Causes and consequences of autonomic dysfunction in CFS

Posted on 11/02/2016 by wames

Thesis abstract:

Introduction:
Chronic Fatigue Syndrome (CFS) is an incapacitating condition characterised by extreme fatigue. In the absence of an objective diagnostic test CFS remains a clinical diagnosis based on a broad spectrum of symptoms, including autonomic dysfunction and cognitive
impairment. This has given rise to significant challenges, not least the development of multiple sets of diagnostic criteria that may represent different disease phenotypes. This thesis examines autonomic and cognitive features between subgroups that meet different diagnostic criteria to better understand this possibility. It also examines the overlap between symptoms of CFS and depression, a potential confounder.

Methods:
A subset of data from a larger Medical Research Council funded observational study Understanding the pathogenesis of autonomic dysfunction in CFS and its relationship with cognitive impairment was examined. Patients were screened using the SCID-I assessment tool to exclude major depression prior to the main study. Depressive symptoms were compared to CFS Fukuda criteria. The DePaul Symptom Questionnaire (DSQ) was used to differentiate between diagnostic criteria. COMPASS and COGFAIL questionnaires were administered for self-reported autonomic and cognitive features respectively. The Task Force(r) Monitor was used for autonomic assessment and a battery of neuropsychological tests administered for objective cognitive assessment.

Results:
Subjective autonomic and cognitive symptoms were significantly greater in CFS subjects compared to controls. There were no statistically significant differences in objective autonomic measures between CFS and controls. There were clinically significant differences between DSQ subgroups on objective autonomic testing. Psychomotor speed was significantly slower in CFS compared to controls. Visuospatial memory, verbal memory and psychomotor speed were significantly different between DSQ subgroups.

Conclusion:
The findings indicate phenotypic differences between DSQ subsets and suggest that elucidating the symptoms seen in CFS, or its disease spectrum, will support research into its underlying pathophysiology and enable more tailored treatment. The absence of significant differences in objective autonomic function between CFS and controls in this cohort contrasts to findings of some other studies and may reflect study exclusion for depression. Together with the overlap between CFS and depressive symptoms, this reinforces the need to better understand the underpinning causality to allow appropriate identification and management.

Causes and consequences of autonomic dysfunction in Chronic Fatigue Syndrome, by Laura Maclachlan, Newcastle University thesis January 2016

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A patient’s experience of ME/CFS and gaslighting

Posted on 10/31/2016 by wames

The Mighty blog post, by Siobhan Simper, 18 Oct 2016: We cannot continue to let doctors ‘Gaslight’ chronic illness patients

Author’s warning: This post contains experiences of gaslighting and abuse.

Recently, I saw an all-too-common meme on social media: the inspirational disabled person. The image was of a Paralympic horse rider, with the caption, “no excuses.” Much has been written about the problematic nature of disability “inspiration porn.” What shocked me was when I tried to explain the issue with this post, I was attacked as “angry” and “fucked up.” But being labelled “crazy” for having a chronic illness or disability is nothing new.

For centuries, it has been common practice to dismiss people who were considered “rabble-rousing” as being “mad.” Women especially bore the brunt of these attitudes. During the Salem Witch Trials, the women hanged as witches were likely to have epilepsy or dissenting views. In the 1800s, women who challenged the status quo were at risk of being declared “insane” and committed to a mental asylum. Their husbands, fathers and brothers were usually the ones to request institutionalization, whereby an unruly woman would learn to submit to male authority. Many opinionated women were silenced in asylums.

At the time, women were considered inherently unstable. Symptoms of legitimate medical conditions were lumped under the pseudo-psychiatric label “hysteria” – an easy way to invalidate the struggles of thousands of women. It was far more convenient to dismiss genuine pain as the result of women’s fragile nature, caused by a rampant womb wandering unchecked through their bodies.

“Gaslighting” is a form of psychological abuse, whereby the perpetrator attempts to convince their victim to doubt their own perceptions, with the intent of making them believe they are in fact “crazy.” As the victim comes to doubt their sanity, they become more reliant on their abuser and less connected with the outside world. The term comes from the 1938 play-turned-film “Gaslight,” in which a husband convinces his wife she is going “insane,” by manipulating her and controlling her environment. It is not hard to see how this plays out for the chronically ill.

A chronically ill person is already in a uniquely vulnerable position, whereby medical professionals act as gatekeepers to proper treatment. Doctors hold an inordinate amount of power over someone with a chronic illness, and it doesn’t take much to tip the balance further in their favor.

Last year, I had the bad luck of being booked in with a registrar, who took the opportunity to continually tell me how I felt. “You’re doing well,” he accosted ad nauseam, in response to my continued protests that my health was, in fact, not good. I have paid $120 for the privilege of consulting with a general specialist who, after listening to me explain I could not walk for five minutes without collapsing, informed me there was nothing wrong with me a little exercise couldn’t fix.

For those with a mental illness, it gets worse. We already know physicians are less likely to believe a patient has a serious illness if they have a history of psychiatric problems. And when we are already primed to view people with mental illnesses as “fundamentally unstable,” gaslighting is the next logical leap.

A friend on a mental ward was accused of being a pathological liar by the head psychiatrist, merely because she had a habit of touching her face when nervous. Another was told she had no hope of recovery, so she should stop trying. When the abuser is a medical professional, or someone in a position of power, why wouldn’t we believe their word over that of someone whose testimony is considered so unreliable already?

Every time a patient is told their symptoms are not real: abuse. Every time someone with a chronic illness is told their illness is a result of them not trying X, Y, Z therapy: abuse. When a young woman is called “fucked up” for finding a disability stereotype offensive: abuse. And what’s worse is it is clear when disabled people are denied their lived experiences are real, they are also denied adequate treatment.

The latest trend in treatment of myalgic encephalomyelitis/chronic fatigue syndrome(ME/CFS) is combining graded exercise therapy (GET) and cognitive behavioral therapy (CBT). The therapies were popularized by the PACE trials, an extensive, government-funded study, which examined GET and CBT as treatments for ME/CFS. Their results were best summarized by The Guardian’s headline: “Chronic fatigue syndrome patients’ fear of exercise can hinder treatment.” The PACE trials confirmed what so many medical professionals already believed: that ME/CFS was nothing more than a psychological disorder, a combination of mental and physical deconditioning which could be easily remedied with a bit of exercise and right thinking. Except, it didn’t.

Criticism of the PACE trials has been building ever since it was published. Scales for measuring illness were so poorly designed that patients could be simultaneously qualified as disabled enough for participation and well enough to be “cured.” These measures were tinkered with as the study progressed. Those who were unwell enough to attend regular appointments at the hospital were discounted, meaning only the most well people with ME/CFS were studied. Patients were given brochures promoting the effectiveness of CBT and GET as treatments for their illness. The patients who were determined “cured” were deemed as such solely on the basis of a subjective survey, not objective measures such as employment and exercise tests.

