The Unexpected Benefits of Supplementing with Colostrum

Colostrum is the fluid produced by new, nursing mothers in the first days after the birth of their child. Humans produce colostrum, along with all other nursing mammals. If you or your partner has ever nursed a baby, you may remember that in the first few days of nursing, the milk is thick and a soft yellow color reminiscent of good, grass fed butter. 

Cows, being mammals, also produce colostrum the first few days of nursing, and dried bovine colostrum is available as a supplement in tablet or powder form. Goat colostrum is also available. Bovine and goat colostrum are very similar in composition to human colostrum. Supplementing with colostrum may seem a bit, well,  gross to some, but the benefits are so valuable to your immune system and gut that it’s worth exploring. This article will go over some colostrum benefits for your health.  

Colostrum Benefits

1. Leaky Gut

As colostrum is the very first substance to go through a newborn’s intestinal tract, it makes sense that it helps to set your little one up for digestive health and wellness. In fact, babies who are only fed formula and miss out on the colostrum in breast milk are more susceptible to a wide range of illnesses. 

Later in life, colostrum supplementation may help heal a damaged gut lining by supporting tight junctions between the cells that compose the lining of the intestinal tract. Supplementing with colostrum may help heal “leaky gut syndrome” – a condition where small food particles are able to slip between intestinal cells that are not tightly joined and enter the body cavity or the bloodstream, causing an allergic or inflammatory response.

2. Immune Health

The colostrum in human breast milk helps to establish a newborn’s innate immune system in a number of ways. Supplementing with colostrum later in life may help support immunity as well. Two possible ways colostrum can support your immune system are listed below:

1. Colostrum may support natural killer cell (NK cell) activity. NK cells are lymphocytes – white blood cells responsible for identifying and destroying pathogens such as bacteria, viruses, fungi, and parasites. Supplementing with colostrum may help support NK cell activity, thereby increasing resistance to pathogens.

A 2014 study on mice infected with the influenza virus demonstrated that colostrum supplementation enhanced NK cell cytotoxicity — the ability of NK cells to kill pathogens. The mice treated with colostrum lost less weight than controls while they were sick, and developed less of a viral burden in their lungs.

2. Colostrum may increase available immunoglobulins. Breast feeding, and specifically the colostrum in breast milk, builds and supports a newborn’s immune system in part by delivering immunoglobulin proteins. Immunoglobulins are antibodies that bind to pathogens and allergens and aid in their destruction. They are present in bovine colostrum.

A 2018 review of the effect of bovine immunoglobulins on the human immune system determined that taking colostrum delivered functionally active immunoglobulins to the intestinal tract.

3. Inflammation

Colostrum is filled with proline rich polypeptides (PRPs), which have been shown to help combat inflammatory response mechanisms. PRPs help to regulate the production of cytokines, key components of inflammation. PRPs may also inhibit the production of damaging reactive oxygen species, which also cause inflammation.

Colostrum also contains lactoferrin, an antioxidant potentially helpful for decreasing inflammatory reactive oxygen species. Lactoferrin has been shown to have an inhibitory effect on autoimmune responses and may be helpful with detoxification.

Allergic Reactions to Colostrum

Colostrum is not milk — it contains almost zero lactose. However, if you are lactose intolerant or have a dairy allergy, check with your doctor to make sure colostrum will be safe for you. Many people who do not tolerate dairy may find that they don’t react badly to colostrum, and goat colostrum may be even easier to digest. Be aware that lower quality colostrum supplements may contain additives such as dairy or soy — so read the small print for all allergen information.

Choosing the Best Colostrum Supplement

A quality colostrum product will be one that comes from organic, grass-fed milk sources, and uses humane, ethical practices when it comes to how the animals are treated, including making sure baby calves get the colostrum they need before harvesting what’s left for human use. 

Colostrum is available in tablet or powder forms. The colostrum powder is reminiscent of the taste of powdered milk. I’ve added it to protein shakes and smoothies, where I can’t even taste it at all.

Colostrum is a powerful substance that may help support immunity, improve gut health, and lower inflammation. Supplementing with high quality colostrum may improve your overall health and wellbeing. 


Shona Curley lives and works in San Francisco. She is co-owner of the studio Hasti Pilates, and creator of the website www.redkitemeditations.com. Shona teaches meditation, bodywork and movement practices for healing Lyme disease, chronic illness and pain.

 

 

References:

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3 Surprising Benefits of The Ancient Herb Astragulus

Astragalus roots have been used in Traditional Chinese Medicine (TCM) for millennia to balance a myriad of symptoms and complaints, particularly stress and immune dysfunction. The plant they come from, Astragalus membranaceus, is native to Northern China, as well as to Mongolia and Korea. Its roots are a distinctive pale yellow, and according to TCM, their medicinal properties are most potent when harvested from four-year-old plants. 

As TCM has become more widely accepted and practiced in the West, scientists have begun to study how astragalus works in the body, and the plant has found its way into the practices of Western herbalists, acupuncturists, and naturopathic doctors. This article will explore some of the benefits of astragalus, the forms in which you can take it, and who should be most careful of its effects.

Astragalus As An Adaptogen

In TCM, astragalus root is considered an adaptogen. Adaptogens are herbs thought to assist the body in coping with stress from various sources: physical, emotional, or mental. In TCM, astragalus root may be administered for a wide range of ailments. TCM practitioners believe that astragalus root supports the body in coping with whatever stress is causing an imbalance and to appropriately self-heal.

Astragalus As An Antioxidant

Astragalus is full of antioxidants – phytochemicals that help to prevent oxidative stress in the body. Oxidative stress occurs naturally during immune response and other natural cellular processes. It involves the creation of free radicals; unstable molecules that, when left unchecked, can damage cell tissue. The body has its own way of cleaning up free radicals, but under stress, we can always use a little extra boost. The antioxidants in astragalus may reduce the number of free radicals circulating in the body, which, in turn, can help lower chronic inflammation. Perhaps this contributes to astragalus’s power as an adaptogen as well.

What Do Scientific Studies Say about Astragalus?

Research on astragalus is promising as to its ability to improve immunity, lower inflammation, and maintain a healthy heart. Here, we’ll take a look at some of the emerging areas of interest for this ancient herb.  

1. Activates Immune Response

A 2012 study looked at astragalus extract’s effect on macrophages – white blood cells in our immune system that destroy pathogens such as viruses, bacteria, fungi, or parasites. The study determined that astragalus extract both increased cell migration in macrophages, and increased their immune response, which may play a role in bolstering our defenses against infections. 

2. Lowers Inflammation

A 2009 study on inflammatory colitis in rats demonstrated that both oral and intracolonic application of astragalus had significant protective effects through modulation of inflammatory cytokine response in the colon. The study showed that the herb balanced the expression of certain anti-inflammatory chemicals in the body, allowing for a reduction in colitis symptoms. However, more research is needed to determine if astragalus would be an effective therapeutic intervention in humans.   

