Ik dacht eens een nieuw supplement uit te proberen om de bloedsomloop te stimuleren en mijn brein wat aan de praat te houden. Het plantje dat een fytotherapeut had aangeraden was panax ginseng, de aziatische. De siberische, die mocht ik zeker niet nemen. Zo gezegd, zo gedaan.
Twee dagen later ben ik gezegend met een acute aanval van reumatoide artritis aan mijn hand blijkt nu. Eerst een mega-ellendige nacht waarbij elke cel van mijn lijf pijn deed alsof ik in de prikkeldraad lag. De volgende ochtend dikke vingers met gezwollen aders, enkele uren laten een griepaanval van jewelste. Dan een paar dagen zeer pijnlijke en stijve vingers. Vandaag is het voor het eerst weer wat beter.
Zo, voor diegenen die hun immuunsystem willen stimuleren: neem panax ginseng
En als je zeker bent dat je aan Crohn of lupus lijdt, a.f.b.l.i.j.v.e.n.
donderdag 16 februari 2012
Neuron memory key to taming chronic pain
http://www.mcgill.ca/newsroom/news/item/?item_id=214078
Neuron memory key to taming chronic pain
Feb. 13, 2012
Study suggests erasing neuronal memories may help control persistent pain
For some, the pain is so great that they can’t even bear to have clothes touch their skin. For others, it means that every step is a deliberate and agonizing choice. Whether the pain is caused by arthritic joints, an injury to a nerve or a disease like fibromyalgia, research now suggests there are new solutions for those who suffer from chronic pain.
A team of researchers led by McGill neuroscientist Terence Coderre, who is also affiliated with the Research Institute of the McGill University Health Centre, has found the key to understanding how memories of pain are stored in the brain. More importantly, the researchers are also able to suggest how these memories can be erased, making it possible to ease chronic pain.
It has long been known that the central nervous system “remembers” painful experiences, that they leave a memory trace of pain. And when there is new sensory input, the pain memory trace in the brain magnifies the feeling so that even a gentle touch can be excruciating.
“Perhaps the best example of a pain memory trace is found with phantom limb pain,” suggests Coderre. “Patients may have a limb amputated because of gangrene, and because the limb was painful before it was amputated, even though the limb is gone, the patients continue to feel they are suffering from pain in the absent limb. That’s because the brain remembers the pain. In fact, there’s evidence that any pain that lasts more than a few minutes will leave a trace in the nervous system.” It’s this memory of pain, which exists at the neuronal level, that is critical to the development of chronic pain. But until now, it was not known how these pain memories were stored at the level of the neurons.
Recent work has shown that the protein kinase PKMzeta plays a crucial role in building and maintaining memory by strengthening the connections between neurons. Now Coderre and his colleagues have discovered that PKMzeta is also the key to understanding how the memory of pain is stored in the neurons. They were able to show that after painful stimulation, the level of PKMzeta increases persistently in the central nervous system (CNS).
Even more importantly, the researchers found that by blocking the activity of PKMzeta at the neuronal level, they could reverse the hypersensitivity to pain that neurons developed after irritating the skin by applying capsaicin – the active ingredient in hot peppers. Moreover, erasing this pain memory trace was found to reduce both persistent pain and heightened sensitivity to touch.
Coderre and his colleagues believe that building on this study to devise ways to target PKMzeta in pain pathways could have a significant effect for patients with chronic pain. “Many pain medications target pain at the peripheral level, by reducing inflammation, or by activating analgesia systems in the brain to reduce the feeling of pain,” says Coderre. “This is the first time that we can foresee medications that will target an established pain memory trace as a way of reducing pain hypersensitivity. We believe it’s an avenue that may offer new hope to those suffering from chronic pain.”
The full article can be found at: http://www.molecularpain.com/content/7/1/99
Other contributing researchers on this study include Andre Laferrière, Mark H Pitcher, Anne Haldane, Yue Huang, Virginia Cornea, Naresh Kumar, Fernando Cervero (all from the Alan Edwards Centre for Research on Pain at McGill) and co-author Todd C Sacktor (State University of New York Downstate Medical Center).
This research was supported by grants from Canadian Institutes of Health Research (CIHR), the Louise and Alan Edwards Foundation, National Institutes of Health (NIH) and an Astra-Zeneca/AECRP fellowship.
