to back you up.

However well you both stick to the agreement, it’s worth having a review some time in the future to go through the CUDSAIR model again and see if things can’t be improved further.

Source:BBC Health News

 

 

 

 

 

 

 

 

 

 

 

Small Heart With Low Cardiac Output for Orthostatic Intolerance in Patients With Chronic Fatigue Syndrome

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The etiology of chronic fatigue syndrome (CFS) is unknown. Orthostatic intolerance (OI) is common in CFS patients. Recently, small heart with low cardiac output has been postulated to be related to the genesis of both CFS and OI.

Hypothesis:

Small heart is associated with OI in patients with CFS.

Methods:

Study CFS patients were divided into groups of 26 (57%) CFSOI(+) and 20 (43%) CFSOI(−) according to the presence or absence of OI. In addition, 11 OI patients and 27 age- and sex-matched control subjects were studied. Left ventricular (LV) dimensions and function were determined echocardiographically.

Results:

The mean values of cardiothoracic ratio, systemic systolic and diastolic pressures, LV end-diastolic dimension, LV end-systolic dimension, stroke volume index, cardiac index, and LV mass index were all significantly smaller in CFSOI(+) patients than in CFSOI(−) patients and healthy controls, and also in OI patients than in controls. A smaller LV end-diastolic dimension (<40 mm) was significantly (P<0.05) more prevalently noted in CFSOI(+) (54%) and OI (45%) than in CFSOI(−) (5%) and controls (4%). A lower cardiac index (<2 L/min/mm2) was more prevalent in CFSOI(+) (65%) than in CFSOI(−) (5%, P<0.01), OI (27%), and controls (11%, P<0.01).

Conclusions:

A small size of LV with low cardiac output was noted in OI, and its degree was more pronounced in CFSOI(+). A small heart appears to be related to the genesis of OI and CFS via both cerebral and systemic hypoperfusion. CFSOI(+) seems to constitute a well-defined and predominant subgroup of CFS.

source:Clinical Crdiology