3. Promotes a Healthy Heart

Astragulus’ antioxidant status may be an essential component that allows this herb to promote heart health. Antioxidants hold promise when it comes to reducing the risk of plaque buildup in the arteries and protecting the blood vessels against cardiovascular conditions. For example, astragalus injections, along with conventional treatment options, helped to combat viral myocarditis (inflammation of the heart muscle) more effectively than conventional treatments alone, reports a 2014 study in the Chinese Journal of Integrative Medicine. Additionally, astragalus may also hold promise for lowering blood pressure and reducing elevating fat triglyceride levels.

A word of caution: As with most traditional herbal remedies, more studies are needed to better understand why and how astragalus works and to determine dosage. 

How Do You Take Astragalus?

Astragalus is an edible root, so you can chop it up and add it to soup, or mix a little of the powder into a smoothie. It does have a slightly bitter and earthy taste, which will not be to everyone’s liking. If eating it isn’t your thing, you can supplement with astragalus in tincture form, in tablets, as a powder, or boiled as a tea.

Side Effects and Contraindications

Astragalus may increase immune response. As a result, people with the following conditions should avoid it: 

  • Those with autoimmune disorders
  • Those who have had organ transplants
  • People taking corticosteroid medications

Also, no studies have been done on the safety of astragalus for pregnant or nursing women, so it may be best in those cases to avoid it as well. Again, your healthcare provider can give you the best counsel about whether astragalus is right for you.

In general, astragalus could be a safe and natural way to help your body handle stress, boost immunity, lower inflammation, and stay heart healthy. It’s relatively inexpensive in its whole or powder forms and is easy to boil into tea or include in soups or smoothies. Talk with your doctor, and decide how best to safely include it in your health and wellness routine.


Shona Curley lives and works in San Francisco. She is co-owner of the studio Hasti Pilates, and creator of the website www.redkitemeditations.com. Shona teaches meditation, bodywork and movement practices for healing Lyme disease, chronic illness and pain.

 

 

References:

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Chronotropic Intolerance: An Overlooked Determinant of Symptoms and Activity Limitation in ME/CFS?

Chronotropic Intolerance: An Overlooked Determinant of Symptoms and Activity Limitation in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome?

Abstract

Post-exertional malaise (PEM) is the hallmark clinical feature of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). PEM involves a constellation of substantially disabling signs and symptoms that occur in response to physical, mental, emotional, and spiritual over-exertion. Because PEM occurs in response to over-exertion, physiological measurements obtained during standardized exertional paradigms hold promise to contribute greatly to our understanding of the cardiovascular, pulmonary, and metabolic states underlying PEM.

In turn, information from standardized exertional paradigms can inform patho-etiologic studies and analeptic management strategies in people with ME/CFS. Several studies have been published that describe physiologic responses to exercise in people with ME/CFS, using maximal cardiopulmonary testing (CPET) as a standardized physiologic stressor. In both non-disabled people and people with a wide range of health conditions, the relationship between exercise heart rate (HR) and exercise workload during maximal CPET are repeatable and demonstrate a positive linear relationship.

However, smaller or reduced increases in heart rate during CPET are consistently observed in ME/CFS. This blunted rise in heart rate is called chronotropic intolerance (CI). CI reflects an inability to appropriately increase cardiac output because of smaller than expected increases in heart rate. The purposes of this review are to (1) define CI and discuss its applications to clinical populations; (2) summarize existing data regarding heart rate responses to exercise obtained during maximal CPET in people with ME/CFS that have been published in the peer-reviewed literature through systematic review and meta-analysis; and (3) discuss how trends related to CI in ME/CFS observed in the literature should influence future patho-etiological research designs and clinical practice.

Source: Todd E. Davenport, Mary Lehnen, Staci R. Stevens, J. Mark VanNess, Jared Stevens and Christopher R. Snell. Chronotropic Intolerance: An Overlooked Determinant of Symptoms and Activity Limitation in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome? Front. Pediatr., 22 March 2019 | https://doi.org/10.3389/fped.2019.00082 (Full article)

A Former Doctor Goes Through the NIH’s ME/CFS Intramural Study

Reprinted with the kind permission of Simmaron Research.

By Cort Johnson

Robert’s Story

Robert, an MD, is board certified in internal medicine. After the worst flu-like illness he ever had, he ended up in the hospital. A regular exerciser prior to becoming ill, his legs were so weak that he could hardly walk afterwards.

His path to a chronic fatigue syndrome (ME/CFS) diagnosis was rapid. Three months of testing left him no other conclusion – it was clear to him that he had ME/CFS. He was able to work on and off for a few years, but his health has deteriorated. He’s been unable to work for the last three years.

Thankfully, he had a wide array of doctor friends who knew him before he became ill and didn’t encounter the skepticism and invalidation so commonly experienced in our community. He noted that our current medical culture doesn’t offer much for the complex patient. Doctors are busy and often time-constrained and if you don’t fit into one of the medical pigeon-holes, they don’t have much to offer.

Rating his level of health on a scale of 1-10 at 2, he’s one of the sickest, if not the sickest, ME/CFS patient to participate in the grueling two-part intramural study at the NIH. He was the first patient to go through the second phase of the Intramural trial which involved, among other things, the exercise study and an extended stay in a metabolic chamber.

One theme – validation – cropped up several times during Robert’s week long stay at the NIH hospital in Maryland. It was clearly apparent from the gestures of sympathy from the occupational therapist during a test to assess functioning. Given cards which identified an activity, Robert put them into two piles – activities he used to do and activities he still did. The occupational therapist – who has probably given this test hundreds if not thousands of times – registered dismay at the few cards left in his “still do” pile. Those few cards left made the extra level of devastation that ME/CFS is so good at causing clear. It’s rare for people who are not elderly to be so sick.

Given his abysmal level of functioning, Robert’s willingness to participate in a study that Dr. Nath thought few might be willing to undergo was a real testament to the courage and determination that so impressed Dr. Nath. Despite Robert’s low functional level (1-2 on a 10-point scale), he was disappointed that the NIH was not doing a two-day exercise test (!).

The second part of the study is centered around the exercise stressor. Participants do cognitive testing, blood tests, the Seahorse mitochondrial test, a functional MRI and transcranial magnetic stimulation before and after the maximal exercise test. (The NIH communicated with the Workwell Foundation on doing the exercise test with ME/CFS patients).

Exercise is finally getting its due in ME/CFS, and over the next couple of years several large studies should tell us much. With its extensive blood draws and millions of data points, Dr. Klimas’s exercise studies have informed her models of ME/CFS and laid the foundations for her clinical trial. With help from the Solve ME/CFS Initiative, David Systrom has added gene expression to his already complex invasive cardiopulmonary exercise testing. Maureen Hanson has incorporated exercise into her large NIH Research Center studies at Cornell, as well. None of these studies, though, can match the sheer breadth of this NIH exercise study with its brain scans, lumbar punctures, Seahorse data, blood draws, etc..

