Friday, 18 August 2017

Join me on August 21, 2017 7:00pm the day of the solar eclipse...



Join me on August 21, 2017 7:00pm the day of the solar eclipse with thousands of women around the world authentically connecting and practicing being in Sacred Sisterhood.
 We will embrace the #solareclipse2017 with a very fitting topic of Embracing the Shadow:
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MEA Summary Review: Cytokine signature associated with disease severity in ME/CFS | 18 August 2017

 

There has been a lot of talk recently about a new research paper from Stanford University concerning cytokine signatures and disease severity. In this review, we hope to break down some of the main aspects of that study, question some of the science behind it, and explain a little more about what it means for the future of ME/CFS research.

  • Research published in Proceedings of the National Academy of Sciences of the USA (PNAS), 31 July, 2017
  • Study authors: Jose G. Montoya, Tyson H. Holmes, Jill N. Anderson, Holden T. Maecker, Yael Rosenberg-Hasson, Ian J. Valencia, Lily Chu, Jarred W. Younger, Cristina M. Tato, and Mark M. Davis
  • This summary review has been written by Charlotte (who has M.E. and holds a degree in biochemistry), who has been volunteering at the ME Association to help produce our recent series of lay reports on key research publications
  • The review is also available as a download that might help people with M.E. to absorb the information it contains

Montoya et al. published the paper on the 31st of July and it has since featured in a lot of scientific, as well as mainstream, media outlets. The study was significant and involved measuring the levels of 51 cytokines in 192 patients and 392 healthy controls.

Although the study found little overall difference in the average levels of each cytokine between the two groups, the researchers found an interesting correlation when they divided patients into subcategories based on symptom severity.

There have been many studies over the years that have suggested an inflammatory role in M.E. However, conventional markers of inflammation commonly used in general practice, such as CRP and ESR (markers your GP would look for) are not often elevated in M.E.

⇒ This suggests the profile of inflammation in M.E., you guessed it, is far from straight-forward.

Therefore, these researchers used an extensive panel of cytokines (not your run-of-the-mill markers) – analysed using the latest immune-profiling approach – to see if an abnormal panel of circulating cytokines could be identified.

What are Cytokines?

Cytokines are chemical messengers, or cell signalling molecules, that aid cell to cell communication of immune responses and stimulate the movement of cells towards sites of inflammation, infection and trauma.

There are many different types of cytokines with different names, based on which type of cells produced them, such as lymphokines, monokines and interleukins.

There are both pro- and anti- inflammatory cytokines, and cytokines are responsible for triggering fever, inflammation and pain during an infection, and/or can demonstrate immune-system activity etc.

 


The stars of the show

Only two cytokines were found to be different in patients compared to controls on average; TGF-β (TGF-Beta) was raised and Resistin was lowered.

TGF-β has been mentioned several times over the years in relation to M.E. – a recent review of papers involving cytokines and M.E. found TGF-β was reported as raised in 5 out of 8 studies, making this the 6th study to make this finding.

⇒ An Australian paper published earlier this year found Activin, a member of the TGF-β “superfamily”, to be raised in M.E. patients, further confirming this to be a common finding.

It seems that we keep confirming what we already know; TGF-β was found to be raised in M.E. patients in a study in 1997, 20 years on and still the same kettle of fish.

The Stanford study, however, used the latest technology, was on a bigger scale, was more accurate and employed a new assay property called ‘nonspecific binding’.

 

What is TGF-β
Transforming growth factor beta is a cytokine that is primarily immunosuppressive (anti-inflammatory). It has many functions but of most relevance perhaps is that it suppresses inflammatory cytokines and is thought to have neuroprotective properties.

 

It is produced by many different cells, including Macrophages, a type of white blood cell that has a central role in the immune system, fighting against foreign bodies, cancerous cells and infections. TGF-β also helps in the regulation of T-cells, another key player in the immune system helping to fight infection. And it is involved in pathways important in the regulation of glucose and energy balance.

 

However, TGF-β may not be such a “good guy” as it has been shown to have pro-inflammatory roles. Although TGF-β suppresses inflammation on a systemic level (in the body as a whole), it can actually stimulate immune and inflammatory responses at the local level – and so it may be important to find out where these high levels of TGF-β are being produced.

