Mast cell dysfunction in ME/CFS

Posted on 07/11/2016 by wames

Research abstract:

BACKGROUND: Mast cells (MCs) mediate inflammation through neuropeptides and cytokines, along with histamine and reactive oxygen species (ROS).

Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME) is an illness characterized by an unexplained disabling fatigue with multiple physiological impairments as well as dysregulated cytokine profiles.

OBJECTIVE: To determine mast cell phenotypes in isolated human PBMCs, in healthy controls and in CFS/ME patients. Second, determine receptor expression of RAGE and its ligand high mobility group box 1 protein (HMGB1).

METHOD: Moderately severe CFS/ME patients (n=12, mean age 39.25±SD3.52 years), severe CFS/ME patients (n=6, mean age 43.00±SD4.02 years) and healthy controls (n=13, mean age 42.69±SD3.87 years) were included in this study. CFS/ME patients were classified according to the 2011 International Consensus Criteria.

LSRFortessa X-20 Flow cytometry was used for the identification of phenotypic peripheral mast cell population in PBMCs using an exclusion marker Lin2 cocktail (anti-CD3, anti-CD14, anti-CD19, anti-CD20 and anti-CD56) and inclusion markers (CD117, CD34, FCεRI, chymase, HLA-DR and CD154) following comparative investigation. HMGB1 and soluble RAGE expression in plasma was measured by sandwich ELISA assay.

RESULTS: There was a significant increase in CD117+CD34+FCεRI-chymase- mast cell populations in moderate and severe CFS/ME patients compared with healthy controls. There was a significant increase in CD40 ligand and MHC-II receptors on differentiated mast cell populations in the severe CFS/ME compared with healthy controls and moderate CFS/ME.

There were no significant differences between groups for HMGB1 and sRAGE.

CONCLUSIONS: This preliminary study investigates mast cell phenotypes from PBMCs in healthy controls. We report significant increase of naïve MCs in moderate and severe CFS/ME patients compared with healthy controls. Moreover, a significant increase in CD40 ligand and MHC-II receptors on differentiated mast cells in severe CFS/ME patients.

Peripheral MCs may be present in CFS/ME pathology however, further investigation to determine their role is required.

Novel characterisation of mast cell phenotypes from peripheral blood mononuclear cells in chronic fatigue syndrome/myalgic encephalomyelitis patients, by Nguyen T, Johnston S, Chacko A, Gibson D, Cepon J, Smith P, Staines D, Marshall-Gradisnik S in Asian Pac J Allergy Immunol. 2016 Jun 30. [Epub ahead of print]

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Dr David Systrom’s exercise intolerance research

Posted on 07/08/2016 by wames

Health rising blog post, by Cort Johnson: The Exercise intolerance in ME/CFS, Fibromyalgia and POTS Explained?

Dr. Systrom’s huge study on people with unexplained exercise intolerance suggests that the current explanation (deconditioning, lack of effort) couldn’t be more wrong. In fact, Systrom’s study suggests that when these peoples hearts were asked to pump more blood during exercise they couldn’t.

He concluded that the problem was every bit as functionally debilitating as heart failure and other major diseases. He also concluded that the problem was not in the heart. Is he explaining what’s going on in ME/CFS and FM?

Introduction:

It’s always  encouraging to see established researchers from outside the chronic fatigue syndrome (ME/CFS) and fibromyalgia fields converging on them. David Systrom, a pulmonologist at Brigham and Women’s hospital in Boston, has been interested in idiopathic or unexplained exercise intolerance for at least a decade.

A significant number of people who cannot exercise have been a medical mystery to cardiologists and pulmonologists

He and Oldham recently published their magnus opus on exercise intolerance; a study employing over six hundred patients that stretches back nine years.