Metabolic Chamber

Robert spent about three days in the metabolic chamber – a sparse box containing a bed and a toilet that’s designed to produce precise measures of metabolic activity – before and after the exercise test. (I will expand on the metabolic chamber). He wore an EEG, blood pressure and Holter monitor, while in the chamber.

Only thirty metabolic chambers exist in the world, and three of them are at the NIH. With 400 metabolic chamber studies underway every year, they’re pretty much in use all the time. These airtight 11-by-11.5-foot rooms aren’t much to look at or stay in: they come with a bed, an exercise bike, a toilet, and nothing else. Precisely measured meals are delivered through a small, air-locked opening in the wall.

Metal pipes running along the ceiling that measure oxygen consumption and CO2 production allow researchers to precisely calculate an individual’s metabolic rate. From the O2 and CO2 readings, researchers can calculate calories burned and what type of fuel (carbs/fats) was used to burn them. Urine is collected to assess protein oxidation.

Metabolic chamber studies have demonstrated how flexible the body is with respect to metabolism. One reporter wrote, for instance, that they’ve debunked the idea that ketogenic diets (high-fat/low-carb) cause the body to burn more fat than high-carb diets.

Energy is burned in our body in three ways. It turns out that simply staying alive is pretty energy intensive. Most of the calories we burn (65-80%) are used simply to keep our body running (basal metabolism). Digestion is no walk in the park either; digesting our food takes up about 10% of the calories we burn in a day, with physical activity accounting for the remainder (10-30%).

If ME/CFS patients’ metabolic production and ability to produce energy is altered by exercise – as Workwell’s and Dr. Keller’s tests suggest it is – that will hopefully be picked up by the metabolic chamber.

Robert noted that if they can pair the findings from the metabolic chamber – which is measuring the metabolic effects of exercise – with the Seahorse tests- which are measuring energy production on the cellular level, they may really be onto something.

Brain Scan

The functional MRI – which Robert said was combined with a cognitive test – will assess the impact of exercise on a) cognitive functioning and b) brain functioning. A similar study by the CDC suggested that exercise negatively impacted both cognitive and brain functioning.

People who do cognitive tests tend to improve the more they do them but not in this case – not in people with ME/CFS after exercise. Familiarity did not breed more competence. Despite doing the tests multiple times, the people with ME/CFS did worse and worse on them after exercise and the brain scans indicated why. Exercise had knocked out one area of the brain devoted to sustained attention causing the brain – in a mostly futile attempt to compensate – to increase activity in other parts of the brain (devoted to executive functioning).

The end result was that people with ME/CFS expended more effort during the cognitive test and yet did worse. By the end of the test they were making about double the errors of the healthy controls.

The repetitive transcranial magnetic stimulation (rTMS) test proved enormously interesting but physically draining. Robert reported that in a process that took hours, data from a previous fMRI was used map the exact location of his motor cortex in order to stimulate the muscles of his right hand/fingers. The goal was apparently to determine the speed at which the signal traveled from the brain to the muscle of his finger before and after exercise. A time delay after exercise would presumably indicate that exercise had interfered with the ability of the motor cortex to activate the muscles.

A 2003 study, in fact, suggested that reduced muscle recruitment due to reduced motor cortex output was occurring in ME/CFS. The motor cortex, it turns out, plans our movements in advance. The study, titled “Deficit in motor performance correlates with changed corticospinal excitability in patients with chronic fatigue syndrome“ suggested that problems in the “motor preparatory areas of the brain” might be hampering physical movements in ME/CFS. It has never to my knowledge been followed up on.

rTMS has relieved pain in fibromyalgia but it had the opposite effects in Robert. He wasn’t clear whether it was the effects of the rTMS or the rigors of setting up the test itself or both which triggered for him what turned out to be an extraordinary bout of PEM (post exertional malaise). The 2 hours it took – sitting up – to get the electrodes correct was in itself draining. (He suggested that they use a reclining chair for future patients if possible.)

At the end of test Robert felt exhausted and experienced transient vertigo, auditory disturbance, headache and sensitivity to light and noises. His nurse was shocked at how poorly he looked. He’d mentioned the documentary Unrest to her the day before. After seeing the movie, she said she could better appreciate what he was going through. (Hopefully she knows that watching the film will get her continuing medical education (CME) credits)

The rTMS test proved immediately much more exhausting than the exercise test, the effects of which took a day to kick in. The rTMS specialist/researcher was surprised at the effect the test had on Robert and its cause is unknown. Was it the long preparatory period or the activity of the rTMS machine on the muscle activation pathways or both? It’ll be fascinating to see how other patients fare.

Robert was also tested for small fiber neuropathy via skin biopsy, underwent a post exercise lumbar puncture and quadricep muscle biopsy. The possibility of integrating the brain scan, cerebral spinal fluid, Seahorse and metabolic chamber results after exercise – not to mention the immune tests – is an enticing one for sure.

Plus there are the muscle biopsy results. Robert’s experience of a rather hefty muscle biopsy suggests that the NIH is not stinting on this area – which Dr. Nath believes may tell us much about ME/CFS.

Plenty of rest periods were provided during the study but at times the testing was lengthy, and the study, predictably, ended up being a rather grueling seven days for this courageous but very disabled ME/CFS patient. Participating in it wasn’t easy but the fact that Robert, even with his abysmal level of functionality, made it through it and recovered, was a good sign. Robert said he was touched by a chaplain who stopped by to see how he was doing.

He’s stayed in touch with the investigators from time to time alerting them of developments in the ME/CFS field.

Participating in the Study

The NIH needs more participants. If you’re interested in helping to further ME/CFS research by participating in the study, check out the study criteria below.

All participants must be 18-60 years old and have at least a 7th grade education. People whose ME/CFS started after an episode of infection and who have severe symptoms lasting from 6 months to 5 years are eligible to participate in the study.

Find out how to participate here.

The Brainstem, Vagus Nerve, Neuroinflammation and Chronic Fatigue Syndrome: The VanElzakker Way

Reprinted with the kind permission of Simmaron Research.

By Cort Johnson

In 2013, Michael VanElzakker produced one of the most intriguing hypotheses to date in ME/CFS. His Vagus Nerve Hypothesis proposed that an infection/inflammation near the vagus nerve was causing it to send an unending stream of messages to the brain, telling it to essentially shut the body down by producing fatigue, pain and other symptoms. Since then, he’s been particularly interested in the connection between the vagus nerve, the brainstem and the ME/CFS.

He’s not the only one interested in the brainstem. In 2019 once his brainstem compression was alleviated, Jeff completely recovered from his severe ME/CFS, POTS and MCAS. Since he published his story over a dozen people have been diagnosed with craniocervical instability – a condition which compresses the brainstem.