 

TGF-β is involved in the development of cancer, which could help to explain why older patients with M.E. are often predisposed to certain types of cancer.

 

What is Resistin?
Resistin is a cytokine originally thought to be primarily produced by adipocytes (fat cells) which causes insulin-resistance and is linked to diabetes.

 

However, it has since been shown to also be released by many immune cells and is now thought to play important regulatory roles in a variety of biological processes; cardiovascular disease, autoimmune disease, cancer and inflammatory bowel disease. It is also known to stimulate other pro-inflammatory cytokines, such as IL-6 and TNFα.

 

 


The significant finding

What caused the most excitement, was that 17 cytokines were found to be linked to disease severity, and that 13 of them are classed as pro-inflammatory (See figure 1 – below).

Interestingly, the levels of these cytokines in mild patients were generally lower than that of the controls. The patients in the moderate category had levels similar to controls, and then the patients in the severe category had higher levels than the controls – creating an overall upward trend in relation to severity.

⇒ Preliminary results coming from a study at ‘younger labs’ – home to Dr Jarred Younger – are also finding similar results relating to severity

This upward trend can be known as “dose-dependence”, meaning as the number of cytokines in the body increases, the number of symptoms – or the severity of symptoms and the impact that M.E. has on a person’s health – increases.

⇒ It is unlikely that cytokines are causing the symptoms in M.E., considering the levels are lower than healthy controls in milder patients, who still have symptoms.

Instead, it is more likely that M.E. causes the altered cytokine profiles because of another mechanism. Furthermore, although these 17 cytokines showed a clear relationship with severity, they do not distinguish patients from healthy controls and so are unlikely to be used as diagnostic markers.

Fig 1. Shows the varying levels of each of the 17 cytokines associated with disease severity. Each line shows the values for controls, mild, moderate and then severe patients in an upward linear trend.

Quick statistics lesson; The “p-value” is showing the statistical significance of each of the trends; the lower the number (closer to 0.0001, further away from 1), the more significant the trend. The more significant something is, the more important, or worthy of further attention it is.

 


The cytokine that’s also a hormone…

Leptin was one of the cytokines found to correlate with disease severity. Another study (from Dr Younger) also found fluctuating levels of Leptin to be associated with fatigue severity. Leptin plays a key role in energy homeostasis (stability) and lowered levels of Leptin are also associated with reduced cognition, as well as anxiety and depression.

⇒ Interestingly, Leptin levels are decreased by sleep deprivation, as well as low food input, which could again suggest that this lowered level is a result of M.E. and not a cause of it. However, as Leptin was only found to be lowered in Milder patients, this cannot be an explanation for all patients.

Adipokines (cytokines originating mainly from fat cells) have long been implicated as mediators of chronic inflammation and two of these were found to be important in this study; Resistin and Leptin.

These adipokines have recently been implicated in neuroinflammation and neurodegenerative diseases and so could help explain the cognitive and neurological symptoms experienced in M.E.

⇒ However, the paper comments that it would have been helpful to have BMI data on the patients as Leptin levels greatly correspond to this – as they are produced by fat cells – but they did not collect this data and so correlations were not possible.

Unlike the earlier cytokine study from Hornig et al., this study did not find cytokine levels to be associated with the duration of illness, only severity.

However, this could have been due to the small number of patients who had the illness for under 3 years (30) compared to those who had it for over 3 years (162)  – making uneven sample sizes which could have affected their data.

Therefore, they were unable to rule out the possibility of cytokine levels differing between different fatigue durations.

 


Theories relating to TGF-β and ME/CFS

– TGF-β – fighting our battles or leading an army against us?

The Stanford research presents two contrasting theories for the finding of raised levels of TGF-β:

‘The TGF-β elevation in ME/CFS patients may represent down-regulation by these patients’ immune systems against unremitting inflammation; if so, however, one would expect TGF-β levels to correlate with ME/CFS severity.’

However, TGF-β is also known to be pro-inflammatory, thus a second theory:

‘…elevated levels of TGF-β in ME/CFS patients may actually be detrimental and may be a major factor in promoting relentless inflammation.’