Source : http://www.mcgill.ca/newsroom/news/item/?item_id=214078
Neuron memory key to taming chronic pain
Feb. 13, 2012
Study suggests erasing neuronal memories may help control persistent pain
For some, the pain is so great that they can’t even bear to have clothes touch their skin. For others, it means that every step is a deliberate and agonizing choice. Whether the pain is caused by arthritic joints, an injury to a nerve or a disease like fibromyalgia, research now suggests there are new solutions for those who suffer from chronic pain.
A team of researchers led by McGill neuroscientist Terence Coderre, who is also affiliated with the Research Institute of the McGill University Health Centre, has found the key to understanding how memories of pain are stored in the brain. More importantly, the researchers are also able to suggest how these memories can be erased, making it possible to ease chronic pain.
It has long been known that the central nervous system “remembers” painful experiences, that they leave a memory trace of pain. And when there is new sensory input, the pain memory trace in the brain magnifies the feeling so that even a gentle touch can be excruciating.
“Perhaps the best example of a pain memory trace is found with phantom limb pain,” suggests Coderre. “Patients may have a limb amputated because of gangrene, and because the limb was painful before it was amputated, even though the limb is gone, the patients continue to feel they are suffering from pain in the absent limb. That’s because the brain remembers the pain. In fact, there’s evidence that any pain that lasts more than a few minutes will leave a trace in the nervous system.” It’s this memory of pain, which exists at the neuronal level, that is critical to the development of chronic pain. But until now, it was not known how these pain memories were stored at the level of the neurons.
Recent work has shown that the protein kinase PKMzeta plays a crucial role in building and maintaining memory by strengthening the connections between neurons. Now Coderre and his colleagues have discovered that PKMzeta is also the key to understanding how the memory of pain is stored in the neurons. They were able to show that after painful stimulation, the level of PKMzeta increases persistently in the central nervous system (CNS).
Even more importantly, the researchers found that by blocking the activity of PKMzeta at the neuronal level, they could reverse the hypersensitivity to pain that neurons developed after irritating the skin by applying capsaicin – the active ingredient in hot peppers. Moreover, erasing this pain memory trace was found to reduce both persistent pain and heightened sensitivity to touch.
Coderre and his colleagues believe that building on this study to devise ways to target PKMzeta in pain pathways could have a significant effect for patients with chronic pain. “Many pain medications target pain at the peripheral level, by reducing inflammation, or by activating analgesia systems in the brain to reduce the feeling of pain,” says Coderre. “This is the first time that we can foresee medications that will target an established pain memory trace as a way of reducing pain hypersensitivity. We believe it’s an avenue that may offer new hope to those suffering from chronic pain.”
The full article can be found at: http://www.molecularpain.com/content/7/1/99
Other contributing researchers on this study include Andre Laferrière, Mark H Pitcher, Anne Haldane, Yue Huang, Virginia Cornea, Naresh Kumar, Fernando Cervero (all from the Alan Edwards Centre for Research on Pain at McGill) and co-author Todd C Sacktor (State University of New York Downstate Medical Center).
This research was supported by grants from Canadian Institutes of Health Research (CIHR), the Louise and Alan Edwards Foundation, National Institutes of Health (NIH) and an Astra-Zeneca/AECRP fellowship.
Source : http://www.mcgill.ca/newsroom/news/item/?item_id=214078
zondag 12 februari 2012
donderdag 9 februari 2012
Increased ventricular lactate in chronic fatigue syndrome.
http://onlinelibrary.wiley.com/doi/10.1002/nbm.2772/abstract
Increased ventricular lactate in chronic fatigue syndrome. III. Relationships to cortical glutathione and clinical symptoms implicate oxidative stress in disorder pathophysiology
Dikoma C. Shungu1,*, Nora Weiduschat1, James W. Murrough2, Xiangling Mao1, Sarah Pillemer2, Jonathan P. Dyke1, Marvin S. Medow3, Benjamin H. Natelson4, Julian M. Stewart3, Sanjay J. Mathew2,5Article first published online: 27 JAN 2012
DOI: 10.1002/nbm.2772
Copyright © 2012 John Wiley & Sons, Ltd.
Pathophysiological model of chronic fatigue syndrome (CFS) which attempts to explain the consistent observation of cross-sectional elevations of ventricular lactate in the disorder. Highlighted are the experimentally measurable items, with the red arrows showing the model-predicted outcomes. This series of neuroimaging studies aimed to validate this model by measuring each key item and comparing the results with the model-predicted outcomes.