In this critical review paper, VanElzakker et. al. pick apart some of the research done and provide a guide to successfully getting at the brainstem and other regions of the brain. It’s called a “Critical Review” and is critical, indeed. It finds many past ME/CFS studies wanting, but then points a way to a better possible future. If brainstem problems play a role in ME/CFS these researchers demonstrate how to get at them.

Neuroinflammation and Cytokines in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): A Critical Review of Research Methods. Michael B. VanElzakker, Sydney A. Brumfield and Paula S. Lara Mejia. Front. Neurol., 10 January 2019 https://doi.org/10.3389/fneur.2018.01033 https://www.frontiersin.org/articles/10.3389/fneur.2018.01033/full

First, VanElzakker et. al. examines one of the sacred cows in the chronic fatigue syndrome (ME/CFS) community – the preferred term for so many: myalgic encephalomyelitis (ME), which refers to muscle pain (myalgia) related to central nervous system inflammation (encephalomyelitis).

While muscle pain is common, it’s not universal. Even people with severe ME may not report pain.

Still, the core part of the definition deals with central nervous system inflammation – a description that, with the emergence of the 2015 Yakatomi and the 2019 Younger studies, seems more and more likely to stick. (A 2018 PET scan study also found neuroinflammation in fibromyalgia as well.)

The idea that inflammation plays a key role in this illness makes sense, given the infectious trigger so commonly (but not universally) found. The authors are just a few among many (Avindra Nath, Jarred Younger, Andrew Lloyd and others) who believe that an infectious event has triggered changes in the brain that are producing fatigue, pain and other problems in ME/CFS.

They point to three ways an infectious trigger could produce central nervous system inflammation in ME/CFS:

A) immune factors (e.g. cytokines) triggered by the infection could get transported across the blood-brain barrier (BBB) that protects the brain. The normally taut blood–brain barrier makes blood-borne infections of the brain rare, but it can, like the gut, become leaky in inflammatory states, allowing immune factors and pathogens entry. Once in the central nervous system, they could trigger a large inflammatory response, or

B) High concentrations of immune factors could allow pathogens to passively diffuse across the BBB, or

C) Immune factors in the blood could trigger the vagus nerve to send signals to the brainstem and brain, which then sparks an inflammatory response.

It’s the last option that primarily concerns these authors. VanElzakker is the author of the Vagus Nerve Hypothesis, which proposes that an infection/inflammation near the vagus nerve is causing it to send an unrelenting stream of signals to the brain, telling it to produce the flu-like symptoms that constitute “sickness behavior” (withdrawal to bed), which isolates infected people from the community and keeps them from spreading an infection.

The largest nerve in the body, the vagus nerve transmits sensory, autonomic, immune and other signals to the brainstem – making it potentially a key player in a possible neuroinflammatory disease like ME/CFS.

Studies indicate that inflammation in the periphery tends to produce a mirror inflammatory response from the immune cells (the glia) in the brain. Even small levels of cytokines in the periphery or body have the potential to activate the chemoreceptors in the vagus nerve, which then activate the immune system in the brain.

That brain activation, interestingly, tends to occur in regions (basal ganglia, limbic system organs (amygdala, hippocampus and hypothalamus), anterior cingulate cortex, prefrontal cortex, and thalamus), which studies suggest are also involved in ME/CFS.

The authors believe the brainstem (which, as it name implies, is found at the very base of the brain, above the termination of the spinal cord), could play a key role in chronic fatigue syndrome (ME/CFS) for four reasons:

  1. Immune signals from the vagus nerve to the brain travel through the brainstem.
  2. The brainstem is dense with mast cells, and mast cell activation syndrome (MCAS) appears to be common in ME/CFS.
  3. The brainstem regulates autonomic nervous system functioning – a common trouble area for ME/CFS and related disorders.
  4. The brainstem also regulates immune functioning; in particular, it triggers an anti-inflammatory response that should limit the inflammatory response.

Whether caused by a structural problem (as in Jeff’s case), inflammation or an infection, the brainstem is a centrally placed brain component that produces many of the issues in ME/CFS.

Seeing the Brainstem in Chronic Fatigue Syndrome (ME/CFS)

Consistent inflammation of the brainstem has not, however, been found in ME/CFS. The authors argue, though, that researchers have rarely used the right kind of imaging needed to investigate this.

The most commonly used method for measuring inflammation in the brain involves measuring the 18kD translocator protein (TSPO) with a PET scan. This protein is produced when the immune cells of the brain – the microglia – become activated. Because the microglia are the chief producers of inflammation in the brain, the TSPO provides a reliable way to indirectly measure neuroinflammation and its effects.

The Nakatomi Study

Nakotomi’s small ME/CFS study using TSPO made a big splash in 2014. Tony Komaroff called the finding of central nervous system inflammation the most important study in decades. Five years later, Van Elzakker et. al. called it “important” and potentially “groundbreaking”. The study used TSPO imaging to find widespread neuroinflammation, particularly in the areas leading from the brainstem to the thalamus.

While the authors regard Nakatomi’s study as potentially groundbreaking, the study is not without significant issues. The authors, in fact, seemed a bit shocked that Nakatomi found as many effects as he did, given the techniques used.

The neuroimaging techniques Nakatomi used (and which most researchers use) were not designed to address brainstem inflammation. Nakatomi used a spatial “registration” technique that aligns the image on the neocortex or upper part of the brain. This kind of alignment is typically done because researchers tend to focus on the upper, “higher” functioning areas of the brain. It can, however, impair the sensitivity of imaging done on the lower, more densely packed, primitive areas of the brain, such as the brainstem, and lead to false negatives.

Nakatomi also used an older tracer (PK-11195) which does not penetrate deeply into the brain and can bind to unintended elements in the brain. Differences in blood-brain barrier permeability between the ME/CFS patients and healthy controls – a distinct possibility – could have confounded the results, as well. Nakatomi’s use of the cerebellum as a kind of baseline measure could have introduced further issues if problems with the cerebellum (another possibility) exist in ME/CFS.

Plus, the hypometabolism believed present in ME/CFS could have resulted in lower amounts of the tracer being metabolized than usual – causing higher amounts of the tracer to reach the brain – and producing a false positive. Because exercise may affect how much of the tracer is taken up into the cells, Nakatomi’s use of healthy, non-sedentary controls instead of sedentary controls introduced another issue.

Finally, because the brainstem actually pulses with every heartbeat, that movement needs to be accounted for – and usually isn’t in ME/CFS studies. The very small but important nuclei in the brainstem are also often not picked up with the standard imaging techniques used in ME/CFS research.

Nakatomi’s study results make sense given what we know, and were given a sort of validation by Jarred Younger’s recent results using thermal mapping – a new technology – but we need more validation.