Yet it is only now, after years of campaigning, that the researchers behind PACE are being forced to release their raw data. The belief that ME/CFS was psychosomatic was so ingrained, that it has taken five years for their research methods to be brought into question. Meanwhile, this research has had real implications for ME/CFS patients. Treatments such as GET have been documented to cause real harm to people with ME/CFS. And who knows how many seriously ill ME/CFS patients were denied a diagnosis or real treatment on the basis of these trials?

On a more personal note, the full force of gaslighting hit me when I was admitted to hospital three years ago. My severe ME/CFS had affected me to the point where I was in bed 24/7, so weak I was unable to sit upright, talk, or feed myself. I was wasting away to nothing. My GP decided I needed admission, so I feebly agreed, knowing my health insurance meant I would have a private, quiet room in the local private hospital. But once I was admitted, my GP went on holiday, and I was immediately whisked from my cosy room to an open room in ICU in the public hospital. I remember crying and begging mum to not take me there, as I knew full well how I would be treated – or at least I thought I did. My experiences surpassed even my wildest nightmares.

A psychiatrist came to my bed. “You’re depressed, aren’t you,” he insisted. I explained, with my limited ability to speak, that I still wanted to do things, I just physically couldn’t. “That doesn’t mean you aren’t depressed,” he countered. Any first year psych student can tell you that one of the key symptoms of depression is anhodenia – an inability to experience pleasure, even in activities that were formerly enjoyed. I tried in vain to signal I still derived enjoyment from life, but my protests were silenced.

Nurses flocked to bed over the next few days, demanding I admit I was just depressed so this charade could be over. “There’s no shame in being depressed,” one told me. “I know – I’m not!” The psychiatrist visited again. He promised he could help me, he could stop the nurses and other doctors from treating me badly and take me to a safe place – so long as I conceded I was depressed.

Next, I was told of a CFS unit in Melbourne, one which would help me, like they had helped many patients before me. A place where they would understand and treat my symptoms. I just had to agree to go. After a long exhortation from a nurse who I thought genuinely cared for me, I agreed to go. I cannot understate how big this decision was for me. I hadn’t left my bed in a year and my hometown in three years. Going to Melbourne, a four-hour car trip away, was not a decision I took lightly. But I deemed it worth the pain, if they could truly treat me.

Later that day, my parents rushed in to my room. There were tears on their faces. “Why did you agree to go to Melbourne?” they asked. I wanted help, I said. A CFS unit could treat me. “But they’re not sending you to a CFS ward,” my parents cried. “They are admitting you to an eating disorder unit!” An eating disorder. Nothing had been further from my mind as I lay there all those months, in agony. I was so consumed by my ME/CFS I did not notice that I had lost nearly half my body weight. And they thought I had anorexia.

Anyone close to me knows I don’t lie. It’s not that I won’t, but I simply cannot tell an untruth. Lying is antithetical to my nature; the very idea of telling a lie upsets me. So the suggestion that I had formed an elaborate deception to mislead not only doctors, but my parents and everyone I loved, was not only offensive, but impossible. The thought that the nurses and doctors, who were meant to be looking after me, had deliberately deceived me to admit me to a mental hospital made me sick.

The next few weeks, hospital staff exerted all their power over me and my parents to force home their conclusion that I did not have a real physical illness. My parents recall a particularly nasty encounter with a weekend doctor. Dad begged in desperation, “Do you know anything about CFS?” to which the doctor retorted, “Do you know anything about eating disorders? Because your daughter has one!” The only people on my side, my parents, put in complaints to the hospital. They were all ignored.

Despite evidence to the contrary, my medical team were convinced I had a hidden eating disorder that my entire social network was in denial about. But I was so desperate to put on weight, I gladly accepted having a nasal gastric feeding tube shoved down my throat. I was happy to gain weight.

My main doctor later threatened to section me. I was scared. Sectioning someone under the mental health act is a way to strip away all their rights, their autonomy as a person. A person is deemed mentally incapable of making decisions for themselves, and can be enforceably hospitalized by their medical team. It takes a legal appeal to remove this order.

There are some people who are so unwell that they genuinely cannot take care of themselves, and being sectioned can be the difference between life and death. But as a tool to terrify and intimidate a young woman, who is so physically disabled she can’t defend herself, it is the epitome of gaslighting.

I agreed to leave, just to escape that doctor. Upon arrival at the eating disorders unit, it took all of five minutes for the team to determine I had no mental illness.

Recovery from gaslighting is one of the hardest things I’ve ever had to do. Having your own perceptions warped to the point where you start to doubt your own sanity is a long road to come back from. You have been taught to not trust your own convictions, so how can you believe your own thoughts after that? It is little wonder so many chronically ill people buy into therapies based on convincing the ill personthey are not sick at all, or that they can overcome illness with the right kind of thinking.

It would be easy to dismiss gaslighting of disabled people as a relic of the past, something we can shake our heads at while feeling oh-so-civilized. But the sad fact is that even now, people with a disability, including mental illnesses, are being objectified, marginalized, and brushed off as “crazy” for the crime of being unwell. Their treatment is often inadequate or non-existent.

If you think you are being gaslighted in a relationship, please, please seek help. For those with a chronic illness, who are often in a continual state of being gaslighted by doctors, friends and society at large, hold strong and true. Your experiences are real, and your feelings valid. To both you and me.

Read more by Siobhan

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Could gut dysfunction in Parkinson’s overlap with ME?

Posted on 10/28/2016 by wames

ME global chronicle article, October 2016: Parkinson’s disease protection may begin in the gut.

Why an article on Parkinson’s in an ME-magazine, one might ask.

There seems to be more and more suspicion that there’s overlap between Parkinson’s, Alzheimer’s and ALS with ME. The findings in this research only seem to affirm.

Science daily article, 5 October 2016:

Your gut may play a pivotal role in preventing the onset of Parkinson’s disease. And the reason may be its knack for sleuthing.  Researchers at the University of Iowa have found that the gut may be key to  preventing Parkinson’s disease. Cells located in the intestine spark an immune response that protects nerve cells, or neurons, against damage connected with  Parkinson’s disease.

Acting like detectives, the immune intestinal cells identify damaged machinery within neurons and discard the defective parts. That action ultimately preserves neurons whose impairment or death is known to cause Parkinson’s.

“We think somehow the gut is protecting neurons,” says Veena Prahlad,

assistant professor in biology at the UI and corresponding author on the paper published Aug. 30 in the journal Cell Reports.veena-prahladParkinson’s disease is a brain disorder that erodes motor control and balance over
time. It affects some 500,000 people in the U.S., according to the National
Institutes of Health. The disease occurs when neurons — nerve cells — in the brain
that control movement become impaired or die. Normally, these neurons produce
dopamine, and when they are damaged or killed, the resulting dopamine shortage
causes the motor-control problems associated with the disease.