Unexplained exertional dyspnea caused by low ventricular filling pressures: results from clinical invasive cardiopulmonary exercise testing. William M. Oldham,1,2,3 Gregory D. Lewis,3,4 Alexander R. Opotowsky,2,3,5 Aaron B. Waxman,1,2,3 David M. Systrom1,2,3. Pulm Circ 2016;6(1):55-62. DOI: 10.1086/685054.

In it they proposed that a significant subset of patients with exercise intolerance and heart abnormalities have simply slipped through the cracks.  No diagnosis has been able to explain their low energy production (VO2 max) during exercise; they don’t have heart failure or arrythmia or cystic fibrosis or known mitochondrial problems. Aside from telling them that they’re deconditioned or depressed the medical profession hasn’t known what to do with these patients.

How a field that gets over $2 billion in funding year in and year out could let any significant group “slip through” the cracks is unclear. Systrom’s use of invasive cardiopulmonary testing techniques apparently has given him a unique insight into these patients.

“In this study, we tested the hypothesis that failure of these mechanisms to increase cardiac preload during exercise….may be the primary limitation….in an undiagnosed population of patients with unexplained exercise intolerance.”

Some of them, perhaps many of them, have ME/CFS/FM or POTS (or would be diagnosed with it if anyone tried) and those that don’t must have something close.  (At least three people with ME/CFS/FM have ended up in Systrom’s office, and probably many more were in the study.)

Systrom, though, is ignoring the ME/CFS/FM for the moment – and probably rightly so.  He has bigger fish to fry; his goal right now is to enroll his colleagues in the idea that they haven’t been correctly diagnosing a significant subset of their patients.

If my reading of medical history (I highly recommend “The Biography of Cancer” and “The Death of Cancer”) is representative, that conclusion is probably not going to go over well.

Systrom found that hearts of the exercise intolerant patients did not expand when they exercised.  This inability to fill with more blood during exercise was why they exhibited low energy production (VO2 max). (We just saw a similar pattern in ME/CFS in “Chronic Fatigue Syndrome: A Small Heart Disease” and A Mestinon Miracle.)

Read more

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MAGENTA: GET for teenagers research trial protocol

Posted on 07/08/2016 by wames

Research protocol abstract:

Introduction:

Paediatric chronic fatigue syndrome or myalgic encephalomyelitis (CFS/ME) is a relatively common and disabling condition, yet there is a limited evidence base for treatment. There is good evidence that graded exercise therapy is moderately effective in adults with CFS/ME, but there is little evidence for the effectiveness, cost-effectiveness, acceptability or best method of delivery for paediatric CFS/ME.

This study aims to investigate the acceptability and feasibility of carrying out a multicentre randomised controlled trial investigating the effectiveness of graded exercise therapy compared with activity management for children/teenagers who are mildly or moderately affected with CFS/ME.

Methods and analysis 100 paediatric patients (8–17 years) with CFS/ME will be recruited from 3 specialist UK National Health Service (NHS) CFS/ME services (Bath, Cambridge and Newcastle). Patients will be randomised (1:1) to receive either graded exercise therapy or activity management. Feasibility analysis will include the number of young people eligible, approached and consented to the trial; attrition rate and treatment adherence; questionnaire and accelerometer completion rates. Integrated qualitative methods will ascertain perceptions of feasibility and acceptability of recruitment, randomisation and the interventions. All adverse events will be monitored to assess the safety of the trial.

Ethics and dissemination: The trial has received ethical approval from the National Research Ethics Service (South West—Frenchay 15/SW/0124).

Trial registration number ISRCTN23962803; Pre-results.