Chronic fatigue syndrome (CFS) is a complex illness, which is often misdiagnosed as a psychiatric illness. In two previous reports, using 1H MRSI, we found significantly higher levels of ventricular cerebrospinal fluid (CSF) lactate in patients with CFS relative to those with generalized anxiety disorder and healthy volunteers (HV), but not relative to those with major depressive disorder (MDD).
In this third independent cross-sectional neuroimaging study, we investigated a pathophysiological model which postulated that elevations of CSF lactate in patients with CFS might be caused by increased oxidative stress, cerebral hypoperfusion and/or secondary mitochondrial dysfunction.
Fifteen patients with CFS, 15 with MDD and 13 HVs were studied using the following modalities: (i) 1H MRSI to measure CSF lactate; (ii) single-voxel 1H MRS to measure levels of cortical glutathione (GSH) as a marker of antioxidant capacity; (iii) arterial spin labeling (ASL) MRI to measure regional cerebral blood flow (rCBF); and (iv) 31P MRSI to measure brain high-energy phosphates as objective indices of mitochondrial dysfunction.
We found elevated ventricular lactate and decreased GSH (glutathion) in patients with CFS and MDD relative to HVs. GSH did not differ significantly between the two patient groups. In addition, we found lower rCBF in the left anterior cingulate cortex and the right lingual gyrus in patients with CFS relative to HVs, but rCBF did not differ between those with CFS and MDD.
We found no differences between the three groups in terms of any high-energy phosphate metabolites. In exploratory correlation analyses, we found that levels of ventricular lactate and cortical GSH were inversely correlated, and significantly associated with several key indices of physical health and disability. Collectively, the results of this third independent study support a pathophysiological model of CFS in which increased oxidative stress may play a key role in CFS etiopathophysiology.
Copyright © 2012 John Wiley & Sons, Ltd.
http://onlinelibrary.wiley.com/doi/10.1002/nbm.2772/abstract
Increased ventricular lactate in chronic fatigue syndrome. III. Relationships to cortical glutathione and clinical symptoms implicate oxidative stress in disorder pathophysiology
Dikoma C. Shungu1,*, Nora Weiduschat1, James W. Murrough2, Xiangling Mao1, Sarah Pillemer2, Jonathan P. Dyke1, Marvin S. Medow3, Benjamin H. Natelson4, Julian M. Stewart3, Sanjay J. Mathew2,5Article first published online: 27 JAN 2012
DOI: 10.1002/nbm.2772
Copyright © 2012 John Wiley & Sons, Ltd.
Pathophysiological model of chronic fatigue syndrome (CFS) which attempts to explain the consistent observation of cross-sectional elevations of ventricular lactate in the disorder. Highlighted are the experimentally measurable items, with the red arrows showing the model-predicted outcomes. This series of neuroimaging studies aimed to validate this model by measuring each key item and comparing the results with the model-predicted outcomes.
Chronic fatigue syndrome (CFS) is a complex illness, which is often misdiagnosed as a psychiatric illness. In two previous reports, using 1H MRSI, we found significantly higher levels of ventricular cerebrospinal fluid (CSF) lactate in patients with CFS relative to those with generalized anxiety disorder and healthy volunteers (HV), but not relative to those with major depressive disorder (MDD).
In this third independent cross-sectional neuroimaging study, we investigated a pathophysiological model which postulated that elevations of CSF lactate in patients with CFS might be caused by increased oxidative stress, cerebral hypoperfusion and/or secondary mitochondrial dysfunction.
Fifteen patients with CFS, 15 with MDD and 13 HVs were studied using the following modalities: (i) 1H MRSI to measure CSF lactate; (ii) single-voxel 1H MRS to measure levels of cortical glutathione (GSH) as a marker of antioxidant capacity; (iii) arterial spin labeling (ASL) MRI to measure regional cerebral blood flow (rCBF); and (iv) 31P MRSI to measure brain high-energy phosphates as objective indices of mitochondrial dysfunction.
We found elevated ventricular lactate and decreased GSH (glutathion) in patients with CFS and MDD relative to HVs. GSH did not differ significantly between the two patient groups. In addition, we found lower rCBF in the left anterior cingulate cortex and the right lingual gyrus in patients with CFS relative to HVs, but rCBF did not differ between those with CFS and MDD.