Scientists have previously linked Parkinson’s to defects in mitochondria, the energy-producing machinery found in every human cell. Why and how mitochondrial defects affect neurons remain a mystery. Some think the impaired mitochondria starve neurons of energy; others believe they produce a neuron harming molecule. Whatever the answer, damaged mitochondria have been linked to other nervous disorders as well, including ALS and Alzheimer’s, and researchers want to understand why.

Prahlad’s team exposed roundworms to a poison called rotenone, which researchers know kills neurons whose death is linked to Parkinson’s. As expected, the rotenone began damaging the mitochondria in the worms’ neurons.

To the researchers’ surprise, though, the damaged mitochondria did not kill all of the worms’ dopamine-producing neurons; in fact, over a series of trials, an average of only seven percent of the worms, roughly 210 out of 3,000, lost dopamine-producing neurons when given the poison.

“That seemed intriguing, and we wondered whether there was some innate mechanism to protect the animal from the rotenone,” Prahlad says.

It turns out there was. The roundworms’ immune defenses, activated when the rotenone was introduced, discarded many of the defected mitochondria, halting a sequence that would’ve led to the loss of dopamine producing neurons. Importantly, the immune response originated in the intestine, not the nervous system.

pd-gut

“If we can understand how this is done in the roundworm, we can understand how this may happen in mammals,” Prahlad says.

The researchers plan to conduct more experiments, but they’ve got some interesting hypotheses. One is the intestinal immune cells are, according to Prahlad, “constantly surveilling mitochondria for defects.”

Even more, those cellular watchdogs may be keeping their eyes on the mitochondria “because they don’t trust them,” Prahlad suggests. The reason has to do with the prevailing theory that mitochondria originated independently as a type of bacterium and were only later incorporated into the cells of animal, plants, and fungi as an energy producer.

If that theory is correct, the intestinal immune responders may be especially sensitive to changes in mitochondrial function not only for its potential damaging effects, but because of the mitochondria’s ancient and foreign past as well.

“How it’s happening is suggestive of the possibility that the innate immune response is constantly checking its mitochondria,” Prahlad says, “perhaps because of the bacterial origin of the mitochondria”.

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The thyroid question in FM & ME/CFS

Posted on 10/28/2016 by wames

Health rising blog post by Cort Johnson, 24 October 2016: The thyroid question in Fibromyalgia and Chronic Fatigue Syndrome (ME/CFS)

Fatigue, lethargy, mental sluggishness, difficulty tolerating heat and cold, depression, joint pain, headaches, morning stiffness…the list goes on and on. It’s almost a perfect match for chronic fatigue syndrome (ME/CFS) or fibromyalgia (FM) but it’s not either – it’s hypothyroidism; one of the trickiest conditions that people with either disease have to deal with.

If a hypothyroid diagnosis was done purely symptomatically, most if not all people with ME/CFS and FM would be considered hypothyroid. Dr. Teitelbaum’s description of the thyroid gland as the body’s “gas pedal” regulating its metabolic rate resonates strongly with ME/CFS and FM. Few studies on this have been done in FM and almost none have been done in ME/CFS.

Most perplexing for the patient is the considerable disagreement among doctors regarding what constitutes low thyroid and how to treat it. The problem is that giving thyroid hormone to someone who doesn’t need it is can cause their thyroid gland to shut down, leaving them dependent upon thyroid medication for life. Plus, other factors such as low cellular energy production or autonomic nervous system problems can cause similar symptoms.

MD’s with an holistic health slant including prominent ME/CFS/FM practitioners such as Dr. Jacob Teitelbaum, Dr. Kent Holtorf, Dr. Sara Myhill and Dr. Ginerva Liptan – argue that flawed thyroid tests vastly underestimate the amount of hypothyroidism present, and by doing so, keep patients from potentially helpful drugs. Dr. Teitelbaum in a blog titled “The High Cost of Missed Hypothyroid Diagnosis”  calls hypothyroidism “horribly under-diagnosed”. He believes that undiagnosed or poorly treated thyroid problems contribute to unnecessary disability in millions of people with fibromyalgia, chronic fatigue syndrome, and chronic pain.

Most doctors, however, probably believe hypothyroidism is rare in ME/CFS and thyroid supplementation is unnecessary and possibly harmful.

A few simple concepts:

  • Thyroid hormones – affect the activity of virtually every cell in the body. They regulate the basal metabolic rate, protein, fat and carbohydrate metabolism, bone growth, affect protein synthesis and others.  Low thyroid levels can lead to fatigue, mental slowness, pain, depression, weight gain and more.
  • Thyroid Stimulating Hormone (TSH) – is produced by the pituitary gland to stimulate the production of thyroid hormones by the thyroid.
  • Thyroxine (T4) – is a prohormone produced by the thyroid gland which is broken down by deiodinase enzymes to produce the active form of thyroid hormone.
    Triiodothyronine (T3) – The active form of thyroid hormone

Dr. Holtorf’s View of Hypothyroidism
Hormones in Wellness and Disease Prevention: Common Practices, Current State of the Evidence, and Questions for the Future. Erika T. Schwartz, MDa,*, Kent Holtorf, MDb

“Thyroid Disorders” by Kent Holtorf in The LDN Book, ed. by Linda Elsegood

Dr. Holtorf has probably done more work in the area of hypothyroidism than any other ME/CFS practitioner. Please note this overview presents one view of this subject – other doctors will have other views.

Most if not all, patients who suffer from chronic fatigue syndrome, fibromyalgia, diabetes, insulin resistance, depression and stress have immune dysfunction that results in low tissue levels of thyroid hormone.  Kent Holtorf

Most doctors rely on TSH and/or T4 test results to determine if thyroid levels are normal. Testing for TSH is an indirect measure of thyroid status but since TSH regulates thyroid production, testing for it makes sense. If TSH levels are high, then thyroid is probably low. In that case doctors will then test for T4 – the inactive form of thyroid; if T4 levels are low then thyroid hormone is needed.

Not so fast says Dr. Holtorf. Holtorf believes that, at times, serum thyroid levels tell us little about thyroid levels in the tissues and cells. Two of those times are when people have fibromyalgia and/or chronic fatigue syndrome.

TSH, Holtorf asserts, is produced by the one organ in the body – the pituitary gland –   which is able to maintain its thyroid at normal levels while thyroid levels in the tissues around it are plummeting. If that’s so, then assessing thyroid hormone levels by measuring TSH is like measuring the temperature of your refrigerator by measuring the temperature of the kitchen.

The pituitary/thyroid issue revolves around the enzymes which activate and deactivate thyroid hormone. Two of these enzymes, D1 and D2, convert the inactive form of thyroid hormone (T4) to its active form (T3).

While most of the body uses D1 to convert inactive thyroid hormone (T4) to its active form (T3), the pituitary gland uses D2.

Dr. Holtorf believes conditions like fibromyalgia, chronic fatigue syndrome, stress, pain, autoimmune diseases, inflammation, depression, toxins, etc. suppress and down regulate D1 levels in the tissues, causing the levels of the active form of thyroid hormone to plummet. These conditions don’t affect D2 levels in the pituitary at all.