Strengths and limitations of this study

  • This feasibility study is the first trial to investigate graded exercise therapy in children with chronic fatigue syndrome or myalgic encephalomyelitis (CFS/ME) in the outpatient setting.
  • Integrated qualitative methodology is being used to optimise recruitment and retention, and to investigate the feasibility and acceptability of the study processes and interventions.
  • This is a multicentre study which will test the feasibility of running this trial in different National Health Service (NHS) settings.
  • The participants and clinicians will not be blinded to allocation.
  • Participant outcomes are self-reported

Managed Activity Graded Exercise iN Teenagers and pre-Adolescents (MAGENTA) feasibility randomised controlled trial: study protocol, by Amberly Brigden, Lucy Beasant, William Hollingworth, Chris Metcalfe, Daisy Gaunt, Nicola Mills, Russell Jago, Esther Crawley in BMJ Open Volume 6, Issue 7 2016 [Published 4 July 2016]

University of Bristol MAGENTA website with information about the trial, questionnaires & information sheets.

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How mestinon helped one ME/CFS patient exercise

Posted on 07/07/2016 by wames

Health Rising blog post, by Cort Johnson, 17 June 2016: A mestinon miracle: vagus nerve stimulating drug helps long time ME/CFS patient exercise.

She’d had chronic fatigue syndrome (ME/CFS) for twenty-eight years and has left no stone unturned in her attempts to get well. She’s traveled widely and seen some of the best ME/CFS doctors in the world. Despite being connected to the hilt in the ME/CFS, her results have been all too familiar; her health has improved a bit but she, a former fitness buff, has never been able to exercise.

She’d had a really tough year. Multiple surgeries including a gall bladder removal, multiple emergency room visits and a mysterious drug reaction had laid her as low as she had ever been.

Many people might have given up after that (and several decades of mostly fruitless searching) but last year there she was in a pulmonary specialist’s office with a catheter in her arm working away on an exercise test.

There she was, almost 30 years later, doing an exercise test in an attempt to figure what had gone wrong.

Her goal – to determine if the latest hot topic in ME/CFS – mitochondrial issues – were it for her. It turned out that they weren’t – her mitochondria appeared to be working fine.  Nor, despite the sarcoidosis she had, was her lung capacity diminished – she still had the lungs of an athlete.

Her autonomic nervous system, however, was  decidedly off. Her heart was beating way too fast and her blood was pooling in her legs instead of getting pushed back up to her heart, leaving her heart without much blood to pump. Her doctor, David Systrom at Brigham’s Women’s Hospital in Boston,  turned to her and suggested Mestinon (pyridostigmine bromide). It’s helped, he said, with fatigue in patients like you have.

Mestinon turned out to be something of a miracle for her.  She took too much at first – had some rather drastic side-effects but then ratcheted it down and then back up again.

Now she’s at the upper limit prescribed for people with myasthenia gravis (180 mgs/day).  She hasn’t been able to exercise without paying for it for almost three decades but it was clear within a couple of weeks that something was different. She described suddenly feeling like “going for a run” – a feeling she hadn’t had in decades. She was tired afterwards but the dreaded PEM never materialized.

Then she went cross-country skiing – one of the most energy intensive exercises there is.  She’s now running 3 plus miles a couple of days a week and working out in the gym. She has one side effect that’s apparently caused by the medication; after exercise sometimes she feels lightheaded.

Other symptoms improved. She does take sleeping pills but now they seem to be working better and she was able to cut down her sleep by an hour or two a night. She’s able to work full days. Much of her alcohol intolerance has disappeared. Her very high resting heart rate has returned to normal.  She’s not healthy but she’s improved enormously and she can exercise (!).

Imagine her shock when she learned that the drug that has done so much for her has been around for decades. It’s even prescribed for the orthostatic intolerance she has, but until Dr Systrom no one had ever mentioned it.

Read more about mestinon, Dr David Systrom and his research into exercise intolerance

 

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Could new form of magnesium help brain fog in ME-CFS?

Posted on 07/06/2016 by wames

A new form of magnesium improves cognitive powers in old folks, will it also help the brain fog of FM and ME-CFS? asks Dr Richard Podell.

Might it also improve Fibromyalgia pain?

Cognitive function tends to declines as we age. For most people the decline is modest. This “semi-normal” decline is thought to be due in part to a decrease in the ability of cells to form communication contacts called synapses between one cell and another. A similar defect is seen with Alzheimer’s disease.