So, we’re not quite sure yet what TGF-β’s role is and whether it’s the good guy or not!

It could be that all M.E. patients produce TGF-β to try and suppress cytokine secretion, which is being produced in response to something else (let’s call this “factor X”) that also causes its own symptoms.

Mild patients are successful in this suppression, whereas in the severe patients, cytokine production is so high (due to more of factor X or a greater immune ‘challenge’?) that the production of TGF-β isn’t sufficient enough to provide the same degree of suppression, leading to rising levels of inflammation, and adding to symptom severity.

We’ve tried to show this in the diagram below:

– Lipopolysaccharide

One contender for this “factor X”, which has been studied in other papers (here and here), is a molecule called Lipopolysaccharide (LPS). High levels of circulating LPS have been found in M.E. patients, as well as in other infectious and autoimmune diseases.

LPS is an endotoxin released from bacteria during stress or infection and regulates the production of pro-inflammatory cytokines.

Could it be that milder patients are able to adapt to constant stimulation by LPS by down regulating the inflammatory response (possibly through the production of TGF-β), but LPS levels in severe patients are so high that down regulation still isn’t enough?

It would be very interesting to measure levels of LPS in different severity subgroups to see if there is a correlation between the amount of LPS and disease severity.

 


Response to exertion?

Some have suggested that the differences in cytokine profiles between severities may not necessarily be there all the time, they might have in fact been showing a response to exertion.

Although the paper states the blood tests were taken at a baseline, after no physical or emotional stressors, the simple act of travelling to the lab to have blood tests and complete questionnaires may have been enough to put the severe patients above their personal exertion thresholds and trigger post-exertional malaise, whereas this was little exertion for the milder patients and so it did not trigger a response.

⇒ However, it would of course be very tricky to take measurements without ANY exertion for the most severe as it would be impractical (and costly!) to go out to each patient’s home.


The critique  

Although many are saying this study proves M.E. to be a physiological – and not a psychological or even psychiatric – condition, this is contradictory given that depression gives similar, if not worse, differences in cytokine profiles.

This is not to say that M.E. is a psychological or even a psychiatric illness, but that inflammation alone is probably not the cause and is more likely an effect of M.E. or of some other mechanism going on.

 

– Patient selection

As with all M.E. research, one must question the methods by which they deemed patients to have M.E.

⇒ For instance, in the fatigue questionnaire that was used, some of the M.E. patients answered that they did not experience unrefreshing sleep or post-exertional malaise, which many would regard as hallmark symptoms of CFS/ME

Additionally, the way in which the researchers categorised the severities may not have been the most accurate:

⇒ This was done using the “multifunction fatigue index” (MFI-20) questionnaire, which some argue may not be the most specific and sensitive test for measuring severity in M.E.

⇒ It is unclear how they decided the boundaries of each category – might there have been overlaps for example, and how would this have impacted the results?

It would have been useful to know how many patients there were in each category of severity and the extent to which this also might have affected the results.

⇒ For example, if there were only a small number in one category of severity, the results could be seen as a misrepresentation of cytokine levels – as it could skew the average in one direction or the other.

– Controls

Unlike other studies, this study was very rigorous in its controls; matching them very accurately by age, gender and race and correcting for these things in their data analysis. This is good scientific practice and would have helped greatly in increasing the accuracy of the results.

⇒ However, all the patients used in the study were aged around 50, which may have had an influence on the results and so it would have been useful to see the same cytokine profiles in a group of younger patients as this may not be a good representation of the M.E. population as a whole.

– Cross-sectional design

The study is cross-sectional in design, meaning it is only looking at a snapshot of cytokine levels at one moment in time. What we need are more longitudinal studies, building up a picture of fluctuating levels over a long period. More studies are also needed that examine cytokine levels “before and after” exertion.

Clark et al. recently carried out a study in the UK looking at cytokine levels before and after exertion.

They concluded there to be no differences in expression and that cytokine levels in general (with the exception of our old friend TGF-β) to be no different to that of controls.

However, the Clark study has been criticised for its poor execution and scientific errors, such as dividing the samples into batches that were looked at years apart by different lab technicians! 