We found no differences between the three groups in terms of any high-energy phosphate metabolites. In exploratory correlation analyses, we found that levels of ventricular lactate and cortical GSH were inversely correlated, and significantly associated with several key indices of physical health and disability. Collectively, the results of this third independent study support a pathophysiological model of CFS in which increased oxidative stress may play a key role in CFS etiopathophysiology.
Copyright © 2012 John Wiley & Sons, Ltd.
http://onlinelibrary.wiley.com/doi/10.1002/nbm.2772/abstract
Heart failure explained and proven
http://www.cfids-cab.org/MESA/DrMyhill-373.pdf
Heart failure in ME is caused by poor muscle function.
Traditional tests like ECG, ECHO's, angiograms, ... will be normal.
Impedence cardiography however accurately measure cardiac output by measuring the electrical impedence across the chest wall.
Do the test in upright position and then again supine.
Disability can be proven with this test. It is completely independent and reliable.
Heart failure in ME is caused by poor muscle function.
Traditional tests like ECG, ECHO's, angiograms, ... will be normal.
Impedence cardiography however accurately measure cardiac output by measuring the electrical impedence across the chest wall.
Do the test in upright position and then again supine.
Disability can be proven with this test. It is completely independent and reliable.
dinsdag 7 februari 2012
The relationship between the liver, exercise and candida
The relationship between the liver, exercise and candida
The liver is a ingenious detox factory. Through two steps, Phase I and II, toxins, pesticides, heavy metals, additives are dismantled and disarmed and removed from the body via the urine e.g.
Phase I
During this process toxic substances undergo a treatment which converts them into bio-active substances. This makes them much more toxic but it is necessary to be able to bind to water in stage II. The cytochrome P 450 enzymes get in action during this phase.
Phase II
The bio-active substances are converted into bio-inactive substances. For example, they can bind to water and avoids toxic loads that are stacked in the liver. During this phase the toxins lose their fragrance.
The enzymes responsible for the conversion of glutathione, glutathione transferase, in particular, are also active during the second phase of detoxification. They need a co-enzyme to function, in particular: selenium, zinc, magnesium, vitamin B (3, 6, 8, 11, 12), and alpha-lipoic acid.
Phase II proceeds via glutathione transferases but on one condition only. It needs (daily) exercise to be useful. Glutathione is as we know, composed of three amino acids: cysteine, glycine and glutamic acid. Glutathione is as we know, composed of three amino acids: cysteine, glycine and glutamic acid.
Cysteine is a troublemaker if there is no exercise. How come? Cysteine can always be present into the cell. Outside the cell, only if there is sufficient cysteine to be converted via exercise.
If the person moves insufficiently, then the cell imports cystine. The cell is equipped with cystine channels. Only 1 cystine can pass at a time. This in turn gives a glutathione.
A cystine => a cysteine => 1 glutathione
Suppose the person exercises enough, no need to import cystine. Cysteine passes via specific channels, 10 cysteine enter at the same time the cell. Thus, it produces 10 times more glutathione.
Someone who has little chance to move or exercise, will detox 10x less than a active person. This is not without consequences.
Another stumbling block for Phase II of the detoxification is Candida or fungus. This causes leaky gut and too little recognized by mainstream medicine. Fungus produces acetyldehyde via the enzyme pyruvate decarboxylase. Acetyldehyde is dismantled by cysteine. The more candida, the greater the use of cysteine. Moreover, it compeeds with vitamine B6 and affects normal detox processes.
The effects of candida are far-reaching. The chemical by-products react with serotonin and dopamine. Acetaldehyde is then transformed into opiate substances that affect the functioning of the brains. The neurons are able to communicate less well and influences the red blood cells negatively. They have more trouble to transport oxygen. Thus, you are tired of candida.
Interesting to know is that everyday substances can limit stage II. These are coffee and tea, sugar and lactose (milk and cheese), smoking and alcohol, stress, paracetamol and too little exercise as previously cited.
Nature is generous, and also provides ways to stimulate phase II. Daily exercise is an obvious move with the knowledge what the lack of exercise can do. Vegetables and plants have to offer: onion, garlic, leeks, chicory, endive, artichoke, broccoli, radish, spinach, olive oil, fatty fish, avocado, turmeric, milk thistle, dandelion, Swedish herb, liver herb.
