Saturday, 9 February 2019

Consumer-Contested Evidence: Why the ME/CFS Exercise Dispute Matters So Much

Hilda Bastian

Sometimes, a dispute with a consumer movement comes along that has profound implications for far more than the people in it. I think the dramatic clash between the ME/CFS patient community and a power base in the evidence community is one of those. It points to weaknesses in research methodology and practice that don’t get enough critical attention. It raises uncomfortable questions about the relationship between researchers and policy communities. And it pushes the envelope on open data in clinical trials, too.

All of that underscores the importance of consumer critique of research. Yet the case also shows how conditional researcher acceptance of consumers can be.

ME/CFS is Myalgic Encephalomyelitis (ME) / Chronic Fatigue Syndrome (CFS), a serious, debilitating condition with a complex of symptoms, and a lot of unknowns. The argument about exercise is rooted in competing views about the condition itself.

A biopsychosocial camp has contended since the 1990s that regardless of how it starts, people with ME/CFS dig themselves into a hole with their attitudes and behaviors, leading to physical deconditioning (sort of the opposite of getting fit). They argue that people can dig themselves out of it by changing their beliefs and behaviors with the help of cognitive behavioral therapy (CBT) and graded exercise therapy (GET).

One of the key people from this camp is Peter White, who explained GET this way with Lucy Clark back in 2005:

A vicious circle of increased exercise avoidance and symptoms occurs, which serves to perpetuate fatigue, and therefore CFS….Patients can be released from their self-perpetuating cycle of inactivity if the impairments that occur due to inactivity and their physiological deconditioning can be reversed. This can occur if they are willing to gradually exceed their perceived energy limits, and recondition their bodies through GET.

ME/CFS groups see it differently. For them, the condition is more complex than fatigue and fitness, and believing you can recover won’t overcome it. From their experience and surveys since 2001, GET in practice causes relapses, worsening symptoms for most people; CBT doesn’t change the condition’s symptoms; and self-management “pacing” does help. The UK group, Action for ME, describes pacing this way:

Taking a balanced, steady approach to activity counteracts the common tendency to overdo things. It avoids the inevitable ill effects that follow. Pacing gives you awareness of your own limitations which enables you positively to plan the way that you use your energy, maximising what you can do with it. Over time, when your condition stabilises, you can very gradually increase your activities to work towards recovery. [PDF]

By the early 2000s, the biopsychosocial camp could claim a few small trials in support of their position, but it was a very weak evidence base. They saw their treatment approach as a good news story for patients, though, and they had a lot of supporters. Exercise is something of a sacred cow to many – including in the evidence community. So there was a constituency that wasn’t going to be as critical of studies claiming advantages of exercise as they might be for other treatments.

There was another powerful camp that was attracted to the idea that cheap short interventions could get rid of ME/CFS, if only the person was willing to make an effort: insurance and welfare stakeholders. It was in their interests to reduce treatment expenditure and income dependency for this fairly common condition. The close associations disclosed by ME/CFS researchers in the biopsychosocial camp with these policy communities have the potential to be conflicts of interest – and they are certainly seen that way by many.

For people with ME/CFS, as George Faulkner explained, “unreasonable expectations of recovery” based on weak research was “presenting policies which reduce their options and income as benevolent and empowering interventions”. [PDF] Yet, even the most optimistic estimates show the overwhelming majority don’t benefit. And believing ME/CFS is a condition that can be cured by attitude and effort is stigmatizing, no matter how carefully you try to frame it. That’s harmful, for individuals who blame themselves (or get blamed) for their suffering, and for the collective of people deeply affected by a condition in effect tagged as “all in the mind”.

A small evidence base means the pool of researchers focusing on the topic is small, and the field can be relatively under-developed. White’s group, who were convinced CBT and GET were beneficial, had tried, unsuccessfully, to get a UK trial of the 2 therapies funded in 1998. That same year, the UK’s Chief Medical Officer established a working group to advise on the ME/CFS. Its report in 2002 was followed by the establishment of a Medical Research Council (MRC) research advisory group that recommended larger treatment trials – and stressed the importance of consumer involvement.

White’s group then brought the consumer group, Action for ME, on board, adding arms to study pacing and specialist medical care alone, plus a greater focus on adverse effects. (This development is described by White’s group here, and by Action for ME here.) The alliance wouldn’t survive the coming storm.

White and colleagues’ proposal became the PACE trial in 2005, after the MRC awarded it the biggest grant ever for an ME/CFS trial. Ultimately, the MRC contributed £2,779,361 (US$3.6 million), a substantial chunk of which came from the Scottish Government’s Chief Scientist Office, the National Institute for Health Research (NIHR), the Department of Health, and the Department for Work and Pensions. Previous trials each had at most about 40 participants comparing 2 treatments. The PACE trial was shooting for more than 600 people who weren’t severely affected, comparing 4 options. So right or wrong, that trial’s result was going to dominate the evidence base.