It would have been far more useful if this study had not been published, but had been repeated once the problems had been identified and corrected – enabling more accurate conclusions to be reached.

N.B. We are hoping to bring you a more thorough review of this research as soon as we can.

 


Conclusion: where do we go from here?

The paper concludes:

‘Findings in this study provide further evidence that ME/CFS likely involves a systemic inflammatory process’ and ‘support the suitability of exploring immunomodulation as a primary or adjuvant therapy.’

Although this study does not provide a diagnostic test for M.E., and it is doubtful that cytokine markers ever will, it has highlighted the importance of looking at different severities of M.E. – as different subgroups who present differing disease profiles – which may respond differently to treatment.

The research also provides further evidence for immune and inflammatory involvement in M.E. and supports the suitability of treatment using immunomodulatory therapies, such as that being investigated in Norway using Rituximab.

As usual, the findings are not straightforward and could leave scientists wondering what they all mean. They are significant and exciting, of course, albeit puzzling and adding to the mystery of a case that no one seems currently able to crack.

⇒ It is very likely that inflammation is just one of a multitude of contributing factors; a small piece of the puzzle that is slowly being pieced together, one break-through study at a time.

The Stanford Symposium

In a recent conference at Stanford, Dr Mark Davis, one of the lead researchers on the paper and a top immunologist, said:

“The increased cytokine levels that correlate with disease severity indicate a strong inflammatory component to M.E.”

He then went on to present his theory of an autoimmune component to ME, where our T cells (important players in the immune system that help to identify and destroy foreign cells) are actually attacking cells in our own tissues.

Many studies have found increased numbers of circulating cytotoxic CD8+ T cells (White blood cells that kill infected or damaged cells) bearing activation antigens; suggesting the body is actively fighting something.

  • Interestingly, TGF-b and Leptin (Two of the cytokines found to be different in M.E.) have both been shown to have regulatory roles in T cells, further supporting this T cell theory.

In MS (multiple sclerosis), there are T cells activated which attack the myelin sheath (a protective layer around nerve cells) and Davis proposes a similar mechanism may be happening in M.E., but targeting a different cell type.

  • Dr Davis then spoke of some research currently underway to try to identify which tissues these T cells are targeting, which sounds very promising!

At the very least, the wide press-release and positive media attention this study has received, along with the fact that it’s published in a highly respectable journal, is very encouraging and provides hope for more funding and more biomedical research.

The Stanford study has certainly made its mark in the scientific world, grabbing people’s attention, generating more interest in the disease among researchers and making the voices of M.E. sufferers that bit louder; things are looking up!


We have made this comprehensive review of cytokines in ME/CFS available as a download, which might make it easier for people with M.E. to take in. 


If you have found this information useful, then please donate – whatever you can afford – to help us continue with our work and make the UK a better place for people with ME/CFS. Just click the button below:

Or why not join the ME Association as a member and become part of our community?
For a monthly (or annual) payment you will not only be helping to keep us doing what we do best, but you will receive ME Essential magazine – with exclusive content – delivered straight to your door. 


 

 



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CMRC 2017 Update: Look who’s flying-in to present at the ME/CFS research conference next month! | 18 August 2017

 


“I am very excited to attend the CMRC conference and welcome the chance to talk about our research with other researchers from around the world. M.E./CFS can turn a life of productive activity into one of dependency and desolation, and it is only through collaboration that we can challenge the horrors of this very real disease and improve lives for the thousands of patients living with it on a daily basis.” Professor Jose Montoya.


The annual CMRC research conference takes place Wednesday 13 and Thursday 14 September at the Future Inns, Bristol.

Both days are open to anyone with an interest in M.E. You can find out more and/or book your place now on the CMRC conference website. 

Professor Jose Montoya (pictured) has just announced he will give the Anne Faulkner Memorial Lecture on the second day of the conference.

Dr Montoya will be explaining his widely reported recent study on ME/CFS and cytokines – research that we will be reviewing in a blog on our website later today!

The purpose of the conference is to increase collaboration between researchers in the ME/CFS field and with those from other research/illness areas. This event provides an opportunity to learn more about latest published and unpublished research, meet potential collaborators and contribute to future developments.

 


The conference will not be livestreamed this year, instead the organisers will be producing better quality videos to be released as soon as possible once the conference has ended.