The liver is a ingenious detox factory. Through two steps, Phase I and II, toxins, pesticides, heavy metals, additives are dismantled and disarmed and removed from the body via the urine e.g.
Phase I
During this process toxic substances undergo a treatment which converts them into bio-active substances. This makes them much more toxic but it is necessary to be able to bind to water in stage II. The cytochrome P 450 enzymes get in action during this phase.
Phase II
The bio-active substances are converted into bio-inactive substances. For example, they can bind to water and avoids toxic loads that are stacked in the liver. During this phase the toxins lose their fragrance.
The enzymes responsible for the conversion of glutathione, glutathione transferase, in particular, are also active during the second phase of detoxification. They need a co-enzyme to function, in particular: selenium, zinc, magnesium, vitamin B (3, 6, 8, 11, 12), and alpha-lipoic acid.
Phase II proceeds via glutathione transferases but on one condition only. It needs (daily) exercise to be useful. Glutathione is as we know, composed of three amino acids: cysteine, glycine and glutamic acid. Glutathione is as we know, composed of three amino acids: cysteine, glycine and glutamic acid.
Cysteine is a troublemaker if there is no exercise. How come? Cysteine can always be present into the cell. Outside the cell, only if there is sufficient cysteine to be converted via exercise.
If the person moves insufficiently, then the cell imports cystine. The cell is equipped with cystine channels. Only 1 cystine can pass at a time. This in turn gives a glutathione.
A cystine => a cysteine => 1 glutathione
Suppose the person exercises enough, no need to import cystine. Cysteine passes via specific channels, 10 cysteine enter at the same time the cell. Thus, it produces 10 times more glutathione.
Someone who has little chance to move or exercise, will detox 10x less than a active person. This is not without consequences.
Another stumbling block for Phase II of the detoxification is Candida or fungus. This causes leaky gut and too little recognized by mainstream medicine. Fungus produces acetyldehyde via the enzyme pyruvate decarboxylase. Acetyldehyde is dismantled by cysteine. The more candida, the greater the use of cysteine. Moreover, it compeeds with vitamine B6 and affects normal detox processes.
The effects of candida are far-reaching. The chemical by-products react with serotonin and dopamine. Acetaldehyde is then transformed into opiate substances that affect the functioning of the brains. The neurons are able to communicate less well and influences the red blood cells negatively. They have more trouble to transport oxygen. Thus, you are tired of candida.
Interesting to know is that everyday substances can limit stage II. These are coffee and tea, sugar and lactose (milk and cheese), smoking and alcohol, stress, paracetamol and too little exercise as previously cited.
Nature is generous, and also provides ways to stimulate phase II. Daily exercise is an obvious move with the knowledge what the lack of exercise can do. Vegetables and plants have to offer: onion, garlic, leeks, chicory, endive, artichoke, broccoli, radish, spinach, olive oil, fatty fish, avocado, turmeric, milk thistle, dandelion, Swedish herb, liver herb.
maandag 6 februari 2012
Kill the virus with
Viri Balance
https://www.gezondheidaanhuis.nl/nl/product/10195/Viri-Balance-Pervital-30-ml
Lymfo Balance
https://www.gezondheidaanhuis.nl/nl/product/13749/Lymfo-Balance-Pervital-30-ml
Detox Balance
https://www.gezondheidaanhuis.nl/nl/product/11801/Detox-Balance-Pervital-30-ml
Brand: Pervital
http://www.nutramin.nl/
If results are not satisfying, add Elaps Balance.
https://www.gezondheidaanhuis.nl/nl/product/13747/Elaps-Balance-Pervital-30-ml
Also helpful against HPV (human papilloma virus responsible for cervix cancer).
https://www.gezondheidaanhuis.nl/nl/product/10195/Viri-Balance-Pervital-30-ml
Lymfo Balance
https://www.gezondheidaanhuis.nl/nl/product/13749/Lymfo-Balance-Pervital-30-ml
Detox Balance
https://www.gezondheidaanhuis.nl/nl/product/11801/Detox-Balance-Pervital-30-ml
Brand: Pervital
http://www.nutramin.nl/
If results are not satisfying, add Elaps Balance.
https://www.gezondheidaanhuis.nl/nl/product/13747/Elaps-Balance-Pervital-30-ml
Also helpful against HPV (human papilloma virus responsible for cervix cancer).
zondag 5 februari 2012
Living is ...