The academics responsible for the trial were Peter White, Trudie Chalder, and Michael Sharpe. In 1993, Chalder was the lead author of the trial’s primary outcome measure tool – the Chalder Fatigue Scale, [PDF] and in 1991, Sharpe was the lead author of “the Oxford criteria” used to diagnose who was eligible for the trial.

Let’s stop right there. Those 2 research instruments are pivotal for this trial. And the intellectual investment in them by these co-authors doomed this trial before the first participant was ever recruited. Why?

To rely on the trial’s results for decision making in ME/CFS, for starters you would need to know that the people in it really had ME/CFS. The Oxford criteria for ME/CFS used to choose who was included can’t deliver that reliably. This is what the US Agency for Healthcare Research and Quality (AHRQ) concluded in a systematic review of diagnosis and treatment for ME/CFS in 2014, several years after the PACE trial:

None of the current diagnostic methods have been adequately tested to identify patients with ME/CFS when diagnostic uncertainty exists.

AHRQ dug into this further in 2016, after an NIH meeting agreed with them, concluding:

The Oxford (Sharpe, 1991) case definition is the least specific of the definitions and less generalizable to the broader population of patients with ME/CFS. It could identify individuals who have had 6 months of unexplained fatigue with physical and mental impairment, but no other specific features of ME/CFS such as post-exertional malaise which is considered by many to be a hallmark symptom of the disease. As a result, using the Oxford case definition results in a high risk of including patients who may have an alternate fatiguing illness or whose illness resolves spontaneously with time. In light of this, we recommended in our report that future intervention studies use a single agreed upon case definition, other than the Oxford (Sharpe, 1991) case definition. If a single definition could not be agreed upon, future research should retire the use of the Oxford (Sharpe, 1991) case definition. The National Institute of Health (NIH) panel assembled to review evidence presented at the NIH Pathways to Prevention Workshop agreed with our recommendation, stating that the continued use of the Oxford (Sharpe, 1991) case definition “may impair progress and cause harm.”

When they analyzed what this means for the evidence on treatment for people with ME/CFS, it’s devastating:

Blatantly missing from this body of literature are trials evaluating effectiveness of interventions in the treatment of individuals meeting case definitions for ME or ME/CFS.

AHRQ argued that you need specific ME/CFS symptoms in your criteria – like experiencing post-exertional malaise. The PACE trial measured that specific symptom, because it was a secondary outcome. So how many of the trial participants had it before the trial treatments started? The baseline data show it ranged from only 82% in the GET group to 87% in the treatment-as-usual group. That underscores AHRQ’s point about the risk of the Oxford criteria, doesn’t it?

The second blow in this one-two punch is the validity of the Chalder fatigue scale, which they used as a primary outcome. It’s a patient-reported outcome measure (PRO or PROM) – a questionnaire for participants. In 2011, a guideline for how to reliably assess the validity of PROMs was released, called COSMIN for short. And in 2012, Kirstie Haywood and colleagues followed it in their systematic review of PROMs for ME/CFS.

They paint a dismal picture of the quality of PROMs for ME/CFS and a lack of robust enough development and evaluation, including for the Chalder fatigue scale and the first version of the other PROM primary outcome for physical function (SF-36: they used version 2). Neither is strong enough to lean on for ME/CFS. The result for the evidence on ME/CFS treatment, they believe, is as devastating as the implications for AHRQ on diagnosis:

[F]ailure to measure genuinely important patient outcomes suggests that high quality and relevant information about treatment effect is lacking.

Lisa Whitehead did a pre-COSMIN systematic review in 2009: she came to the same conclusion about the lack of adequate evidence to support the Chalder fatigue scale.

Depressing, isn’t it? But it’s not surprising, either. These kinds of weak links in the science of doing research are common, fueling confusion and controversies. When the trial’s results were published in 2011, consumers studying the trial had a wealth of methodological weaknesses to zone in on – and plenty of information on the science of doing research to point the way.

I think this brings us to one of the important lessons from this controversy: involving a consumer organization isn’t likely to be enough, on its own, to prepare for wading into a controversial area where there is a strongly networked community with a lot at stake. If your methods aren’t in very sound scientific territory and your findings aren’t welcome, you will get hammered.

That could, and should, have a positive impact on research standards. “[Taking] sides in pre-existing methodological disputes” is one of the main ways HIV activists came to have such an influence on the conduct of clinical trials, according to Steven Epstein’s analysis.

Let’s jump forward to the current battleground with consumers over the Cochrane review that included the PACE trial, supporting its conclusions about benefits of CBT and GET and lack of effectiveness of its pacing intervention. Systematic reviews like the ones from Cochrane, AHRQ, and NICE are critical influences on the policy and clinical impact of a trial, and potentially for research funding. That’s especially key for one as big as PACE in an area where stronger trials that could confirm or challenge its results can’t be taken for granted.