Animal studies show that one way to increase the number and function of synapses is to raise the brain’s level of the mineral magnesium. When scientists increase brain magnesium in lab rats, the rats become smarter—thinking more rapidly and accurately than they did before.

BUT, most forms of oral magnesium don’t pass easily from the blood into the brain. An exception is a new form of magnesium developed by a research team from MIT specifically for this purpose. This form is magnesium threonate, which is being developed by Neurocentria, Inc., a pharmaceutical company, under the brand name of MMFS-01.

Neurocentria’s team with collaborating researchers from both the U.S. and China
recently published a very important study. Their results strongly suggest that MMFS-01 can substantially improve cognitive function in aging humans.

Press release from Neurocentria Inc.

MMFS-01 is not yet commercially available. However, a “generic” magnesium threonate is available from the Life Extension Foundation under the brand name of Neuro-mag. Likely other “generics” are or will soon be available.

What is truly remarkable about the MMFS-01 study is that improvement in overall  cognitive function was seen within just six weeks. Improvement continued through 12 weeks, the full length of the study. Subjects treated with placebo did not improve much over-all.

More details for the study: The volunteers were age 50 to 70. All had test score evidence of mild cognitive impairment. Twenty five subjects took MMFS-01 and 26 took placebo. The treatment dose was between 1.5 and 2.0 grams per day in divided doses.

Four different cognitive tests were taken before treatment and again at six and twelve weeks. These tests measured executive function, working memory, attention and a concept called episodic memory.

  • With magnesium threonate executive function significantly improved compared to placebo at 6 and 12 weeks
  • Working memory improved significantly at six weeks but at 12 weeks the placebo group had improved also. So, the difference between the groups at 12 weeks was no longer statistically significant
  • Attention improved in the MMFS-01 group compared to baseline, but this improvement was not statistically better than for those taking placebo
  • Episodic memory improved with MMFS-01 by week 12, but was not significantly
    better than that seen with placebo.
  • When over-all cognitive ability was calculated by combining results from the four
    tests, subjects taking MMFS-01 scored significantly better than subjects taking
    placebo. This was true at week 6 (P=.017) and at week 12 (p=.003).
  • As important–subjects taking MMFS-01 who had the largest increase in red blood cell magnesium levels, were also the subjects most likely to show major cognitive improvement. There were no major side effects.

Separate research suggests that magnesium might also help treat fibromyalgia pain. This might be because magnesium tends to inhibit the activity of NMDA receptors. Activation of NMDA receptors is believed to be one mechanism that creates fibromyalgia pain. A recent open label clinical study from Mayo Clinic found that transdermal magnesium chloride spray taken twice daily for 3 weeks was followed by a reduction in fibromyalgia pain.

Key Questions: Should physicians treating FM or ME-CFS “brain fog” be offering  magnesium threonate as a potential treatment?

The arguments against:

  • We don’t know whether brain fog in fibromyalgia or ME-CFS has any relationship to the cognitive decline that is common with aging.
  • We have only one clinical study to support the beneficial effects of
    magnesium threonate.

The argument for:

  • Brain fog is a major problem for our patients
  • We have no proven treatments
  • For most (but not all patients), side effects from magnesium are minimal—
    mainly diarrhea if we get the dose up too high.

Should patients with FM or ME-CFS try magnesium threonate on their own?

I strongly recommend that all patients work with their doctor. Certain patients should not take extra magnesium, especially those with any degree of kidney dysfunction. Also, it would be useful to obtain a baseline red blood cell magnesium level and to monitor that level as treatment proceeds.

Since MMFS-01 is not available, using Life Extension’s or other generic equivalents
would be appropriate. Of course, ideally, some angel would fund a good controlled study.

But, as usual, that’s not likely to happen anytime soon.