Because women tend to have lower levels of the enzyme (D1) that converts the inactive to the active form of thyroid, they’re more likely to suffer from hidden thyroid problems. Holtorf noted a typical patient of his: a woman suffering from what appears to be the symptoms of hypothyroidism (fatigue, inability to lose weight, cold intolerance, etc.) who often has low-normal TSH, high-normal free T4, low-normal free T-3, high normal reverse T-3, plus markers of thyroid resistance and low resting metabolic rates.

As active levels of thyroid hormone in the body decline, they may actually increase in the pituitary.

The pituitary gland, remember, produces thyroid stimulating hormone (TSH) which tells the thyroid gland to produce more hormones when levels of pituitary T3 decline. If pituitary levels of the active thyroid hormone (T3) are unaffected by conditions such as fibromyalgia and chronic fatigue syndrome, TSH readings could falsely suggest that thyroid levels are fine, when tissue levels are, in fact, low.

TSH, of course, is what most doctors first test for to determine thyroid hormone status.

Reverse T3 (RT3)
A third enzyme, D3, complicates matters further. D3 converts the inactive form of thyroid hormone (T4) to a form of thyroid called reverse T3 when levels of T4 are too high.  Holtorf, however, believes that in some conditions such as fibromyalgia and ME/CFS, RT3 becomes pathological as it blocks the active form (T3) from binding to thyroid receptors in the body.

Higher RT3 levels and/or higher RT3/T3 ratio’s may indicate poor availability of the active form of thyroid (T3).

The pituitary gland is also the only tissue in the body which does not contain D3, the enzyme which converts inactive thyroid hormone (T4) to a form of the hormone (reverse T3).

TSH levels, then, have no bearing at all on reverse T3 levels. RT3 levels can be high even when TSH levels are normal. Most doctors, however, do not test for RT3.

Reverse T3 is actually an “antithyroid” — T3 is the active thyroid that goes to the cells and stimulates energy and metabolism. Reverse T3 is a mirror image — it actually goes to the receptors, sticks there, and nothing happens. So it blocks the thyroid effect. Reverse T3 is kind of a hibernation hormone, in times of stress and chronic illness, it lowers your metabolism. So many people seemingly have normal thyroid levels, but if they have high Reverse T3, they’re actually suffering from hypothyroidism. Holtorf

Because even small increases in reverse T3 can block the active form of the thyroid hormone from having an effect, Holtorf believes that severe hypothyroidism can be present even when standard thyroid tests are normal.

Transport in the Cells and Stress
Holforf also cites culture work indicating that physiological or emotional stress can inhibit the transport of inactive thyroid hormone into the cell. This suggests that T4 levels can be normal or even high when little T4 is making it into the cells. At these times neither T4 nor TSH levels reflect this reduced uptake into the cells.

Besides, inflammation, physiological stress and glucocorticoid drugs such as prednisone also suppress the levels of active thyroid hormone in the tissues and increase levels of reverse T-3.

Testing
Dr Holtorf on Thyroid Testing

“…. extreme caution should be used in relying on TSH or serum thyroid levels to rule out hypothyroidism in… A wide range of conditions including stress, chronic fatigue syndrome, fibromyalgia, inflammation, autoimmune diseases, depression, diabetes, insulin resistance, and systemic illnesses.” Holtorf

More traditional sources of medical information such as WebMD mention only TSH and T4 testing. The Mayo Clinic suggests that most doctors will stop at TSH testing if TSH levels are normal.

Dr. Liptan tests for TSH, T3 and T4. Dr. Holtorf includes these tests as well as a variety of others to assess thyroid functioning.

Dr. Holtorf’s Indications of Low Thyroid Activity

  • TSH – >2 = low tissue thyroid levels (Increased TSH can reflect an attempt by the brain to prod the thyroid gland to produce more thyroid. Holtorf believes TSH levels, however, are poor markers of thyroid problems in ME/CFS and FM.
  • T4 – high – may be associated with low levels of active thyroid (T3) if problems with transport into the cells are present.
  • T3 – generally T3 should be in the upper 25th percentile of normal range.
  • Reverse T3  should be less than 150.
  • Free T3/Reverse T3 – >0.2, when the Free T3 is measured in picograms per milliliter (pg/mL).
  • Sex hormone binding globulin (SHBG) – a marker of thyroid tissue levels in women – if <70, low cellular thyroid levels are likely.
  • Leptin – > 12 may indicate leptin is suppressing TSH production.
  • Iron / Iodine – check for deficiencies (ferritin should be above 70)
  • Basal Metabolic Rate
  • Relaxation Phase of Tendon Reflex – Holtorf believes this test is a more accurate measure of thyroid functioning than serum tests; should be above 110 msec
  • Reverse T3 level above 150 — or a Free T3/Reverse T3 ratio that exceeds 0.2 [when the Free T3 is measured in picograms per milliliter (pg/mL)] — may indicate hypothyroidism.

Treatment
If reverse T3 levels are high, then Holtorf believes that thyroid preparations containing the inactive form of the thyroid hormone (T4) should not be given. Instead, only preparations of the active form of time-released thyroid (T3) should be given.

In general, Dr. Holtorf finds that T4 preparations such as Synthroid and Levoxyl rarely work and Armour thyroid, a pig glandular product, is somewhat better, but not adequate for most patients.

That leaves combinations of T4/T3 or straight T3. Holtorf reports that T3 works the best for many of his patients, but that the main source of T3 – Cytomel, a short acting T3 drug, is a poor choice. Instead he usually recommends compounded timed release T3. He believes, though, that standard blood tests are not a good way to assess T3 dosing regimens.

Other Factors
Reducing Inflammation – Because serum thyroid tests may be inaccurate in inflammatory states which alter the levels of thyroid in the tissues, lowering inflammation and normalizing immune function can help with thyroid problems. Holtorf has found that low dose naltrexone is able to normalize thyroid functioning at times.

Because gluten can be such a potent inducer of inflammation, Dr. Liptan recommends that everyone with low thyroid embark on a gluten free diet for 8 weeks.

Iron Deficiency –  Because iron deficiency impairs thyroid activity, iron levels should be checked. Dr. Liptan wants ferritin levels to be in the 50-100 range; Dr. Holtorf wants them above 70. (Note that both are well above what is often considered “low-normal” (10-50) by many doctors.)

Recovery Story
While thyroid supplementation, when needed, is usually just one part of a treatment plan, occasionally it turns out to be the missing factor in  a person’s search for health. Check out a recovery story on the Health Rising website where this turned out to be true.

Eight years of ME/CFS disappears in two hours

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Could one gene help explain ME/CFS, FM, POTS, IBS, EDS, IBS and others?

Posted on 10/27/2016 by wames

ME/CFS, FM, POTS, IBS, EDS and others often exist in a kind of swarm of interconnected illnesses. All have been maligned at one time or another because of the wide range of symptoms they produce. How could a biological disease cause so many different symptoms?