The takeaway is that the brainstem – because of the role it plays in autonomic nervous system functioning, immune regulation and the transmission of motor signals – could play a major role in ME/CFS, but is essentially, according to these authors, still something of a black box.

Barnden’s Brainstem – the Australian Study

It’s not completely a black box, though. Researchers using other techniques have found evidence of brainstem problems in ME/CFS. Barndem in Australia, in particular, has done a series of MRI studies which have found striking brainstem issues in ME/CFS.

(During his talk at the 2019 Emerge conference, Barnden noted how he had to shift his MRI to avoid the alignment problem (that VanElzakker mentioned) which prevented him from getting a good image of the brainstem. )

One study found that reduced brainstem grey matter volume – suggesting that damage to the neurons in the brainstem had occurred – was correlated with autonomic nervous system problems in ME/CFS.

Another study finding of impaired communication from the brainstem nuclei to other nuclei in the brain suggested the same, and found increased signs of myelination in the sensorimotor cortex of the brain. Barnden proposed that decreased signaling from a damaged brainstem provoked a compensatory increase in myelination in the sensorimotor region as it bulked up to try to understand the limited signaling coming from the brainstem. The impaired brainstem-sensorimotor connection might be, Barnden thought, impacting motor functioning in ME; i.e. the ability to carry out physical activity.

Signals to move muscles pass from the motor cortex to the sensorimotor cortex down to the thalamus and then through the brainstem to the muscles. (Signals from the muscles to the brain pass up through the same pathways.) Barnden proposed that the movement problems in ME/CFS could start with the brainstem’s inability to properly relay signals to the motor cortex to activate the muscles.

Barnden’s most recent brainstem study validated the idea that inadequate communication between the brainstem nuclei and other nuclei in the brain, including the vasomotor region, hypothalamus and prefrontal cortex, was affecting autonomic nervous system functioning in ME/CFS.

Other Kinds of Brain Scans

Other kinds of brain scans, such as magnetic resonance spectroscopy (MRS), can pick up signs of neuroinflammation. Although almost 10 MRS studies of the brain in ME/CFS have been done, VanElzakker et. al. report that a clear and consistent picture of metabolite alterations in the brain has yet to emerge.

They believe that’s due largely to a common theme in medical research, found in this disease in particular – lack of standardization. Different diagnostic criteria, different types of healthy controls, different brain regions examined, and different metabolites targeted make it difficult to present a clear picture of the metabolic alterations in the brains of people with ME/CFS.

The Japanese Take

The Japanese probably couldn’t agree with Barnden more. Their studies indicate that, as the healthy controls became more fatigued, two core regions – both of which communicate with the brainstem ( the prefrontal cortex and the anterior cingulate cortex) – shut down.

As these regions begin to shut down, control of autonomic functioning becomes lost. In particular, the ability to activate the parasympathetic nervous system (i.e. the vagus nerve) and tone down the sympathetic nervous system activity, is lost.

The Japanese believe a breakdown in what they call the facilitation system in the brain has occurred. As we become fatigued, the facilitation system jumps in to increase the signals coming from the primary motor cortex to the muscles. This increased “drive” from the motor cortex prompts the muscles to work harder and activates more and more of them so that activity can proceed.

So long as new, fresh muscle fibers remain to be recruited, the activity can continue. If no muscle fibers are left to be recruited or if the brain has a problem recruiting new muscle fibers, fatigue sets in.

A 2003 study suggested that reduced muscle recruitment due to reduced motor cortex output was indeed occurring in ME/CFS. That study suggested that, “… changing motor deficits in CFS has a neurophysiological basis [which] … supports the notion of a deficit in motor preparatory areas of the brain”. That study titled, “Deficit in motor performance correlates with changed corticospinal excitability in patients with chronic fatigue syndrome“, to my knowledge was never followed up on.

Conclusion

Several studies suggest significant brainstem issues may be present in ME/CFS. Problems with the brainstem could produce everything from autonomic nervous system problems to immune issues to problems with movement.

The authors critique past brain imaging studies and provide a “how to” guide to assess the brainstem in ME/CFS. Barnden’s Australian brainstem studies suggest that when done correctly, MRI imaging studies may indeed find extensive damage is present in ME/CFS. Barnden found evidence of brainstem neuron demyelination, a compensatory remyelination in parts of the brain the brainstem connects with, and lastly, a reduced connectivity between these regions in ME/CFS.

VanELzakker et. al. assert that future imaging studies that focus on the specific functional connectivity pathways in the brain which are activated by inflammatory processes should be able to capture the neuroinflammatory processes occurring in ME/CFS. (Two of the three pathways they cite include the brainstem.) The thalamus’s role in sensory stimuli activity presents another fruitful pathway to assess. Lastly, the authors suggest that researchers target the nucleus of the solitary tract (NTS) where the vagus nerve enters the brainstem.

With help from an ME/CFS donor, VanElzakker has been employing brain imagining techniques to assess the brainstem in chronic fatigue syndrome (ME/CFS). He will be speaking at the NIH ME/CFS Conference in Baltimore in April.

Marjoram: A Versatile Herb for Cooking and Aromatherapy

Reprinted with the kind permission of Dr. Mercola.

The marjoram plant (Origanum majorana) is an aromatic herb known for its aromatherapeutic and culinary uses. Its botanical name literally means “mountain beauty.” Interestingly, since marjoram and oregano (Origanum vulgare, which means mountain joy when translated), have often been confused through the years, you may also see marjoram referred to as mountain joy.

In Greek mythology, Aphrodite was believed to have grown this herb, as well as oregano. Romans, on the other hand, believe marjoram was made by Venus.1

Marjoram is classified as a perennial, and can grow up to a height of 24 to 36 inches. It’s closely related to (and often confused with) oregano, because of their similar appearances, most notably because of their oval, flat green leaves.2

To make things even more confusing, as mentioned, their botanical names are quite similar. But even more confusing, Origanum vulgare, which is the common oregano, is also known as wild marjoram. Since it can be very confusing, be sure to do your research before you purchase either of these plants.3

The 6 Health Benefits of Marjoram You Should Know About

Marjoram can be used in cooking or in aromatherapy, in its essential oil form. That being said, depending on how it’s used, marjoram is known to provide the following health benefits:

  1. Antioxidants — A 2005 study showed that marjoram contains various antioxidants. Most notably, Egyptian varieties contained more antioxidants compared to Hungarian ones.4
  2. Antimicrobial — Extracts of marjoram have been found to be effective against several species of fungi and bacteria.5
  3. Anti-inflammatory — In vitro examination of marjoram showed that it may help manage inflammation. Researchers discovered that the plant suppressed pro-inflammatory cytokines. Sabinene hydrate and terpineol have been identified as the main anti-inflammatory compounds.6
  4. Better digestion — A mice study showed that marjoram extract exhibits antiulcer properties, as well as reducing basal gastric secretion and acid output. In addition, marjoram may help repair the gastric mucosa.7
  5. Reduced risk of cancers — A PLOS One study showed that marjoram has promising potential in modulating breast cancer growth and metastasis.8 Another study shows that marjoram extracts have beneficial effects against human lymphoblastic leukemia cell line.9
  6. Better heart health — A study found that marjoram helped alleviate erythrocytosis, granulocytosis, thrombocytosis and myocardial oxidative stress, as well as other cardiovascular factors.10