Robert Courtney and Tom Kindlon are both people with lives severely affected by ME/CFS, who critiqued the PACE trial intensively. They posted detailed analyses of the Cochrane review and its verdict on the PACE trial and other evidence in Cochrane’s commenting system. Their comments from 2015 to 2016 raised important issues, but the review’s authors rather brushed off their concerns.

There is only 1 Cochrane review journal, but the reviews are produced and edited in Cochrane review groups, not centrally. There are 53 of those groups. The group that deals with ME/CFS is the Common Mental Disorders group, reflecting the disproportionate power base that psychiatry and psychology have established around this illness and its treatment. Courtney complained to the editor in chief in February 2018, when the review group was so unresponsive.

In November 2018, Cochrane reported action. Sadly, Courtney didn’t get to see this: he died by suicide in March, after a long struggle with health-related problems. Cochrane attached a note to the review, stating that Cochrane’s editor in chief, David Tovey, was not satisfied that the authors had made enough revision to their review in response to Courtney’s feedback, and a full update was in the works:

The Editor in Chief and colleagues recognise that the author team has sought to address the criticisms made by Mr Courtney but judge that further work is needed to ensure that the review meets the quality standards required, and as a result have not approved publication of the re‐submission. The review is also substantially out of date and in need of updating.

That update hasn’t been published yet. It could take a while, especially if a new set of editors is dealing with it in a new review group. That’s not just because of different people. Cochrane review groups have some standardized methods they are supposed to adhere to, but there can be big differences, too.

Courtney’s complaint also raised concerns about another review in progress at Cochrane. It was a review based on individual patient data from the exercise review. Tovey and his colleagues reviewed the version that had been submitted for publication by Cochrane too, and it was rejected. The already-published protocol for that review was then retracted (withdrawn in Cochrane-speak, with no reason given). And finally, the review group and Tovey agreed to transfer the responsibility for ME/CFS Cochrane reviews to a different review group, in acknowledgment of the fact that it isn’t a mental health disorder.

That’s a lot to achieve from consumer pushback on research, so kudos to Courtney and Kindlon for their effort. But will the changes in the updated review be critical enough of the evidence base, and closer to the AHRQ position? I think they should be. And I think the reasons for that are included in Courtney’s and Kindlon’s comments. There are a lot of them, but I’ll focus on one major one: the risk of selective reporting bias. (Note: I’ve removed and described or linked the references in quotes below for simplicity.)

From Kindlon’s comment (page 72 of PDF of the Cochrane review):

I don’t believe that White et al. (2011) (the PACE Trial) should be classed as having a low risk of bias under “Selective reporting (outcome bias)”. According to the Cochrane Collaboration’s tool for assessing risk of bias, the category of low risk of bias is for: “The study protocol is available and all of the study’s pre-specified (primary and secondary) outcomes that are of interest in the review have been reported in the pre-specified way”. This is not the case in the PACE Trial.

He’s right. The criteria for “low risk of bias” he referenced came from the table in 8.5 of the Cochrane Collaboration’s handbook.

The PACE trial began recruiting participants – and therefore collecting data – early in 2005, and the protocol was published in 2007. Data collection ended in January 2010. There was a data analysis plan, but it wasn’t published till 2013 (after the results of the trial). At some point between the protocol and the final data analysis, they dropped a primary outcome and elevated a secondary one to primary status, and lowered the thresholds for what would be classified as “recovery”.

Before and after this change, there were different ways of interpreting the data from the Chalder fatigue scale. The one in the protocol set a higher bar for benefit than the one they swapped over to: had they stuck with it, it would be harder to conclude one treatment option had better results than another. And that was, according to their first results publication, the intent:

Before outcome data were examined, we changed the original bimodal scoring of the Chalder fatigue questionnaire (range 0–11) to Likert scoring to more sensitively test our hypotheses of effectiveness.

Here, responding to criticisms about this, they said they made the change:

…because, after careful consideration and consultation, we concluded that they were simply too stringent to capture clinically meaningful recovery.

Here, they wrote that the first way of using the fatigue scale came from levels in the small 1993 Chalder paper, and a larger Chalder paper in 2010 was responsible for re-calibrating their approach. That 2010 paper didn’t measure fatigue in people in ME/CFS.

Courtney, in his comments on this point (page 78 of the review), wrote that something else happened early in 2010, too – PACE’s so-called “sister trial”, FINE, published their results:

The FINE trial investigators had found no significant effect for their primary endpoint when using the bimodal scoring system for Chalder fatigue but determined a significant effect using the Likert system in an informal post-hoc analysis.

The  same thing happens, apparently, with the PACE data. In 2016, Carolyn Wilshire and colleagues (including Kindlon) published a re-analysis of the data made publicly available after a freedom of information request:

Publications from the PACE trial reported that 22% of chronic fatigue syndrome patients recovered following graded exercise therapy (GET), and 22% following a specialised form of CBT. Only 7% recovered in a control, no-therapy group. These figures were based on a definition of recovery that differed markedly from that specified in the trial protocol…
When recovery was defined according to the original protocol, recovery rates in the GET and CBT groups were low and not significantly higher than in the control group (4%, 7% and 3%, respectively).