After this week, perhaps a better question is how could one gene cause them. Check out an astonishing study that pinpointed a gene that may wreak havoc in some people in all these disorders. For those people, help – perhaps even a cure – might not be that far off.

Health rising blog post, by Cort Johnson, 22 October 2016: One gene many disorders: enetic finding could help explain POTS, EDS, IBS, FM, ME/CFS and others.

First, at least for me, there was chronic fatigue syndrome (ME/CFS) and fibromyalgia (FM). Then I learned about irritable bowel syndrome (IBS), then POTS and in the last five years Ehler’s-Danlos (EDS) and Mast Cell Activation Syndrome (MCAS).

The more researchers looked the more they seemed to uncover a large group of syndromes which tended to flock together. Anyone who has ME/CFS or FM now has to consider whether they also might have dysautonomia, IBS, POTS, MCAS and a host of other disorders (interstitial cystitis, migraine, multiple chemical sensitivities, small fiber neuropathy).

Obviously, this suite of disorders is connected somehow, but the question – what is the tie that binds? – has remained. The wide range of symptoms – from flushing to gut problems to chronic pain to orthostatic intolerance to connective tissue problems – had defied understanding – and helped psychologists to get their feet in the door.

Now the NIH of all groups – never really a friend to any of these – may have uncovered a link – that may explain them for some people.

Family Study

Elevated basal serum tryptase identifies a multisystem disorder associated with increased TPSAB1 copy number. © 2016 Nature America, Inc. All rights reserved.

The researchers did what a Simmaron Research Foundation study is currently doing with ME/CFS; they zeroed on a set of families with these problems and studied them intensively. First, increased levels of an immune factor called tryptase which is sometimes associated with mast cell activation showed up. Researchers did not find signs of altered mast cell growth or morphology or increased IgE degranulation or tryptase expression; i.e., they said they found no indication of mastocytosis or mast cell activation disease (MCAS). Despite the high tryptase levels they believed the disease they uncovered was more akin to connective tissue disorders such as Ehlers-Danlos Syndrome (EDS) than MCAS.

Mast cells have often been implicated in certain functional disorders; however, our patients did not have evidence of clonal mast cell disease or evidence of mast cell activation, whereas many did have connective tissue manifestations overlapping with those seen in EDS III. The authors

Of the 96 people from 35 family’s studies, almost 50% met the criteria for IBS, 65% met the criteria for chronic gastroesophageal reflux, 28% had joint hypermobility, 48% had arthritis, 47% had headache, or body pain, a full quarter had congenital skeletal problems, 46% had autonomic issues and 34% had POTS. Other common issues included flushing and pruritus (51%), itching and sleep disruption (39%) and exaggerated reactions to venom.

Fatigue wasn’t measured but since fatigue is common in all these disorders, it was likely quite high. (Many of these individuals probably would have met the criteria for fibromyalgia or chronic fatigue syndrome (ME/CFS).)

Extra Sequences Spell Trouble

The group’s genetic secrets were not yielded easily. First exome and genome sequencing found no common gene variants but a linkage analysis identified a single “peak” on one chromosome – a section of the chromosome containing the 4 genes responsible for producing tryptase.

Further testing found that individuals containing multiple copies of a tryptase encoding sequence were highly, highly, (highly) likely (p<.000001) to have high tryptase levels. This is the kind of probability that’s probably considered a slam dunk in genetics; everyone who carried multiple copies of this tryptase-producing sequence had high tryptase levels and a wide range of sometimes bizarre symptoms. Plus, the more copies of the copies of the sequence an individual had, the worse they were off symptomatically. None of the family members without these sequences had any symptoms.

Tryptase is the most common enzyme found in mast cells and is often used as a marker for mast cell activation. Interestingly, none of the individuals had evidence of mast cell activation syndrome. If tryptase was causing their symptoms, it was doing so in a different way than is ordinarily associated with MCAS. (MCAS is apparently called a syndrome for a reason.).

After identifying a genetic anomaly associated with high tryptase levels in families it was time to see if it showed up in other groups. A retrospective analysis of people who’d had genomic analyses done for other disorders indicated that all the individuals with increased serum tryptase levels had multiple copies of the tryptase encoding sequence.

Next, the researchers turned to a healthy control group, and again found that all the individuals with increased tryptase levels had multiple copies of the tryptase encoding gene. (Three of the “healthy controls” turned out to have similar symptoms as the original cohort; the rest were either normal or had minor problems).

New Disease

It’s rare that genetic effects are so clear. In fact, the genetic effects were so clear that the condition is now called hereditary-a tryptasemia. This disease is “exclusively caused” by increased copy numbers of the tryptase-producing sequence.

Exactly how elevated tryptase levels are causing pain and autonomic nervous symptoms is not clear but may involve “protease-activated 2 receptor pathways” (if that’s any help (lol). The study highlights, though, that it’s not necessary to understand a disease to find a treatment for it. Knowing that elevated tryptase levels cause pain, connective tissue problems and orthostatic intolerance, even if we don’t know how, can allow researchers to develop anti-tryptase blockers that could conceivably stop these symptoms in their tracks.

Tryptase can be tested for, and in fact, around five percent of the population, or over 15 million people in the U.S. have high tryptase levels. Most of them are probably asymptomatic but those who are ill could benefit greatly from this finding. It’s very rare to find such a clear genetic link and such a clear treatment pathway.

NIH Admits It Was Not All in Their Head After All

The NIH itself noted that this study should give hope to people with complex multi-system disorders who, too often, have ended up being told their unusual symptoms must be “all in their head”. It was obviously high on this work. It’s not often that a clear cause of an illness – let alone a spectrum of illnesses – may have been found. In fact, the NIH was so excited that it produced a video about the finding, and sent out a press release featuring none

Chronic fatigue syndrome’s relationship with NIAID and Fauci is a complex one; NIAID is the only Institute to ever fund ME/CFS research centers, but its abandonment of ME/CFS in the early 2000’s ushered in 15 years of declining funding. That obviously didn’t endear anyone to Fauci or NIAID, but now NIAID and NINDS do appear to be doing the lion’s share of the work in the ME/CFS Working Group at the NIH.

Plus, seeing NIAID crow over its genetic finding for a complex multi-symptom condition is a good thing. One of the reasons NIAID abandoned ME/CFS was because it was a complex multi-symptom, multi-systemic condition. The multiple system issue gave NIAID an out; because ME/CFS clearly wasn’t simply an immune disease it decided it was no longer responsible for it. Fifteen years later, ironically, as NIAID begins to welcome ME/CFS back, it has found an immune factor that causes multiple symptoms and produces a multiple system disease.

Next up for this group: developing a diagnostic test to detect alpha tryptase gene copies and finding ways to block tryptase production. For people with extra copies of this gene and who are ill the news is good indeed. Few diseases, after all, can be traced to one factor. Pharmaceutical companies are surely combing their drug databases for drugs with tryptase-inhibiting pathways.