4 Ways to Use Marjoram Effectively

The beauty of marjoram is that it can be added to various dishes and can be used for different cooking methods, such as:

  1. Soups — It gives vegetable soups more flavor.11
  2. Roasted meats — Marjoram can add an herbal aroma to roasted meats, such as chicken.12
  3. Sautéed vegetables — Side dishes such as sautéed vegetables become more flavorful with a dash of marjoram.13
  4. Marinades — Upgrade the taste of your marinated meat and fish dishes by adding marjoram to the marinade.14

Planting marjoram in your garden can reap benefits as well. Not only does it create a beautiful atmosphere, but it also helps attract butterflies and other insects that feed on pests and decomposing matter, and can even pollinate plants.15,16

Oregano can be used as a substitute for marjoram if you don’t have it at the moment. But remember that although these two plants are very similar in appearance, they do have slight differences in flavor. Oregano has a pungent, spicy taste, while marjoram is sweeter and floral. If you want to use oregano in place of marjoram, only use a small amount to mellow out its strong taste.17

Growing Marjoram in Your Home

Marjoram is quite easy to grow in the comfort of your own home. It can be placed in an indoor container, window box or outdoors in your garden.

Start by making sure your soil has good drainage. Sunlight exposure must be at its fullest for the plant to grow well.18 Plant marjoram seeds during the late winter or early spring, because the extremely cold temperatures will damage the plants and may even cause seedlings to die out.19

If you’re just starting out, plant indoors first and when the snow has melted, you can transfer your site outdoors. Make sure that the location has plenty of sunlight, and the soil follows the appropriate conditions.20

Start planting seeds by placing them just beneath the surface of the soil. As the seedlings grow, remember to clear up space by placing each of them 10 inches apart in all directions. The plants are ready for harvesting once they reach a height of 3 inches. To get the best flavor, pick them before the flowers start to open.

Once picked, dry them to seal in their taste and aroma. Simply group plants in small bundles and hang them upside down in a dark room with good ventilation. Afterward, remove the stems, then crush or grind before using.21

Try This Healthy Recipe: Spicy Roast Chicken With Tomatoes and Marjoram

This recipe from Bon Appétit uses marjoram to provide roast chicken with a wonderful aroma and flavor. With the addition of tomatoes and red pepper, this dish is not only delicious, but warm and inviting as well.22

Ingredients

4 pasture-raised chicken breast halves with ribs
24 ounces cherry tomatoes (about 4 cups), stemmed
1/4 cup coconut oil
5 garlic cloves, pressed
1 1/4 teaspoons dried crushed red pepper
2 tablespoons chopped fresh marjoram
Himalayan salt and freshly ground pepper, to taste

Procedure

  • Heat the oven to 450 degrees Fahrenheit.
  • Toss the tomatoes, coconut oil, garlic, crushed red pepper and a tablespoon of marjoram in a large bowl.
  • Place the chicken slices on a rimmed baking sheet.
  • Pour the mixture over the chicken, while arranging the tomatoes in a single layer on a sheet around the chicken.
  • Sprinkle the chicken slices generously with salt and pepper.
  • Roast until the chicken slices are cooked through and the tomatoes are blistered, for about 35 minutes.
  • Transfer the chickens to plates.
  • Spoon the tomatoes and juices over.
  • Sprinkle the plates with the remaining tablespoon of marjoram and serve.

Marjoram Essential Oil Has Unique Benefits, Too
Marjoram oil has been a popular fixture in folklore medicine for a long time. Research shows that it has been used as an antimicrobial as well as anti-inflammatory. A 2017 study summarizes the main possible benefits of marjoram essential oil:23

  • Antioxidant
  • Antimicrobial
  • Anticancer
  • Anti-inflammatory
  • Hepatoprotective

How to Make Marjoram Essential Oil

Modern manufacturing of marjoram essential oil is achieved through steam-distilling the tops of the plant. Depending on the source, the final product is a yellow to yellow-green oil. Spanish varieties produce an orange color.24

Using Marjoram Essential Oil Properly

Before using marjoram essential oil (or any essential oil), you need to be aware of any potential allergic reactions. If you have any pre-existing medical conditions or are pregnant, it’s important to consult with your doctor first and let them know of your intention to use marjoram essential oil.

Once you’ve gotten permission from your doctor, do a skin patch test on your arm with a drop of the oil and check for any allergic reaction or irritation. Should a negative reaction occur, stop using the oil immediately.

This article was brought to you by Dr. Mercola.

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Vitamin B12 deficiency could increase risk of infection

Reprinted with the kind permission of Life Extension.

March 18 2019. An article published on March 13, 2019 in PLoS Genetics describes a study involving the roundworm Caenorhabditis elegans (C. elegans) which uncovered a link between insufficient dietary intake of vitamin B12 and a greater risk of potentially lethal infections. Caenorhabditis elegans are similar to humans in their need to obtain vitamin B12 by dietary means.

“We used C. elegans to study the effect of diet on a host and found that one kind of food was able to dramatically increase resistance to multiple stressors — like heat and free radicals — as well as to pathogens,” reported lead researcher Natasha Kirienko, who is an assistant professor of biosciences at Rice University in Houston.

By feeding C. elegans diets consisting of either the OP50 or HT115 strains of the bacteria E. coli, Dr Kirienko’s team found that E. Coli HT115, which provided vitamin B12, improved the worms’ survival after exposure to the bacteria Pseudomonas aeruginosa or Enterococcus faecalis OG1RF. It was determined that a lack of vitamin B12 lowers the worms’ ability to metabolize branched chain amino acids (BCAAs), resulting in an accumulation of partially metabolized BCAAs that damage the mitochondria of the cells. Conversely, increasing vitamin B12 availability improved mitochondrial homeostasis and resistance to infection.

“The key difference between the two diets is the ability of HT115 and OP50 to acquire B12 from the environment,” commented coauthor Alexey Revtovich, a research scientist. “We showed that HT115 is far more efficient at this.”

“Some labs use OP50 as their standard food, and others use HT115 or even another strain of E. coli,” observed coauthor Ryan Lee. “Our results show there are significant metabolic differences between these diets, and it’s likely those differences could contribute to substantial uncertainty in research outcomes.”

—D Dye

Dr Nath Talks on the ME/CFS NIH Intramural Study

Reprinted with the kind permission of Simmaron Research.

By Cort Johnson

It looked like we were going to be late … again. It was pouring cats and dogs as we eased the van around tangled web of streets that is the NIH campus scanning glumly at the rain-obscured buildings. Even our guide on the phone seemed to be lost.