The second threshold for fatigue had been lowered so much, they point out, that 13% of the participants were “recovered” by that measure before the trial treatments started.

The PACE trial authors responded, accepting the accuracy of the re-analysis. They pointed out, as they did in their original paper, that there is no gold standard way of measuring recovery from ME/CFS. They also wrote a paper on recovery in the PACE trial, which is about more than the primary outcomes.

The Cochrane review authors defended their assessment of low risk of reporting bias by arguing that it was a reported protocol variation, and therefore not a problem. Their note on their risk of bias judgement quotes a sentence from the trial publication which points to a second source of selective reporting:

“These secondary outcomes were a subset of those specified in the protocol, selected in the statistical analysis plan as most relevant to this report.” Our primary interest is the primary outcome reported in accordance with the protocol, so we do not believe that selective reporting is a problem.

This is problematic for several reasons. Firstly, the primary outcomes differed from those in the protocol. The review authors argue because they were still specified before data analysis, “it is hard to understand how the changes contributed to any potential bias”.

The Cochrane Handbook states clearly in the rationale about selective outcome reporting: “The particular concern is that statistically non-significant results might be selectively withheld from publication”. What if you change your mind about an outcome after data collection has ended, for a trial going on in your own clinic, because you are now concerned that your results won’t be significant? As Courtney pointed out “Investigators of an open-label trial can potentially gain insights into a trial before formal analysis has been carried out”.

Secondly, the Cochrane reporting bias criteria are for the study as a whole – not just for primary outcomes. What’s more, they did rate one other study (Wearden 1998) at high risk of reporting bias – and that was based on concerns about secondary outcomes (here). And that was valid. That is explicitly stated in the Handbook, too:

Selective omission of outcomes from reports: Only some of the analysed outcomes may be included in the published report. If that choice is made based on the results, in particular the statistical significance, the corresponding meta-analytic estimates are likely to be biased.

I think rating the PACE trial at high risk of selective outcome reporting bias would be consistent with Cochrane methods and the rating for Wearden 1998.

Where does all this leave us? We’re still only arguing about subjective measures: there still isn’t much evidence of benefit on objective outcomes at all. That leaves us in uncertainty. We don’t know how different approaches to exercise, “graded” or “paced”, really compare yet. There is too much uncertainty.

A similar message has been coming from multiple trials of GET – but only one particular form of pacing has been tested in a trial. The message could be fairly consistent on GET because it really does have a small amount of benefit for a minority of people (about 15% over and above regular care in PACE). Or the message could be fairly consistent because the trials have all relied on similar and deeply flawed methods. We won’t know till there are more rigorous methods to use to test these questions, and strong large trials are done that learn from the errors in the story so far.

This clash around the PACE trial raised other critical issues about the practice of science – especially around openness and response to consumer criticism. Activists pounded away to get access to data, using a variety of official channels and a lot of pressure. There’s a lot to learn from this. We obviously still haven’t got open data practice sorted out yet.

In this case, defensiveness won out over transparency, and that was throwing gasoline at a fire. Although official processes have seen important data and other information released, the researchers have also removed a lot of material that used to be in the public domain. So much so, that it’s now impossible to assess for yourself some of the concerns, because the materials have disappeared. That’s bad enough for any research, but it’s unacceptable for a publicly funded clinical trial.

Instead of responsiveness to criticism, some – not all – researchers have put massive effort into discrediting the whole community and rallying other researchers to their defense. It’s been a collective ad hominem attack. Being responsive when consumers are making mistakes or unjustified criticisms isn’t always easy, especially when there’s a barrage, with extremists in the mix. But it’s not only consumers who do that, is it? And there are important and legitimate issues here – not just people who don’t agree with the results.

This kind of clash happened to me early in my involvement in research, and I’ve written about that before. I don’t think there’s any shortcut. People need to keep listening and responding though, and as many bridges need to be built as possible. Carolyn Wilshire, a psychologist co-author of the PACE trial data analysis, has written of the concerns about researchers’ therapeutic allegiances and other relevant points. People’s positions can make it very difficult for them to be fair when developing and doing research. Even if they weren’t entrenched beforehand, they can quickly become so when their research is under attack. People shouldn’t take it personally, but they do. And the time that it will soak up isn’t usually factored into the research process.

As Epstein pointed out from analyzing the battles over HIV clinical trials, getting these relationships right can advance science and social progress – even though that’s not always easy. As he said, you can’t grab onto a consumer group in a controversial area “solely in passive terms – as a resource available for use, or an ally available for enrollment”. But that’s too often how public involvement in science is approached. (A recent systematic review on patient and public involvement in clinical trials, for example, had as its primary outcomes effects on recruiting and retaining participants.) We have to get past that, and deal better with these kinds of clashes. They are inevitable.