Thanks to The SolveME/CFS Initiative for highlighting this study on their website. Without their doing that, I would have missed it entirely.

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Severe ME in Australia: suffering ignored and denied help

Posted on 10/26/2016 by wames

ME Australia blog post, by Sasha Nimmo, 13 September 2016: Severe ME: Suffering ignored and denied help

Myalgic Encephalomyelitis is estimated to affect between 0.4% and 1% of the population, according to the International Consensus Criteria primer for medical practitioners, endorsed by Australian patient organisations. In Australia, that is between 96,700 and 241,800 people (ABS population figures). Of those, 25% are so severely affected that they cannot leave their homes or even their bed.

Between 24,000 – 60,000 Australians have severe ME.

Speaking to patients around Australia, a major hurdle is simply finding a GP who can visit them at home for basic medical care.

“The most difficult thing for me when I was completely bedbound was having no medical professional who could come and see me as I was too ill to travel to the doctor. Advocating for myself to receive basic medical care was exhausting and stressful and very taxing on my health,” patient in Victoria.

“What frustrates me most is how many doctors just do not understand how much we deteriorate after each visit, even if they say they understand severe ME. If they did they would do home visits,” patient in South Australia.

“My GP said he’d be able to visit me at home as he could see I was deteriorating and getting to his practice was difficult. But when I rang to book a home appointment, he wouldn’t see me at home and I was left without any medical care and without any help from the practice to find a new GP.”

“The pain medication I was on ran out, leaving me in severe pain and unable to walk the couple of steps to the kitchen to get food and water,” patient in the ACT.

“I cannot see a doctor at the time I’m having symptoms because I’m too unwell to get out of the bed and get ready for the appointment. Of course, I’m looked at with suspicious eyes when my symptoms ease and I can get in for an appointment.

“I don’t have medical degree or training so that I can explain my suffering the way they can get it…” patient in Queensland.

All of these patients would only speak on the condition of anonymity.

“I wish to remain anonymous as I don’t want to be mistreated by healthcare practices and/or government agencies for advocating for ME anymore,” patient in Queensland.

For those who can find doctors, finding ones who understand the impact is hard.

“Educating doctors about ME, and particularly severe ME is crucial to patients being able to access appropriate care, which is sensitive to the unique disabilities severe ME brings,” patient in Victoria.

“Canberra is the national capital but there are no specialists who know about ME here,” patient in the ACT.

“If the hospital and Disability SA had accepted how much I needed an electric wheelchair ages ago when I tried to apply repeatedly, both through hospital OT and Disability advocate from MALSSA, then I would not have deteriorated so far. Sad really, probably common everywhere. People overseas I think have the impression Australia, especially Adelaide, has all these researchers. That doesn’t matter if none understand severe ME and can visit,” patient in South Australia.

“I’m scared, to be honest,  as no one really seems to understand just how really dangerous severe ME is,” South Australian patient.

“All specialists I have been referred to (psychiatrists, cardiologists, neurologists, rheumatologists) either had the wrong idea or had no idea about ME nor CFS and they are supposed to deliver the best care for the patients,” South Australian patient.

“Sadly, the NCNED Clinic has closed its doors due to overwhelming demand. We need funds to train more clinicians and establish facilities, hopefully one in each state/territory.

“Very rare GP specialists are very expensive, too far to travel, and possibly their diagnosis and treatment protocol are not the same,” Queensland patient.

What is needed: education, in-home support and policies for hospitalisation

“We need Centre for Excellence in ME in Australia, where medical and healthcare service providers can rely on facts and case studies about ME. I hope NCNED will take up on this role.” Queensland patient.

Patients say they need:

  • Standardised, up-to-date diagnostic criteria
  • Safe and effective treatment/management guide
  • Designated ME specialists in Australia
  • In home care for cooking, cleaning, community care of patients with staff who are educated in ME sensitivities e.g. noise, light, chemical sensitivities (some patients  have been denied services as they asked for no perfumes/deodorants and the care service refused to comply under ‘occupational health and safety policies’
  • Nursing assistance for administering medications/bathing etc.
  • Regular in-home treatments which are affordable e.g. saline infusions for POTS
  • Case management services to coordinate all of the severe patients’ needs so they (or their carers) don’t have to organise all of this when they are cognitively compromised
  • 24 hour care for the most severe patients
  • Respite care for carers of severe patients
  • Hospitalisations where patients are located in suitable rooms, for example on the infectious disease wards where they are away from other patients, noise, light and the risk of infection is kept low
  • In-hospital care for severe patients that does not involve contempt from treating doctors and numerous visits from psychiatrists
  • Provide the right and critical information about severe ME for DSP/NDIS approval
  • Financial support for mobility aids (items such as slings for beds, railing, noise cancelling headphones, heated rugs, cooling vests, mattresses designed for bedbound people to prevent pain/bedsores, walkers, reclining electric wheelchairs) climate control at home, noise control at home and for off label prescriptions, which are still very expensive for people with financial challenges, which most severe ME patients have.
  • Attitudes impacting health
  • Misinformation and ignorance about severe ME make it much more difficult to access healthcare, services, insurance payments and daily living support.

“Having to negotiate my way through application for disability payments and also then temporary and permanent disability insurance applications was horrendous and impacted my health,” Victorian patient.

“From the treatment I received and experienced, severe ME doesn’t exist in Australia. They have no idea about our suffering and many are seriously and dangerously confused it with depression or other mental illnesses. And they don’t listen to me when I explain. They deny my experience and suffering as if I was making things up. But, I think this is the general attitude towards chronic illnesses in society; if you don’t get better, die quietly.”

Outdated, harmful government guidelines

Nationally, in the 1990s, the federal government commissioned guidelines. In 2002 the Australian chronic fatigue syndrome clinical guidelines were published and adopted by the the National Health and Medical Research Council. They were heavily criticised for having a bias towards the psychological, dismissing biological evidence and omitting severely affected patients.

At the moment, Australia has no official government clinical guidelines as they ‘expire’ after 10 years and the government has not replaced them.

I asked state government health ministers questions about caring for people with severe ME. WA and Tasmania were the only states to respond. Their answers show they are using potentially harmful treatments and have no clinical criteria for diagnosis. Instead, they consult papers which refer to ‘contested illnesses’, despite the fact that Myalgic Encephalomyelitis has been recognised by the World Health Organisation since 1969. The guidelines on the WA health website recommend psychological treatments for children, which have no basis in science.

Read more about care for people with ME in regions of Australia

 

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Welsh Ambulance Trust booklet & app to aid communicating health needs

Posted on 10/26/2016 by wames

In 2013 The Welsh Ambulance Trust developed a bilingual Pre Hospital Communication Guide in the form of a small booklet.

They have now developed an App version of the guide, which is available for everyone to use, you can download it to your phone for free!

pre-_hospital_communication_guide_coverThe App is a tool to help para medics and other healthcare staff to communicate with those who have additional communication needs including:

  • People who are Deaf or hard of hearing
  • People for whom English is not their first language
  • People with learning disabilities
  • People whose illness or injury affects their communication

A person may use a mixture of speech, gesture and pictures to communicate. The App uses images and a small amount of text to help you find out important information about someone or what has happened if they have had an accident.