The ME Association is providing funding for six medical and research students to attend and we will be producing a written report of the conference.

Dr Avi Nath (pictured) will also be speaking. He hails from the National Institutes of Health, and is overseeing the latest developments in ME/CFS research from the American equivalent of the UK’s Medical Research Council.

Other presentations include:

  • Autonomic intolerance from Dr Peter Rowe, John Hopkins Children’s Centre
  • Imaging in research from Dr Matt Wall, Imanova, a translational research company that specialises in applying PET and MRI scanning techniques to improve drug development and health research
  • The challenge of chronic pain : how neuroscience can help from Prof Maria Fitzgerald, University College London
  • Learning from other illness fields from Prof John Gallacher, Oxford University
  • An overview of fatigue in arthritis: insights for ME/CFS from Prof Alan Silman, Nuffield Department of
    Orthopaedics, Rheumatology and Musculoskeletal Science

And,

  • Transient receptor potential ion channels and impaired calcium signalling in natural killer (NK)
    cells from Prof Don Staines from Griffith University, Brisbane.

The full conference programme can be viewed from the conference website page where you can also book your tickets.


For more information about the CFS/ME Research Collaborative, please visit the CMRC section of our website.

The ME Association is a board member of the CMRC and strongly believes in the importance of this working partnership – especially in helping to bring ME/CFS to the recognition of mainstream science as a legitimate biomedical disease in desperate need of increased funding.


 

 

 

 

 



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How to Ask for What You Want and Need (No, It’s Not Selfish)

“It’s not selfish to put yourself first—it’s self-full.” ~Iyanla Vanzant

I’ve always thought of myself as individualistic. When I was a teenager, I often felt the desire to go against the grain, dressing alternatively and shunning bands my peers liked because I felt they were too popular. So it came as a huge surprise to me when my therapist called me a people pleaser the other day.

I recently started cognitive behavioral therapy for insomnia, and during the first session my therapist identified that I put other people’s needs and wants ahead of my own.

He’d asked me to give an example of a situation that is currently making me anxious (since anxiety is both a cause and symptom of insomnia), and I told him a landscaper made a mistake in my yard and I was feeling bad asking him to fix it.

I’d hired the landscaper to build a fence and incorporate a parking pad into my backyard space. While the fence turned out awesome, the landscaper brought too much loam and turned the parking pad area into a hill that sloped down from the fence to the garage. When I asked him to level it, he got angry and said he had already spent man-hours on the project and would be losing money.

I started to feel bad. Was his business doing okay? Did he have kids?

“The job you agreed upon was for him to level it,” my therapist said. “It has to be level.”

“But what if he is losing money?”

“That’s none of your business. You wanted it level. It has to be level.”

It took him repeating that sentence to me a few more times before the concept clicked, and I knew he was right. I was putting someone else’s wants and needs above my own. I do it all the time.

“Why don’t I put myself first?” I asked him. “It’s like I think I don’t deserve to be treated as well as other people.”

I expected my therapist to say I have low self-esteem and needed to work on that, but instead he said, “Because you’re framing it wrong.”

Then he asked, “What’s your favorite ice cream?”

Thrown off by the change in topic, I stammered something about Maple Walnut.

“And is there an ice cream flavor you dislike?”

“Tiger.”

“So when you go to an ice cream store, do you ask yourself whether you deserve Maple Walnut or if you should just accept Tiger?”

“Of course not.”

“There you go. It isn’t about whether you deserve to have something, it’s that you want it. Plain and simple.”

It was simple. Suddenly I felt like I’d been let in on the secret all the confident, take-no-crap, boundary-setting people in my life have known forever. If they want something, they go for it. They don’t stand around questioning whether or not they deserve to have it.

In my case, I wanted the parking pad incorporated into my yard so that I could enjoy the added space. Therefore, the backyard has to be level.

“Now that you know your position, the next step is to communicate it correctly,” my therapist continued. “Do not ask, ‘Can you please make this level?’ Simply say, ‘We agreed it would be level, so it has to be level.’”