It had been a wild 12 hours. The night before, reaching up to turn on the fan on my brother’s porch, I’d let loose a rather large bug which tumbled into my eye. Howling with pain I stumbled off to the bathroom where I managed to wash it out – leaving my eye reddened and swollen. The next morning, my eye still swollen, my partner insisted I see an eye doctor.

To our surprise we found somebody. The problem was was that his office was right in the heart of downtown Washington DC. – where parking is scarce and traffic cops take their jobs very seriously. Finding no parking we stopped in a loading zone across from the doctor’s office, hoping that the big yellow van with it’s solar panels, Nevada license plate and all would for the next 15 minutes be taken for a loading van –

After being assured the appointment would be short, I dashed inside where I was  bombarded by frantic calls from my partner (who does not drive the van). She had immediately been accosted by first one then another traffic cop.

After seeing the doctor who informed me (for $250 dollars) that insects in the eyes almost never cause problems (but who did give me drops) I dashed back out to the van to find my now none-too happy partner.

We sped off in the rain – still seemingly on time for the appointment with Dr. Nath. Hauling up to the NIH we tried no less than three entrances – only to be turned away at each them (our oversize vehicle thwarting one attempt) – and directed to the next. Finally, as our appointment time came and went, we found the right entrance – for, ironically, delivery vehicles.

After going through an extensive (and time-consuming) security check we headed off into the labyrinth that is the NIH clutching small hard to decipher maps and immediately got lost. The  minutes continued to tick by and rain strengthened into a deluge and eventually we managed to steer onto the right street. Our guide, still on the phone, told us to stop, we jumped out of the car and looked up, rain pouring down, at a steep, muddy climb.

Five minutes later – 45 minutes late for our hour appointment, we strode, soaked and bedraggled into Dr. Nath’s office. He immediately set us at ease, and with his next appointment running late stayed overtime with us. We were there to talk about the NIH Intramural ME/CFS study.

The NIH Intramural ME/CFS Study

Dr. Nath informed us that the applications to be in the NIH Intramural ME/CFS study have been gratifyingly robust.  Dr. Nath noted that it was entirely possible that this is the most rigorously examined patient group ever assembled for a study.

Then it was up to Canada, where he held a faculty position at the University of Manitoba (1990-97), and then he was at The University of Kentucky (1997-02). In 2002, he became Professor of Neurology and Director of the Division of Neuroimmunology and Neurological Infections at Johns Hopkins.Dr. Nath is leading the study. He has been around. He received his MD degree from Christian Medical College in India in 1981, completed a residency in Neurology from The University of Texas Health Science Center in Houston, did a fellowship in Multiple Sclerosis and Neurovirology at the same institution, and then another fellowship in Neuro-AIDS at NINDS.

in 2011, he became the Clinical Director of NINDS, the Director of the Translational Neuroscience Center, and Chief of the Section of Infections of the Nervous System. His research focuses on understanding the pathophysiology of nervous system infections and their outcomes, and the development of new diagnostic and therapeutic approaches for these diseases. He’s heavily involved in HIV research, the role endogenous retroviruses play in neurological diseases, and “undiagnosed neuroimmune and neuroinfectious diseases”.

He recently wrote a paper on Herpes Viruses, Alzheimer’s Disease, and Related Dementias: Unifying or Confusing Hypothesis?, which examined what role herpesviruses might be playing in dementia.

The NIH Intramural Chronic Fatigue Syndrome Study

The study takes place in two parts: a one week part which further assesses the potential participant and another one week section which measures a wide variety of parameters before and after an exercise test.

Requirements for entry are high, however, and not often met. You might say that many have been called – or rather have called – but few have been chosen. That was OK with Dr. Nath. “We need,” he explained, “to make sure that we’re studying the right population. That’s the best way to get to the answer, and then it’ll be broadly applicable.”

The response has been excellent.  Many people are traveling to participate, and they’re coming from all over. The NIH is even getting interest from people in other countries.

As of Dec. last year, 337 people had inquired about the study. One hundred and seventy-three were quickly screened out, and 164 participated in phone interviews. One hundred and twenty-seven made it to the medical record assessment stage.

Multiple reasons thwarted would-be participants from participating in the study.  The study required onset within 5 years which was triggered by infection. One-third had had the disease for too long, 20% had no evidence of infectious process (doctor’s records are required), 9% were too sick to travel, and just 3% were unwilling to have a lumbar puncture.

It is not an easy study! It’s a two-part, two-week plus study on a population, which studies suggest, has the lowest functionality of any disease. The study includes a lumbar puncture, a maximal exercise test, several nights in a metal box (metabolic chamber), tilt table test, muscle biopsy, brain scans, lengthy neuropsychological tests and scads of blood tests. Every part of you is going to be probed.The researchers were surprised at the last two figures. They expected, based on their experience from past studies, much higher percentages of people who were too sick to travel or unwilling to have a lumbar puncture. Dr. Nath well knows how difficult it can be to get people to participate in a study, but that’s not a problem here. Calling the numbers “very good”, Dr. Nath said the ME/CFS community was clearly “very motivated to participate in the study”.

Plus, you have to provide your entire medical history, get interviewed several times, and then, most likely travel.

Dr. Nath said he looked at the study – which is clearly larger and more intensive than most  – and said, “who is going to enroll in this study?” Laughing, he joked that, “I wouldn’t volunteer on my own study!” He was afraid no one was going to show up!  Instead he said the patients were very willing to undergo all the tests and are grateful for it.

Recruitment has been good, but as with any study, Dr. Nath said, it was high at first, and now it’s tailed off. As of March of this year, 19 ME/CFS patients and 21 healthy controls had completed the first phase of the study, and six people with ME/CFS and 7 controls had completed phase II.

Thus far, then, about half the projected participants (n=40 ME/CFS; 40 healthy controls) have gone through the first week of the study and about 15% have completed the entire study.

Quite a few people with autoimmune disorders have shown up during the filtering out process. Nath suggested that could be an interesting cohort to study on its own.  He’s also found quite a bit of head injury and loss of consciousness – which makes MRI and brain scans difficult to assess – and people with seizures and strokes. Interestingly, only one person had had a diagnosis of major depression….

High Percentage of Rare Diseases 

It’s a small sample set but it’s remarkable how many people participating in the first week were diagnosed with a rare disease. In something of a testament to the thoroughness of the study, almost third of week one participants (6/19) were found to have a rare disorder which the researchers believed was probably causing their symptoms and dismissed from the study. One appeared to have Parkinson’s Disease, another a neurological disease and I’m unsure of the others.

Big Data

They are gathering lots and lots of data – which brings its own problem. The study includes two different brain scans, blood, saliva, urine and stool samples, exercise data, tilt table data, spinal taps, Seahorse data, metabolic room data, cognitive testing, muscle and skin biopsies, and I’m probably missing some. I asked Nath, how will they able to integrate all this disparate data?