As for the dispute over the validity of key methods here? I think the balance should, and ultimately will, tip towards the ME/CFS consumer movement on this particular contested evidence.

Wednesday, 6 February 2019

No Faith? Our Struggle With Unbelief

By J.P. Thackway

“And He said unto them, why are ye so fearful? How is it that ye have no faith?” Mark 4:40

The first three gospels record the stilling of the storm on the lake of Galilee. It is one of the most powerful and impressive of the Lord’s miracles. This was especially so for Peter, Andrew, James, and John – fishermen – who well knew, when a storm arose, the terrors of those waters.

The freshwater lake of Galilee is 686 feet below sea level and less than 200 feet deep. It is bounded by high hills, from where cold winds can hit the warm surface of the water and whip up sudden squalls. Luke’s account shows this: “there came down a storm of wind on the lake” (Luke 8:23). Shallow water reacts to winds faster than deep water does, and hapless fisherman can be engulfed before they know it.

In Mark’s account we see how desperate their plight was, “And there arose a great storm of wind, and the waves beat into the ship, so that it was now full” (4:37). The next wave may have sunk the boat. The disciples felt completely at the mercy of the storm. We can spiritualise this, and apply it to our experience.

a] Storms of life do come.

Even to obedient disciples. Remember, they were obeying the Master in crossing the lake (Mark 4:35). We can be in the centre of God’s will and yet in the eye of a storm of trouble! Do not conclude that your maelstrom is because you have sinned. Of course, it could be, as in the case of Jonah, and it is right to examine ourselves (Job 34:32). However, it is not necessarily so, and our kind Lord would not add the burden of false guilt to our trouble (Matthew 11:29,30).

b] The Lord is with us in the storm.

“And he was in the hinder part of the ship” (4:38). In every storm, He is in the same boat with us. John Newton, who knew storms at sea as well as in life, could say,

With Christ in the vessel I smile at the storm.

And so can we because, “The LORD hath his way in the whirlwind and in the storm” (Nahum 1:3). He deals with us like this to subdue sin, draw us closer to Him, make us better Christians, and fashion us for the work of His kingdom.

c] He has power over every storm and can easily deliver us.

“And he arose, and rebuked the wind, and said unto the sea, Peace, be still. And … there was a great calm” (4:39). With His mere word our Lord stilled the storm: “Peace” spoken to the howling wind, silencing it; “Be still” to the tossing waves, calming them to a smooth surface. “The Lord of peace” is with us (2 Thessalonians 3:16). For the One who made heaven and earth no tempest is too fierce to quell (cf Psalm 107:23-31). We can be sure that, real though the storm may be, it will not be allowed to overwhelm us (Isaiah 43:1,2).

Be still, my soul: the waves and winds still know
His voice who ruled them while He dwelt below.

Now let us consider the Lord’s searching question, “Why are ye so fearful? how is it that ye have no faith?” (Mark 4:40). He means that the disciples’ reaction showed a failure of faith. If they had believed, they would not have acted the way they did; neither would they have uttered those hurtful words, “Master, carest thou not that we perish?” (verse 38).

Have we passed through stormy waters this past year? If so, how consistent has our faith been? The New Year of 2019 may bring deep and turbulent trials. One thing is sure, faith is the overcoming grace (1 John 5:4) and is always the difference between victory or defeat. According to our faith we will be brought down, or be wonderfully upheld and brought through. To help us in this, let us consider,


“How is it that ye have no faith?” Does the Lord mean they are unbelievers?

1] Not in the absolute sense.

These are disciples who have left all to follow the Master. They certainly are believers: the gift of faith is theirs (Ephesians 2:8,9; Philippians 1:29). As one of them was to write to Christians years afterwards, this indestructible grace was their treasure: “like precious faith with us” (2 Peter 1:1).

2] However, it was true in a comparative sense.

“No faith.” Our Lord means their faith was not in exercise. Matthew and Luke have, “O ye of little faith” and “Where is your faith?” These good men failed to believe what they knew to be true: that the Son of God was there with them and that all was well. They allowed the storm, and their feelings, to take them over so that they forgot Whose they were and Whom they served!

3] This can easily happen to us.

“No faith.” We fret, we panic, we go down under our circumstances. They control us, and we seem little better than unbelievers. Let us guard our reactions: the Lord has not forgotten nor abandoned us. Let us remember what we know, and reach out to Him Whom we know. Faith must not be dormant but exercised toward Him. As Thomas Watson had it: “Faith … has an eye to see Christ, as well as a wing to fly to Christ” … “Faith, though it hath sometimes a trembling hand, it must not have a withered hand, but must stretch.”

4] This was a test of faith.

It was what they saw versus what they knew was true. And, sadly, what they saw won! (2 Corinthians 5:7). It might seem that the Lord is asleep to our predicament – unaware, indifferent. But it was not so, as the sequel proved! The Lord did not need the terrified, reproachful disciples to waken Him to still the storm! He would certainly have done it.

5] Nothing troubled the Lord.