Richard N. Podell, M.D., MPH
Clinical Professor, Department of Family Medicine
Rutgers-Robert Wood Johnson Medical School
Podell2@gmail.com

Rich’ Reviews: New form  of magnesium, from: ME Global Chronicle No. 17 June 2016 p48

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Video: Prof Warren Tate, researcher & parent of child with ME

Posted on 07/06/2016 by wames

Video: Life with ME/CFS: Professor Warren Tate Talks About ME/CFS

Prof Warren Tate

Professor Tate has a daughter who suffers from ME/CFS. As an award winning biomedical researcher, and close family member of a sufferer, Warren provides an invaluable perspective on the illness. 22 June 2016

 

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Prof Garth Nicolson’s research: ME & restoring mitochondrial functioning

Posted on 07/06/2016 by wames

Prof. Garth Nicolson introduces his research:

We have been involved in research on the role of mitochondrial function in ME/CFS for some time and have found that restoring inner mitochondrial membrane (IMM) trans-membrane potential is essential. When mitochondrial membrane lipids are damaged, the IMM becomes leaky and the membrane potential cannot be sustained, which results in loss of ATP production and increases in fatigue.

Since 2003 we have published several scientific papers that show that ME/CFS and other chronic illness conditions, including chronic infections like Lyme disease, chronic Mycoplasma and other complex infections, cause IMM dysfunction that can be repaired by Membrane Lipid Replacement (MLR) with NTFactor Lipids, resulting in improvements in fatigue, cognition, short-term memory and mood

Membrane Lipid Replacement: clinical studies using a natural medicine approach to restoring membrane function and improving health by GL Nicholson in International Journal of Clinical Medicine, 2016; 7: 133-143.

NTFactor Lipids is an all-natural membrane glycerolphospholipid product (for example, Patented Energy,). This has been reviewed recently in our article in Discoveries 2016

Clinical uses of Membrane Lipid Replacement supplements in restoring membrane function and reducing fatigue in chronic diseases and cancer, by GL Nicholson et al in  Discoveries 2016; 4(1): e54.

There are other potential useful benefits of MLR that we rarely discuss, such as the removal of excess, potentially toxic, cholesterol from cellular stores. (Presumedly similar mechanisms exist for removal of the damaged membrane glycerolphospholipids and their secretion and eventual excretion).

As quoted in an article just published in Lipid Insights by Thomas A. Lagace of the University of Ottawa Heart Institute,

“Phosphatidylcholine plays a critical role in cellular cholesterol sinks that buffer against cholesterol-induced ER stress and assist in the maintenance of cellular cholesterol gradients that drive interorganelle cholesterol transport.”

(Lagace, T.A. Phosphatidylcholine: greasing the cholesterol transport machinery. Lipid Insights 2015; 8(S1): 65-73. doi:10.4137/LPI.S31746).

Phosphatidylcholine is the most prevalent lipid in NTFactor Lipids, and it plays an
essential role in cholesterol transport and its removal at the cellular level and at the organ and systems levels. This may be due to a rather simple concentration gradient mechanism that sequesters cholesterol and oxidized glycerolphospholipids into Lipid Droplets for their eventual removal.

This could explain why our ME/CFS patients have better cholesterol, homocysteine and other blood tests after 6 months on MLR. (Blood homocysteine and fasting insulin levels are reduced and erythrocyte sedimentation rates are increased with a glycophospholipid-vitamin formulation: a retrospective study in older subjects, by Ellithorpe, R.R, Settineri R.,  Ellithorpe, T. and Nicolson, G.L. in Functional Foods in Health and Disease 2015; 5(4): 126-135.)

Eventually the use of MLR may enhance and hopefully replace costly cholesterol reducing
drugs (with side effects) that Big Pharma has been pushing for some time. For years ME/CFS patients have benefited from NTFactor lipid products without adverse reactions or events.