The App can be used to identify if the person uses a specific communication method or the language they speak. Anyone can download and use the App for free! Its available on iOS, Android and Blackberry.

  • iOS – search for ‘PreHospApp’
  • Blackberry – search for ‘pre hospital app’
  • Android – search for ‘Pre-Hospital Communication App’
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Dr Bested’s experience of treating gut symptoms in ME/CFS

Posted on 10/26/2016 by wames

Altered Gut Microbiome in ME/CFS, by Alison C Bested, October 2016

In 2007 as a doctor specialized in treating patients with Myalgic Encephalomyelitis (ME)/
Chronic Fatigue Syndrome (CFS), I was curious to see if there was a relationship of the patients’ irritable bowel symptoms and their degree of fatigue and pain. Clinically I had noticed that when parasites were found in a patient’s stool and treated, that afterwards, often in addition their fatigue going up a notch, sometimes their headache pain and general pain symptoms improved. I was intrigued.

Dr. Alan Logan was able to secure private funding to look at a small group of my patients with ME/CFS and irritable bowel symptoms. We had 20 patients as controls and 20 patients that we treated with billions of probiotic bacteria: Lactobacillus casei strain Shirota for two months. We were hoping to see improvements in fatigue and pain in the
patients.

There was a rise in Lactobacillus levels as expected with the supplementation given to the patients. We were surprised to see an increase in the Bifidobacterium levels. We do not
see improvement in their fatigue or pain levels. With experience, looking back, a two month protocol for supplementation with a probiotic was far too short a time.

What did surprise us was that the patients who were treated with a probiotic had significant improvement in their anxiety scores. It was possible that the decreased anxiety was a direct result of improved bowel function. We postulated that perhaps this was an example of enteric neuroscience with the bowel communicating directly with the brain through the vagal nerve.

Perhaps, we wondered, if by changing the microbiota in the bowel, it helped to restore normal intestinal health, decrease intestinal permeability, reduce inflammation and cytokines and indirectly reduce anxiety. We knew that there was lots of room for further studies in this area.

A Venket Rao, Alison Bested, Tracey Beaulne, Martin Katzman, Christina Lorio, John Berardi,  Alan Logan. A randomized, double-blind, placebo-controlled pilot study of a probiotic in  emotional symptoms of chronic fatigue syndrome. Gut Pathogens, 2009, 1:6.     DOI: 10.1186/1757-4749-1-6

I was thrilled with this new article about gastrointestinal disturbances or irritable bowel
syndrome and altered microbiota in patients with ME/CFS. Gastrointestinal disturbances are present in many patients with ME/CFS. According to the article by Giloteaux et al. dysbiosis or altered gut microbiome (types and numbers of bacteria present in the gut) is present in patients with ME/CFS. Dysbiosis of the gut microflora may contribute to ongoing symptoms of inflammation in patients with ME/CFS.

Potentially, in the future, this could lead to better investigation and treatment for symptoms of dysbiosis or IBS in patients with ME/CFS.

Ludovic Giloteaux, Julia K. Goodrich, William A. Walters, Susan M. Levine, Ruth E. Ley and Maureen R. Hanson. Reduced diversity and altered composition of the gut microbiome in individuals with myalgic encephalomyelitis/chronic fatigue syndrome. Microbiome (2016) 4:30 DOI 10.1186/s40168-016-0171-4

Alison C. Bested MD FRCPC
Hematological Pathologist
Clinical Associate Professor
Faculty of Medicine
University of British Columbia

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NICE takes a dim view of foreign work on ME/CFS

Posted on 10/25/2016 by wames

ME Association news blog post, 24 October 2016: NICE takes a dim view of foreign work on ME/CFS – Robin Ellis Freedom of Information request

The main supplier of England’s drugs and treatment guidelines, the National Institute for Health and Clinical Excellence (NICE), tends not to take foreign research into account when it produces work on ME/CFS.

In internal correspondence released this month under the Freedom of Information Act (FoI), the agency admitted that it has not yet considered the results of important US studies when deciding what is best for British M.E. patients.

NICE are holding back the review of their guidelines on ME/CFS until some time in 2017, saying the evidence to justify earlier reconsideration isn’t strong enough.

“It is not really for the NHS to respond to a report commissioned in another country and not yet examined by its commissioner”, the agency’s director for clinical practice wrote to colleagues as they were assembling their reply to a FoI request from Robin Ellis.

Professor Mark Baker wrote: “We would take seriously the views of the relevant esteemed medical associations in the UK, principally the RCP (Royal College of Physicians) and the RCPsych,(Royal College of Psychiatrists) when looking at reviewing this guidance.

“I am not aware of any reason to do anything before then unless some major new evidence on treatment emerges, and we know that no major studies are in progress”.

The applicant, Mr Ellis, filed three FoI requests earlier this year seeking the release of information held by NICE about the PACE Trial.

This time he wanted to know if NICE allowed its thinking on M.E. to be influenced by overseas research using easily observable symptoms – like testing for post-exertional fatigue using the 48-hour exercise test – the 2015 US Institute of Medicine report on the “devastating severity” of M.E – and the National Institutes of Health report which “retired” the Oxford criteria for CFS believing it to be harmful to people with the illness.

Mr Ellis also pointed to another US agency that had recently determined that CBT and GET were ineffective treatments given the poor outcomes reported all round – including in the PACE Trial.

Mr Ellis’s latest FoI request was formally entitled: Unique characteristics of pw ME/CFS as defined by the CCC and ICC and exercise physiologist experts eg Workwell Foundation, Snell, VanNess, Stevens, Klimas. He wanted to see what papers were held by NICE on these matters.

In the papers released by NICE, there is an intervention from the Countess of Mar, who chairs the Forward ME Group of charities.

The Countess wrote to NICE:

“I have to assume that you must agree that patients with ME/CFS are very much the same wherever they are in the world, and that there will be no difference between UK and US patients.

“I also assume that you must agree that very many more resources have been applied to this issue in the US than in the UK. Professor Baker reiterated his belief that there is no evidence that GET makes some patients worse.

“Absence of evidence is no evidence of absence, and there is plenty of evidence from the two major charities in the UK – Action for ME and the ME Association – which have both done major surveys of their members…”

Professor Baker replied that NICE will conduct a critique of the American work to consider “whether it adds anything to what we already know”.

He added: “You will be aware that the British academic establishment holds an entirely different view, though not necessarily any better informed.”

On October 19, Mr Ellis formally requested an internal review of NICE’s handling of his FoI request. “I asked for information around the decision NOT to update the NICE Guidelines, none was provided.”