We are flummoxed and perplexed, but the Lord is not. Although asleep as Man – as God would He have allowed the boat, and them, to sink? Did He really care for these men less than they cared for themselves? Far from it. Mark tells us He was “in the hinder part of the ship” (verse 38) – this is where the helmsman steers the boat! Faith in exercise will say with George Herbert,

When winds and waves assault my keel,
He doth preserve it, He doth steer,
Ev’n when the boat seems most to reel.
Storms are the triumph of His art;
Though He may close his eyes, yet not His heart.


“How is it that ye have no faith?” What do we say to this? Why do we tend not to exercise faith when we need to most? Here are some reasons which may help us avoid this for the future.

1] Because of fear.

verse 40 “Why are ye so fearful?” The emotion of fear and the exercise of faith are opposites; and mutually exclusive. Where one is, the other cannot be. In this instance, fear pushed out faith. Therefore, before fear takes hold, remember the Lord, and do what the prophet says, “I will trust, and not be afraid” (Isaiah 12:2; cf Psalm 56:3). If you go from fear to faith, you go from fear to Him.

2] Unbelief remains in us.

It is part of the “sin that dwelleth in me” (Romans 7:17). Being our old nature, it will always make exercising faith a struggle. Every grace has its opposite corruption to oppose it. And faith has to contend against unbelief. This is why the father of the demon-possessed boy “cried out, and said with tears, Lord, I believe; help thou mine unbelief” (Mark 9:24). The encouragement, though, is that the Lord heard this man’s struggling prayer OF faith! The Lord is greater and kinder than our faltering faith.

3] We forget past deliverances.

These disciples had already seen instances of the Lord’s power. For example, the deliverance of the demoniac in the synagogue (Mark 1:23-28); Peter’s mother-in-law healed (1:30,31); many people healed, and delivered from demons (1:32-34); a leper cleansed (1;40-45); the sick of the palsy made whole (2:2-12); the man with the withered hand cured (3:1-5). For our part, we have seen His grace and goodness many times. Do we think our current storm of trouble is unique and beyond the Lord’s ability to come in for us? Having proved Him in the past, let us rise to the opportunity of proving Him in the present. Let faith go back to its Ebenezers and on to its henceforths!

4] Because faith looks beyond what is seen and temporal.

The Puritans called faith “our spiritual optic.” It enables us to see “him who is invisible” (Hebrews 11:27). Thomas Adams said, “It is the office of faith to believe what we do not see, and it shall be the reward of faith to see what we … believe.”

In this instance, however, what the disciples saw with their eyes took them over. They did not use the eye of faith that looks beyond to Him. David, too, was aware of this, “I had fainted, unless I had believed to see the goodness of the LORD in the land of the living” (Psalm 27:13). Let us look beyond and above our present distress, and believingly look to the Lord!

5] We are not enough in the Bible.

We should not underestimate our great enemy in this. Satan stirs up our carnal sense to undermine confidence in the Lord. Only God’s word can answer and silence him. As David Dickson said, “When Satan borrows sense to speak one thing, let faith borrow Scripture to speak the contrary.”

God’s word is the greatest faith-building means of grace: “faith cometh by hearing, and hearing by the word of God” (Romans 10:17). The Scriptures bring us into heart-acquaintance with Him Who is the great Object of our faith (Acts 20:32). The word of God leads us to the God of the word; it makes Him real to the soul.

Yet, when all is said, the disciples’ reaction was prayer, “they awake him and say unto him, Master, etc.” (verse 38). If at least our fear drives us to Jesus, is not all wrong. The cry to Him, even of half-believing panic, brings us His help. Their faith was weak, but their prayer was strong. The comfort is that despite His gentle question, He did not rebuke them, but the storm.

Let us humble ourselves and confess our unbelieving fears and sinful distrust. Let us pray to the Lord to increase our trust, that we might be strong in faith, and give credit and glory to God.

They never forgot this lesson. Peter especially, years afterwards wrote, correcting the unworthy reflection on the Lord, and knowing better now, “Casting all your care upon him; for he careth for you” (1 Peter 5:7).

Dear reader, believe that it will be so for you as well. We do not minimise the deep and dark trial that waves and billows can be. But as those in Psalm 107:27-30 found, they were “at their wits end,” but not at their faith’s end. Believe it is so for you as well,

… and he bringeth them out of their distresses. He maketh the storm a calm, so that the waves thereof are still. Then are they glad because they be quiet; so he bringeth them unto their desired haven.

And that haven is into His arms, upon His bosom – to be safer in the storm with Him than in the calm without Him.

The storm may roar without me,
My heart may low be laid;
But God is round about me,
And can I be dismayed?

by Rev. John Thackway, Pastor of Holywell Evangelical Church

Used with kind permission of the author

Friday, 1 February 2019

Myalgic Encephalomyelitis: A Baffling Syndrome With A Tragic Aftermath

[This article by Dr Melvin Ramsay (1901 – 1990) was first published in 1986. I thought that it would be helpful, with all the current confusion about ME and mixing it up with various fatigue syndromes and states, to reproduce it here.]