We ran through hypothetical life situations where I could apply this technique, and each time I made the mistake of asking the other person to “please” grant my wishes instead of communicating my wants and needs. Every time I smiled sheepishly at the mistake, it hammered home how I unconsciously present myself to other people.

While trying to be polite and accommodate everyone else, I might actually be telling people I’m a doormat. Of course people are going to walk all over me because I haven’t given them guidance on where they can and cannot step!

At the end of the appointment, I resolved to start setting boundaries and ask for what I want in life, and I saw results immediately. When I told the landscaper the yard had to be level, he fixed it. By no longer questioning whether or not I “deserved” the same treatment as everyone else and simply asking for it, I gained self-confidence.

Granted, not all situations in life are as clear-cut as standing up for yourself with a landscaper. There are times to stand your ground and times to compromise, and the trick is to learn to tell the difference.

Sometimes our wants and needs can directly affect other people, or their wants and needs can be in conflict with our own. In this case, it’s important to remember to balance healthy self-assertihttps://tinybuddha.com/blog/5-myths-setting-boundaries-steal-joy-lead-resentment/on with consideration and respect for others.

For someone who habitually puts other people’s wants and needs ahead of her own, putting myself first simply means treating myself the same way I treat them—not trampling on everyone else!

The ice cream story has changed my perception on putting myself first. It’s not selfish—it’s self-full. Sometimes I slip back into old habits and wonder if I deserve something, but then I remind myself I wouldn’t accept Tiger when I want Maple Walnut.

Here are a few simple steps to setting boundaries and asking for what you want and need in life:

1. Know your position.

The most important step in setting boundaries is to know your position—what you want—and to stick with it. That way when someone comes back at you trying to change your mind, you can simply go back to your position.

Imagine you’re at a dealership and you tell the salespeople that your budget is 10K. If they respond, “We have a newer model with leather seats and a sunroof for 13K,” your response should be, “My budget is 10K.” If they tell you only rust buckets go for 10K, tell them your budget is 10K and then walk away.

Don’t forget what you want or need. It’s easier not to be bullied or walked on when you are confident in your position.

2. Communicate your position.

Communicate your position properly is just as important. When you ask someone to honor your wishes or approve of your position, you’re asking them to make you happy. But when you tell them what you want or need, you’re making yourself happy.

If a friend asks you to go to a party with them but you don’t want a late night, you can choose to say no or agree to go on your own terms. Rather than asking if it’s okay if you leave early, tell them that you will go with them for a bit but you want to get a good sleep.

If a friend is having an elaborate and expensive birthday and you can’t afford to attend multiple events, tell them. You do not have to apologize. Simply communicate what you can and cannot do.

People don’t necessarily aim to walk on you, but if you don’t communicate what you want and expect, there is a better chance it will happen. Have you ever felt taken advantage of but didn’t communicate your feelings, and the frustration built up inside of you until you finally snapped? Or worse: snapped at the wrong person? I’ve definitely been guilty of that.

By setting boundaries and communicating them, everyone knows where they stand and it will prevent future blowups.

3. Stop asking if you “deserve” what you want.

In my opinion, this is the most important principle. Do not question whether or not you deserve things in life. Simply know what you want and go for it.

People who don’t set boundaries often don’t feel they “deserve” to set boundaries, and they feel that way because they’re used to always putting other people first. Their low self-esteem has been reinforced by their own inability to state what they want. It’s a vicious cycle.

We can’t always get what we want in life, but we definitely won’t get it if we don’t ask. By focusing on what you want or need in life, rather than questioning whether you’re worthy to receive, you will help guide your own success and self-confidence will follow!

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About Alexandra Baker

Alexandra (Lex) Baker is a freelance writer and author of both young adult and adult fiction. As a sensitive person with a genuine interest in people, her novels tend to be character-driven, focusing on coming of age and growth. Her debut young adult novel Instalove was published by Bloomsbury. Learn more about her at lexbaker.com or @lexbakerwrites.

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Thursday, 17 August 2017

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Tapping Research Shown to Ease Your Public Speaking Fears

This is your moment. They’ll all be looking at you. Will you shine? This research study shows how to greatly increase your chances of public speaking success by decreasing your anxiety.

It’s 2:45 and you’re up in 15 minutes.