The full exchange of correspondence can be read here: www.whatdotheyknow.com/request/unique_characeristics_of_pw_mecf#incoming-883778

The papers released can be read here:
www.whatdotheyknow.com/request/357691/response/883778/attach/2/FOI%20EH73066%20Redacted%20documents%20for%20release.pdf

The papers have been slightly redacted by NICE. The agency wrote that it did not want to show details of junior staff involved in the correspondence nor a third party who was consulted as part of the exercise.

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The ‘extreme’ side-effects of antidepressants

Posted on 10/24/2016 by wames

BBC news article, By Lesley Ashmall (BBC Victoria Derbyshire programme), 19 October 2016: The ‘extreme’ side-effects of antidepressants

Claire Hanley says she tried to take her own life twice after taking antidepressants
People who say their lives have been ruined by commonly prescribed antidepressants, known as SSRIs, are taking their case to Parliament on Wednesday. Some users say the tablets have made them suicidal.

“I was getting seizure-like symptoms, where my muscles were jolting around of their own accord,” Claire Hanley tells the BBC’s Victoria Derbyshire programme, explaining the effects she says antidepressants had on her body.

She had begun taking them while caring for her seriously ill mother and studying for her final exams at Cambridge University, but suffered severe side-effects after her GP prescribed a stronger dose of tablet.

“Within two weeks I’d tried to take my own life twice,” she says.

“I felt disorientated and sick and had digestive problems and infections, it was really extreme. I don’t even know how to begin. All I can remember is being on the bedroom floor in a kind of semi-conscious state having seizure after massive seizure.”

It has been 20 years since she first took the tablets, but Ms Hanley says she still suffers from the consequences of a cocktail of drugs doctors have prescribed to try to treat the side-effects of the original antidepressants.

She says she has constant muscle ache and fatigue, and spends most days in bed.

It is thought about one in 100 people experiences severe side-effects as a result of taking SSRIs.

The drugs are designed to increase serotonin levels in the brain, which can improve symptoms of depression.

Some experts, however, now believe many more people than was previously thought are suffering negative consequences.

Prof David Healy, from the psychiatric unit at Bangor University, believes the drugs make “one in four people become more anxious, rather than less”.

“Some people become very agitated and some go on from that to become suicidal,” he says.

“The drugs can become the problem that they’re then used to treat.”

The drugs companies have declined to comment, but Dr Sarah Jarvis, a GP in West London, is keen to point out that doctors do not prescribe antidepressants lightly.

She also stresses the vital role they can play in helping people with depression – saying, if untreated, “moderate depression and severe depression wreck lives, and very regularly cost lives”.

Dr Jarvis adds that for most people, the drugs are effective.

“I think for people with severe depression, they may need to try two or three [different types of antidepressant] before they find one that does work for them, but for most people we can find a medicine which will help them and for whom the benefits will outweigh the risks,” she says.

Antidepressants

  • Antidepressants cost the NHS £780,000 per day
  • Between 2005 and 2012, there was a 54% increase in the number of children prescribed antidepressants in the UK
  • Common side-effects include dizziness, headaches and feeling sick. These generally improve with time
  • Antidepressants can cause serotonin syndrome, which – while uncommon – can lead to seizures, an irregular heartbeat and unconsciousness in the most severe cases
  • In rare instances, some people experience suicidal thoughts and a desire to self-harm when they first take antidepressants. People under the age of 25 seem particularly at risk

Sources: Health and Social Care Information Centre, World Health Organization, NHS Choices

But according to some experts, such as Prof David Healy, the side-effects of antidepressants are not just felt when someone is taking them, but also when they try to reduce the dose or come off the tablets altogether.

“There’s a large number of people – and it seems to be more women than men – who have great difficulties trying to reduce the dose,” he says.

“And if they halt the treatment, they can become terribly agitated, they can become suicidal.”

“When you look at the clinical trials that have been done, the taper phase – the point where the person is trying to come off the drug – is the riskiest period.

“That’s the point where the person is most likely to commit suicide, or the most likely to do terrible things.”

Gemma – not her real name – says her withdrawal symptoms were so bad that she is now back on the tablets.

“I was told I could come off [antidepressants] no problem,” she says.

“But I was in a mess basically. I reached a point where I could barely function. I was incredibly anxious – I was highly anxious all the time, so I was very panicky, very agitated. I could barely sleep.”

Gemma had followed medical advice and come off the tablets slowly, but she suffered severe consequences nevertheless.

She says: “I was petrified. I was crying my eyes out. I didn’t know what on Earth was happening to me. I guessed it could be the medication, but I thought I had some kind of terminal illness. I just didn’t know what was happening.”

Gemma eventually decided to go back on the drugs, and the withdrawal symptoms quickly disappeared.

“I was shocked. All the migraines, the muscle aches – everything – just stopped instantly,” she says.

Many people find the effects manageable, but others – some of whom got in contact with us – say they have been severely affected. Here are a few.

Brigitte, from Exeter, said: “I couldn’t walk and was experiencing the most horrendous sensory sensations. My muscles were burning, I had facial twitches, terrible night sweats and numbness on my forehead.”

Pauline, from Hertfordshire, said: “I look and feel like a drug addict, I can’t focus my eyes. My eyes are like slits even if I’ve not been crying. I cannot sleep at all, and because it seems my body realises it is not getting the drug, every day is living hell.”

Christine said: “The fatigue is so bad that I have to go to bed in the afternoons and can do very little. I feel dizzy, nauseous, have blurred vision and a headache at the back of my head and on top.”

But others believe people who need medication should not be put off by those who have experienced severe symptoms.

Mehran, from south-east London, said: “I have been on and off antidepressants for over a decade. It is only natural to have withdrawal effects as the brain becomes comfortable with a certain level of chemicals. Usually, those people, like myself, who withdrew abruptly actually still needed the medication. I worry [that the stories of those with severe symptoms] put fear into the people that need medication.”

Mark, from London, said: “[When I started taking antidepressants] I did feel more, rather than less, anxious for the first two to three weeks – which was accompanied by muscle twitches, nausea and a general feeling of dissociation. But then I felt fine, I could function again and I got better. I believe SSRIs provided a crutch to support me through a difficult time, while I worked on finding a longer-term solution using psychotherapy.” Mark does not recall experiencing any withdrawal symptoms.

For Dr Jarvis, however, while some individuals may suffer prolonged side-effects from antidepressants – lasting months or, on occasion, years – she would be surprised if all of the reported effects related to the tablets.

“What we need to bear in mind is that some patients who have taken these have been very vulnerable, they’ve been very anxious and it can be very difficult to tell what is anxiety and what is the tablets,” she says.

But for Ms Hanley, the dangers must be taken more seriously by medical professionals.

“It may be a minority of people who have these extreme reactions, but they exist,” she says.

“If you look at the leaflets in the packets, and it says one in 100 will have this symptom, they’ve got to realise that that one person could be their patient. It does happen.”

NB In the ME Association survey of patients symptoms in 2010:

  • 46% found depression a major problem
  • 40% found depression a minor problem

Many were taking anti depressants.

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