Myalgic Encephalomyelitis: A Baffling Syndrome With A Tragic Aftermath


Melvin Ramsay, M.A., M.D. Hon Consultant Physician,

Infectious diseases Department, Royal Free Hospital

Myalgic Encephalomyelitis leaves a chronic aftermath of debility in a large number of cases. The degree of physical incapacity varies greatly, but the dominant clinical feature of profound [paralytic muscle] fatigue is directly related to the length of time the patient persists in physical effort after its onset; put in another way, those patients who are given a period of enforced rest from the onset have the best prognosis.

Although the onset of the disease may be sudden and without apparent cause, as in those whose first intimation of illness is an alarming attack of acute vertigo, there is practically always a history of recent virus infection associated with upper respiratory tract symptoms though occasionally there is gastro-intestinal upset with nausea and vomiting. Instead of making a normal recovery, the patient is dogged by persistent profound fatigue accompanied by a medley of symptoms such as headache, attacks of giddiness, neck pain, muscle weakness, parasthesiae, frequency of micturition or retention, blurred vision and/or diplopia and a general sense of 'feeling awful'. Many patients report the occurrence of fainting attacks which abate after a small meal or even a biscuit, and in an outbreak in Finchley, London, in 1964 three patients were admitted to hospital in an unconscious state presumably as a result of acute hypoglycaemia. There is usually a low-grade pyrexia [fever] which quickly subsides. Respiratory symptoms such as sore throat tend to persist or recur at intervals. Routine physical examination and the ordinary run of laboratory investigations usually prove negative and the patient is then often referred for psychiatric opinion. In my experience this seldom proves helpful is often harmful; it is a fact that a few psychiatrists have referred the patient back with a note saying 'this patient's problem does not come within my field'. Nevertheless, by this time the unfortunate patient has acquired the label of 'neurosis' or 'personality disorder' and may be regarded by both doctor and relatives as a chronic nuisance. We have records of three patients in whom the disbelief of their doctors and relatives led to suicide; one of these was a young man of 22 years of age.

The too facile assumption that such an entity - despite a long series of cases extending over several decades - can be attributed to psychological stress is simply untenable. Although the aetiological factor or factors have yet to be established, there are good grounds for postulating that persistent virus infection could be responsible. It is fully accepted that viruses such as herpes simplex and varicella-zoster remain in the tissues from the time of the initial invasion and can be isolated from nerve ganglia post-mortem; to these may be added measles virus, the persistence of which is responsible for subacute sclerosing panencephalitis that may appear several years after the attack and there is a considerable body of circumstantial evidence associating the virus with multiple sclerosis. There should surely be no difficulty in considering the possibility that other viruses may also persist in the tissues. In recent years routine antibody tests on patients suffering from myalgic encephalomyelitis have shown raised titres to Cocksackie B Group viruses. It is fully established that these viruses are the aetiological agents of 'Epidemic Myalgia' or 'Bornholm's Disease' and that, together with ECHO viruses, they comprise the commonest known virus invaders of the central nervous system. This must not be taken to imply that Cocksackie viruses are the sole agents of myalgic encephalomyelitis since any generalised virus infection may be followed by a period of post-viral debility. Indeed, the particular invading microbial agent is probably not the most important factor. Recent work suggests that the key to the problem is likely to be found in the abnormal immunological response of the patient to the organism.

A second group of clinical features found in patients suffering from myalgic encephalomyelitis would seem to indicate circulatory disorder. Practically without exception they complain of coldness in the extremities and many are found to have abnormally low temperatures of 94 or 95 degrees F. In a few, these are accompanied by bouts of severe sweating even to the extent of waking during the night lying in a pool of water. A ghostly facial pallor is a well known phenomenom and this has often been detected by relatives some 30 minutes before the patient complains of being ill.

The third component of the diagnostic triad of myalgic encephalomyelitis relates to cerebral activity. Impairment of memory and inability to concentrate are features in every case. Many report difficulty in saying the right word and are conscious of the fact that they continue to say the wrong one, for example 'cold' when they mean 'hot'. Others find that they start a sentence but cannot complete it, while some others have difficulty comprehending the written or spoken word. A complaint of acute hyperacusis is not infrequent; this can be quite intolerable but alternates with periods of normal hearing or actual deafness. Vivid dreams generally in colour are reported by persons with no previous experience of such a phenomenon. Emotional lability is often a feature in a person of previous stable personality, while sudden bouts of uncontrollable weeping may occur. Impairment of judgement and insight in severe cases completes the 'encephalitic' component of the syndrome.