Your palms and temples are wet, and you’re hoping your deodorant is doing its job.

You review your notes for the 411th time and try to remember your mental cues: slow down if they laugh… pause at the end of an idea… look at individual members of the audience… keep breathing…

But these reminders don’t seem to be slowing down your pulse. You sit back down, waiting, wondering if this will be the time that you pass out or lose your cookies.

The scenario above might seem funny from a reader’s perspective, but for people with public speaking anxiety, it’s actually quite serious.

Most of us in our everyday adult lives have to occasionally get up and speak in front of a group. Even if it’s something informal, like toasting a family member at an event, to somebody with this degree of anxiety, the task can seem as insurmountable and frightening as climbing Mount Kilimanjaro.

Because this particular fear, known as “glossophobia,” affects such a large number of people (10% of adults in the US according to Forbes Magazine, which would be about 32 million), researchers have been working on understanding and treating it for years.

Enter Energy Psychology, an alternative way of understanding and treating a variety of illnesses through restoring flow to the body’s natural life force.

In the early 1980’s, a psychologist named Roger Callahan devised a method of balancing the body’s energy by linking mental health issues to acupressure points. Clinicians would have the patient talk about the issue while they tapped on the corresponding point, which would unblock the flow of energy.

The developer of Emotional Freedom Techniques, Gary Craig, took this one step further by simplifying it so that anyone in the health care field could apply it and teach clients how to do it themselves.

It takes some time for a treatment modality to earn the respect and legitimacy of society and the medical community. Because of the many research studies conducted, however, EFT has been rapidly accepted as an “evidence-based treatment,” particularly by the American Psychological Association for specific phobias.

But is public speaking one of them? Let’s find out…

To Be or Not to Be… A Study

Researchers of this study in Australia recruited 36 volunteer students to fill out a questionnaire about public speaking and fear.

The group was divided into two: the first would receive EFT as a treatment and the other was the wait list/control group. All students were given several questionnaires that are considered reliable measures in research about public speaking anxiety. They were also asked to predict how effective they thought the treatment would be for them on a scale of 0-10.

The students in the EFT group were asked to give a four-minute speech before the treatment. Then they were shown how to use EFT.

One interesting aspect of this study was having the students rate their anxiety at three points during the treatment itself: 15 minutes into it, 30 minutes into it, and at the end, at 45 minutes.

After treatment, the students filled out all of the questionnaires again. Finally, they were asked to give another short speech in front of a small group that was video recorded.

Using this recording, the researchers then scored students on observable anxious behaviors, like wetting their lips, swaying, gesturing awkwardly, or pacing.

The control group followed the same protocol, but without treatment. One week later, they came back to the counseling center and also received the Tapping Therapy. They then filled out the questionnaires and gave their video recorded speeches, being evaluated just like the first group.

Toastmasters for Tapping

The overall findings in this study showed that EFT was a highly effective treatment for public speaking anxiety.

Researchers noted the particularly short treatment time and the fact that individuals can even give themselves the treatment without a therapist.

In comparing the questionnaires, researchers found that students who received the EFT treatments felt less anxious in general, and specifically calmer about public speaking post-treatment. There were improvements in anxiety levels, statistically significant ones, on all measurement tools they used.

The anxiety measurements taken at each 15-minute interval during the treatment process showed a steady decline of anxiety throughout. Interestingly, there was a big drop in just the first 15 minutes of doing the tapping.

Applause!

Given how easy it is to teach and learn, and how quickly the treatment begins to work, Tapping is a fabulous tool that could save millions of people from the suffering they experience every time they are required to speak in front of a group of people.

Even when I have to take the stage for a talk or conference presentation, I still tap beforehand because it just simply helps to calm the nerves and provides me with better focus.

If you’d like to try Tapping for your public speaking anxiety, we’ve got a free Tapping Meditation to help you.

Go ahead and give it a try the next time you have to get up to speak in front of others. Your voice and your words could be just what someone else needs to hear.

Until next time…

Keep Tapping!

Nick Ortner


Tell me about a time where you had to speak publicly. How did it go? Do you think Tapping could have helped?

The post Tapping Research Shown to Ease Your Public Speaking Fears appeared first on The Tapping Solution.



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