Prof. Emeritus Garth Nicolson, PhD, MD (H)
Department of Molecular Pathology, The Institute for Molecular Medicine

ME & mitochondrial functioning  from ME Global Chronicle No. 17 June 2016 p54

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Gut bacteria spotted eating brain chemicals for the first time

Posted on 07/05/2016 by wames

New Scientist article, by Andy Coghlan, 1 July 2016: Gut bacteria spotted eating brain chemicals for the first time:

Bacteria have been discovered in our guts that depend on one of our brain chemicals for survival. These bacteria consume GABA, a molecule crucial for calming the brain, and the fact that they gobble it up could help explain why the gut microbiome seems to affect mood.

Philip Strandwitz and his colleagues at Northeastern University in Boston discovered that they could only grow a species of recently discovered gut bacteria, called KLE1738, if they provide it with GABA molecules. “Nothing made it grow, except GABA,” Strandwitz said while announcing his findings at the annual meeting of the American Society for Microbiology in Boston last month.

GABA acts by inhibiting signals from nerve cells, calming down the activity of the brain, so it’s surprising to learn that a gut bacterium needs it to grow and reproduce. Having abnormally low levels of GABA is linked to depression and mood disorders, and this finding adds to growing evidence that our gut bacteria may affect our brains.

Treating depression

An experiment in 2011 showed that a different type of gut bacteria, called Lactobacillus rhamnosus, can dramatically alter GABA activity in the brains of mice, as well as influencing how they respond to stress. In this study, the researchers found that this effect vanished when they surgically removed the vagus nerve – which links the gut to the brain – suggesting it somehow plays a role in the influence gut bacteria can have on the brain.
Strandwitz is now looking for other gut bacteria that consume or even produce GABA, and he plans to test their effect on the brains and behaviour of animals. Such work may eventually lead to new treatments for mood disorders like depression or anxiety.

“Although research on microbial communities related to psychiatric disorders may never lead to a cure, it could have astonishing relevance to improving patients’ quality of life,” said Domenico Simone of George Washington University in Ashburn, Virginia.

Read more: Psychobiotics: How gut bacteria mess with your mind

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Dysfunctional low affinity antibodies leads to gut & immune problems in ME/CFS

Posted on 07/05/2016 by wames

Research abstract:

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a heterogeneous illness characterized by a number of comorbid conditions; gastrointestinal (GI) dysregulation make up one subgroup of this disease.

IgA is the most abundant antibody isotype found in mucosal secretions including the gut. In a process of class switch recombination (CSR), that relies on the interaction of plasmacytoid dendritic cells (pDCs) with B cells, in a T cell independent (TI) manner, low-affinity IgA are produced that limit the adhesion of commensal bacteria to intestinal epithelia without neutralizing them. These low-affinity antibodies also limit bacterial overgrowth and potential bacterial translocation thus maintaining gut homeostasis. This process is known as “immune exclusion”.

Two ligands on the surface of pDCs that are obligatory for the process; the membrane bound form of APRIL and BAFF. The upregulation of APRIL and BAFF on the surface of pDCs is dependent on low-level expression of type I interferon (IFN) which is produced by intestinal stromal cells in response to Toll-like receptor (TLR) engagement.

Previous studies suggest that peripheral pDCs are significantly lower in subjects with ME/CFS when compared to controls and studies conducted by us further suggest these cells likely redistribute from the periphery to the gut. We have observed that, in contrast to controls, gut-associated pDCs in subjects with ME/CFS lack APRIL and BAFF expression.

These data support a model of gut pathology in ME/CFS whereby dysregulated pDCs fail to promote the production of low-affinity IgA through the process of TI activation of B cells, thereby leading to bacterial overgrowth, dysbiosis, bacterial translocation and systemic immune activation.