I would like to suggest that in all patients suffering from chronic debility for which a satisfactory explanation is not forthcoming a renewed and much closer appraisal of their symptoms should be made. This applies particularly to the dominant clinical feature of profound fatigue. While it is true that there is considerable variation in degree from one day to the next or from one time of the day to another, nevertheless in those patients whose dynamic or conscientious temperaments urge them to continue effort despite profound malaise or in those who, on the false assumption of 'neurosis', have been exhorted to 'snap out of it' and 'take plenty of exercise' the condition finally results in a state of constant exhaustion. This has been amply borne out by a series of painstaking and meticulous studies carried out by a consultant in physical medicine, himself an ME sufferer for 25 years. These show clearly that recovery of muscle power after exertion is unduly prolonged. After moderate exercise, from which a normal person would recover with nothing more than a good night's rest, an ME patient will require at least 2 to 3 days while after more strenuous exercise the period can be prolonged to 2 or 3 weeks or more. Moreover, if during this recovery phase, there is a further expenditure of energy the effect is cumulative and this is responsible for the unrelieved sense of exhaustion and depression which characterises the chronic case. The greatest degree of muscle weakness is likely to be found in those muscles which are most in use; thus in right- handed persons the muscles of the left hand and arm are found to be stronger than those on the right. Muscle weakness is almost certainly responsible for the delay in accommodation which gives rise to blurred vision and for the characteristic feature of all chronic cases, namely a proneness to drop articles altogether with clumsiness in performing quite simple manoeuvres; the constant dribbling of saliva which is also a feature of chronic cases is due to weakness of the masseter muscles. In some cases, the myalgic element is obvious but in others a careful palpitation of all muscles will often reveal unsuspected minute foci of acute tenderness; these are to be found particularly in the trapezii, gastrocnemii and abdominal rectii muscles.

The clinical picture of myalgic encephalomyelitis has much in common with that of multiple sclerosis but, unlike the latter, the disease is not progressive and the prognosis should therefore be relatively good. However, this is largely dependent on the management of the patient in the early stages of the illness. Those who are given complete rest from the onset do well and this was illustrated by the aforementioned three patients admitted to hospital in an unconscious state; all three recovered completely. Those whose circumstances make adequate rest periods impossible are at a distinct disadvantage, but no effort should be spared to give them the all-essential basis for successful treatment. Since the limitations which the disease imposes vary considerably from case to case, the responsibility for determining these rests upon the patient. Once these are ascertained the patient is advised to fashion a pattern of living that comes well within them. Any excessive physical or mental stress is likely to precipitate a relapse.

It can be said that a long-term research project into the cause of the disease has been launched and there are good grounds for believing that this will demonstrate beyond doubt that the condition is organically determined.

Friday, 25 January 2019

Watch The Debate!

The debate about ME, which was held in the House of Commons, Westminster, London, UK, on Thursday 25 January 2019 can be watched on YouTube; see below. There were a lot of excellent contributions from MPs, many of whom used case histories sent to them by their constituents. Sadly, the one disappointing, weak speech was the response by the Minister of Health. Apart from that, I thought that it was encouraging and well worth watching.

Friday, 18 January 2019

ME Debate In Parliament

From the 25% ME Group website –

Published by Simon Lawrence on 17/01/2019

The Backbench Business Committee has granted a debate on ME. It will take place on the afternoon of Thursday 24th January.

It would be helpful if you could encourage the community to approach their MPs to request their support. Any briefings would also be appreciated.

The motion to be debated next week is as follows: “That this House calls on the Government to provide increased funding for biomedical research into the diagnosis and treatment of ME, supports the suspension of Graded Exercise Therapy and Cognitive Behaviour Therapy as means of treatment, supports updated training of GPs and medical professionals to ensure they are equipped with clear guidance on diagnosis of ME and appropriate management advice to reflect international consensus on best practice, and is concerned about the current trends of subjecting ME families to unjustified child protection procedures.”

Office of Carol Monaghan MP
Member of Parliament for Glasgow North West

Monday, 14 January 2019

Rest Is A Gift

C H Spurgeon's Cheque Book Of The Bank Of Faith Daily Devotional for 14th January

“Come unto Me, all ye that labour and are heavy laden, and I will give you rest.”

Matthew 11:28

We who are saved find rest in Jesus. Those who are not saved will receive rest if they come to Him, for here He promises to "give" it. Nothing can be freer than a gift; let us gladly accept what He gladly gives. You are not to buy it, nor to borrow it, but to receive it as a gift. You labour under the lash of ambition, covetousness, lust, or anxiety: He will set you free from this iron bondage and give you rest. You are "laden," yes, "heavy laden" with sin, fear, care, remorse, fear of death; but if you come to Him He will unload you. He carried the crushing mass of our sin that we might no longer carry it. He made Himself the great Burden-bearer, that every laden one might cease from bowing down under the enormous pressure. Jesus gives rest. It is so. Will you believe it? Will you put it to the test? Will you do so at once? Come to Jesus by quitting every other hope, by thinking of Him, believing God's testimony about Him, and trusting everything with Him. If you thus come to Him the rest which He will give you will be deep, safe, holy, and everlasting. He gives a rest which develops into heaven, and He gives it this day to all who come to Him.