Nath agreed that it was a challenge, but noted that that kind of challenge is a pretty common challenge now. Some of the really big Alzheimer’s and Parkinson’s studies contain thousands of individuals, each of whom has done thousands of tests. Computational biology has become a major part of medical research.

Google, not surprisingly, is collaborating with the NIH to create better ways to analyze data. Many of the discoveries in medicine today, Nath said, actually occur as breakthroughs in physics; MRI and CT scans, for example – came from physics.

Their general hypothesis is that an infection triggers brain and immune system issues (ranging from persistent immune activation to immune dysregulation) that stay stuck.  They don’t believe the nature of the infection is particularly important.

No Preliminary Findings Yet

Nath was unable to give me any preliminary findings. One reason is that they are storing samples so they can run them all at the same time. Another is that, echoing Ron and Mark Davis’s thoughts, they don’t want to even try to come up with hypotheses yet. They simply want to gather more and more data.

Making a conclusion on the basis of small samples is, Nath said, the kiss the death. They will not even try to interpret their findings until about half the study is done.

If, when they get to the end of the study, they see trends but don’t quite have a significant result, they’ll do sample size calculations to determine how many more patients they’ll need to see to get to statistical significance. If the calculation says do another 10 patients, they’ll probably expand the study to do 12 more. If the calculation says do another 100 patients, that’s too much.

They’re preventing another kind of bias by recoding the samples, so the analyst doesn’t know which are from patients and which are from controls.

The Study

Brian Vastag’s visit raised the issue of mitochondrial problems. Nath believes studying the muscle itself may be more important than assessing mitochondrial problems using the blood, and added muscle biopsies to the study. The muscle biopsies will be tested for DNA analysis, structural issues, and staining for various kinds of cells.

The Open Medicine Foundation and Ron Davis apparently believe likewise. They’ve pumped a million dollars into an ME/CFS Collaborative Research Center at Harvard lead by Ron Tompkins which will focus on figuring out what is going on in the muscles.

Because lots of patients have autonomic symptoms, the NIH is doing tilt table tests. Once those turn out positive, Nath said, the next question is why the autonomic nervous system problems are present. They’re doing small fiber neuropathy skin tests and examining the heart, peripheral nerves, adrenal glands, and sympathetic nervous system functioning.

I asked him if there were any surprises, and there were.  As Robert’s story will show, the NIH doesn’t seem to be prepared for the level of devastation ME/CFS can wreak in a relatively young group of patients.

Nath said his personal contact with the patients has led him to develop a real appreciation for the disease. These patients, he said, “are devastated”. Whether or not this study finds a cause, the reality, Nath said, is that the lives of the study patients are “totally messed up.” Then he made an important point.  Seeing the patients in the flesh naturally causes him and other researchers to develop additional empathy for them and “another level of appreciation” for them and their disease.

It was clear that just by being there and exposing the researchers and doctors at the NIH to this disease, the participants in the study are making a difference.  The lengths to which some patients are going to participate in this study are amply illustrated by Robert’s story.

Participating in the Study

The NIH needs more participants. If you’re interested in helping to further ME/CFS research by participating in the study, check out the study criteria below.

All participants must be 18-60 years old and have at least a 7th grade education. People whose ME/CFS started after an episode of infection and who have severe symptoms lasting from 6 months to 5 years are eligible to participate in the study.

Find out more here.

Associations Between Autonomic and Orthostatic Self-report and Physician Ratings of Orthostatic Intolerance in Youth

Abstract

PURPOSE: There is no known biological marker or physical assessment to diagnose chronic fatigue syndrome (CFS), leaving physicians to heavily rely on self-report measures regarding the symptoms associated with CFS. Common symptoms of CFS include difficulty sleeping, joint pain, headaches, sore throat, cognitive dysfunction, physical exhaustion, dizziness, and nausea. Because of the overlap among CFS symptoms and autonomic functioning, we examined the association between 2 self-report measures of orthostatic and autonomic symptoms and a physician’s report of autonomic functioning (measures of changes in blood pressure and pulse) to further understand the association among autonomic functioning within individuals with symptoms of CFS.

METHODS: With data from an ongoing study, we used independent t tests and Pearson correlation tests to assess the association among the orthostatic domain from the DePaul Symptom Questionnaire, Autonomic Symptom Checklist composite scores, and the physician’s assessment of orthostatic intolerance obtained from a sample of 191 participants, 42 who were healthy controls.

FINDINGS: No significant demographic differences were found between the CFS-like group and the healthy controls. Results indicate a significant correlation between orthostatic and autonomic functioning (r = 0.58) and a correlation with a low effect size among autonomic functioning and physician measures of orthostatic functioning (r = -0.01 to 0.29). However, fewer correlations were found between self-reported symptoms of orthostatic functioning and the physician’s measures of orthostatic functioning.

IMPLICATIONS: These results suggest that although orthostatic dysfunction is reported in children and adolescents with CFS-like symptoms, the physical measures of autonomic functioning in this study were unable to detect these symptoms.

Copyright © 2019. Published by Elsevier Inc.

Source: Schultz KR, Katz BZ, Bockian NR, Jason LA. Associations Between Autonomic and Orthostatic Self-report and Physician Ratings of Orthostatic Intolerance in Youth. Clin Ther. 2019 Mar 12. pii: S0149-2918(19)30070-0. doi: 10.1016/j.clinthera.2019.02.010. [Epub ahead of print]

Pharmaceutical Interventions in Chronic Fatigue Syndrome: A Literature-based Commentary

Abstract

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating disorder characterized by prolonged periods of fatigue, chronic pain, depression, and a complex constellation of other symptoms. Currently, ME/CFS has no known cause, nor are the mechanisms of illness well understood. Therefore, with few exceptions, attempts to treat ME/CFS have been directed mainly toward symptom management.

These treatments include antivirals, pain relievers, antidepressants, and oncologic agents as well as other single-intervention treatments. Results of these trials have been largely inconclusive and, in some cases, contradictory. Contributing factors include a lack of well-designed and -executed studies and the highly heterogeneous nature of ME/CFS, which has made a single etiology difficult to define.

Because the majority of single-intervention treatments have shown little efficacy, it may instead be beneficial to explore broader-acting combination therapies in which a more focused precision-medicine approach is supported by a systems-level analysis of endocrine and immune co-regulation.

Copyright © 2019. Published by Elsevier Inc.

Source: Richman S, Morris MC, Broderick G, Craddock TJA, Klimas NG, Fletcher MA. Pharmaceutical Interventions in Chronic Fatigue Syndrome: A Literature-based Commentary. Clin Ther. 2019 Mar 11. pii: S0149-2918(19)30071-2. doi: 10.1016/j.clinthera.2019.02.011. [Epub ahead of print]