Failure of gut-associated pDCs to express membrane bound APRIL and BAFF prevents their ability to promote low-affinity IgA expression in ME/CFS by Vincent C Lombardi, Svetlana F Khaiboullina, Kenny L De Meirleir, Tanja Mijatovic and Jan Hulstaert in The Journal of Immunology, May 1, 2016, vol.196 (1 Supplement) 137.4

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Nausea and sickness: non-drug options

Posted on 07/04/2016 by wames

MEA blog post, 29 June 2016: Dr Charles Shepherd reports on two non-drug options for nausea and sickness in ME/CFS

New guidance from the Royal College of Obstetricians and Gynaecologists adds further weight to the fact that two non-drug options – ginger and acupressure bands – can be helpful in relieving nausea.

BBC report: Ginger and acupressure ‘options for morning sickness’

These are non-drug options which are also worth considering when nausea occurs in ME/CFS.

However, whilst nausea and sickness can be a symptom of ME/CFS, it is important to exclude other possible medical explanations before doctors or patients conclude that this is ‘just another ME/CFS symptom’.

Medical information on acupressure bands: Sea-bands

More information on ginger (from Cancer Research UK):

Some people find ginger very helpful when feeling sick. People say it is particularly good for motion sickness. You can use ginger any way you like, for example as crystallised stem ginger. Or you can add freshly ground ginger to your favourite dishes, or to hot water or tea to make a soothing drink. You can try sipping ginger ale. Fizzy drinks sometimes help to reduce nausea too.

Researchers have been looking at using ginger alongside anti sickness medicines during chemotherapy. But the results so far have been mixed. So more research is needed.

Drug treatment options for nausea and vomiting. Source: patient information UK

* Cinnarizine, cyclizine, promethazine – these medicines belong to a group of medicines called antihistamines. The exact way that they work is not fully understood. It is thought that antihistamines block histamine 1 (H1) receptors in the area of the brain which creates nausea in response to chemicals in the body. They are thought to work well for nausea caused by a number of conditions including ear problems and motion (travel) sickness.

* Hyoscine – this medicine works by blocking a chemical in the brain called acetylcholine. It is a type of medicine called an antimuscarinic (or anticholinergic). It works well for nausea caused by ear problems and motion sickness.

* Chlorpromazine, haloperidol, perphenazine, prochlorperazine, levomepromazine– these medicines work by blocking a chemical in the brain called dopamine. They are useful for nausea that is caused by some cancers, radiation, and opiate medicines such as morphine and codeine. Prochlorperazine (or brand name Stemetil®) is one of the most used medicines for nausea. It works for many causes of nausea, including vertigo, ear problems and sickness in pregnancy.

* Metoclopramide – this medicine works directly on your gut. It eases the feelings of sickness by helping to empty the stomach and speed up how quickly food moves through the gut. It is often used for people with sickness due to gut problems or migraine. It is not usually used for more than a few days.

* Domperidone – this medicine works on the CTZ (an area of the brain known as the chemoreceptor trigger zone). It also speeds up the emptying of the gut. It is not usually used for more than a few days.

* Dexamethasone – this is a steroid medicine. It is a man-made version of a natural hormone produced by your own body. Dexamethasone has a wide range of actions on many parts of the body. The reason why it reduces nausea isn’t clear.

* Granisetron, ondansetron, and palonosetron – these medicines work by blocking a chemical called serotonin (5-HT) in the gut, and the brain. Serotonin (5-HT) has an action in the gut and the brain to cause nausea. These medicines are useful for controlling nausea and vomiting caused by chemotherapy.

* Aprepitant and fosaprepitant – these are newer medicines and work by blocking a chemical that acts on neurokinin receptors in the body to cause nausea. They are sometimes called neurokinin-1 receptor antagonists. They are usually given to people on a certain type of chemotherapy.

* Nabilone – it is still not clear how this medicine works to control nausea. It is normally prescribed for people who are having chemotherapy.

Medicines for nausea are available as tablets capsules, liquids, suppositories and skin patches. Some are given as injections into the muscle or directly into the vein.

Some of these medicines are also available as tablets that dissolve in the mouth against the gum. They are called buccal tablets. These medicines come in various different brand names.

Dr Charles Shepherd
Hon Medical Adviser, ME Association

 

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