"Perhaps it is true that we do not really exist until there is someone there to see us existing;
that we cannot properly speak until there is someone there who can understand what we are saying;
that, in essence, we are not wholly alive until we are loved."
Alain de Botton: On Love
that we cannot properly speak until there is someone there who can understand what we are saying;
that, in essence, we are not wholly alive until we are loved."
Alain de Botton: On Love
woensdag 1 februari 2012
Mitochondrial changes associated with glutathione deficiency
http://www.sciencedirect.com/science/article/pii/092544399500007Q
Abstract
Glutathione deficiency produced by giving buthionine sulfoximine (an inhibitor of γ-glutamylcysteine synthetase) to animals, leads to biphasic decline in cellular glutathione levels associated with sequestration of glutathione in mitochondria. Liver mitochondria lack the enzymes needed for glutathione synthesis. Mitochondrial glutathione arises from the cytosol. Rat liver mitochondria have a multicomponent system (with Ks of approx. 60 μM and 5.4 mM) that underlies their remarkable ability to transport and retain glutathione. Mitochondria produce substantial quantities of reactive oxygen species = damaging free radicals) ; this is opposed by reactions involving glutathione.
Glutathione deficiency leads to widespread mitochondrial damage which is lethal in newborn rats and guinea pigs, animals that do not synthesize ascorbate (= vitamin C). Glutathione esters and ascorbate protect against the lethal and other effects of glutathione deficiency. Ascorbate spares glutathione; it increases mitochondrial glutathione in glutathione-deficient animals. Glutathione esters delay onset of scurvy in ascorbate-deficient guinea pigs; thus, glutathione spares ascorbate. Glutathione and ascorbate function together in protecting mitochondria from oxidative damage.
Abstract
Glutathione deficiency produced by giving buthionine sulfoximine (an inhibitor of γ-glutamylcysteine synthetase) to animals, leads to biphasic decline in cellular glutathione levels associated with sequestration of glutathione in mitochondria. Liver mitochondria lack the enzymes needed for glutathione synthesis. Mitochondrial glutathione arises from the cytosol. Rat liver mitochondria have a multicomponent system (with Ks of approx. 60 μM and 5.4 mM) that underlies their remarkable ability to transport and retain glutathione. Mitochondria produce substantial quantities of reactive oxygen species = damaging free radicals) ; this is opposed by reactions involving glutathione.
Glutathione deficiency leads to widespread mitochondrial damage which is lethal in newborn rats and guinea pigs, animals that do not synthesize ascorbate (= vitamin C). Glutathione esters and ascorbate protect against the lethal and other effects of glutathione deficiency. Ascorbate spares glutathione; it increases mitochondrial glutathione in glutathione-deficient animals. Glutathione esters delay onset of scurvy in ascorbate-deficient guinea pigs; thus, glutathione spares ascorbate. Glutathione and ascorbate function together in protecting mitochondria from oxidative damage.
dinsdag 31 januari 2012
Regular laughter equals regular exercise
In contrast, the subjects who watched the humorous video had changes in blood pressure and also changes in the leptin and ghrelin levels. Specifically, the level of leptin decreased as the level of ghrelin increased, much like the acute effect of moderate physical exercise that is often associated with increased appetite.
Berk explains that this research does not conclude that humor increases appetite. He explains, "The ultimate reality of this research is that laughter causes a wide variety of modulation and that the body's response to repetitive laughter is similar to the effect of repetitive exercise. The value of the research is that it may provide for those who are health care providers with new insights and understandings, and thus further potential options for patients who cannot use physical activity to normalize or enhance their appetite."
Source: http://www.the-aps.org/mm/hp/Audiences/Public-Press/For-the-Press/releases/10/12.html
Definitively an option for many ME and CFS sufferers who are bed- or housebound!
Berk explains that this research does not conclude that humor increases appetite. He explains, "The ultimate reality of this research is that laughter causes a wide variety of modulation and that the body's response to repetitive laughter is similar to the effect of repetitive exercise. The value of the research is that it may provide for those who are health care providers with new insights and understandings, and thus further potential options for patients who cannot use physical activity to normalize or enhance their appetite."
Source: http://www.the-aps.org/mm/hp/Audiences/Public-Press/For-the-Press/releases/10/12.html
Definitively an option for many ME and CFS sufferers who are bed- or housebound!
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