Saturday, January 5, 2008

A doctor on doctors as patients

http://www.sacbee.com/107/story/608309.html

Inside Medicine: Truthful discussions are key to effective treatment
By Dr. Michael Wilkes
 
Over the past 30 years, a great deal has changed in the doctor-patient relationship. However, there remains a social dance that regularly occurs between the doctor and patient. At its core, the dance is driven by a sick person feeling dependent, vulnerable and wanting to be liked by the doctor. The more worried a patient is about his or her health, the more exaggerated the dance – often to the detriment of the patient's health.
A report in the British Medical Journal describes the process patients go through to avoid being perceived as aggressive or pushy because they don't want to upset the doctor. When the doctor asks us how we're doing, we tend to be overly cheery and positive, based on a social norm of not wanting to upset or disappoint someone in an important position. One sick patient explained that the fewer questions he asked, the happier the doctor seemed, the less behind the doctor got in his schedule and the more the doctor seemed to like him.
A secret is that doctors also need to be liked. Believe it or not, we are human and need positive reinforcement. In all fairness, I would be remiss to not point out that our employers are now also interested in measuring how much our patients like us (or how "satisfied" they are with us).
In his new book, "When Doctors Become Patients," Robert Klitzman, a psychiatrist, describes his surprise at learning that when doctors become patients, they also assume this role of not wanting to upset or disappoint their doctor. The doctors-as-patients also avoided asking tough questions and never confronted their physicians directly out of fear of offending or upsetting them.
A patient of mine says she feels that if she brings the doctor a little treat at each visit, the doctor will be more likely to remember her. She doesn't want to be just another patient – she wants to be special in case there is a time when she really needs medical attention. The doctor perceives these favors as signs of admiration – not a bribe or an attempt to curry favor – and such gifts are usually warmly received.
However, if the result of all this verbal and nonverbal social interaction is that the patient leaves my office without asking me important questions, or failing to share additional symptoms, we both lose.
Admittedly, the face time between doctors and patients is at an all-time low. Doctors are rewarded for doing things to people rather than talking with them. Given a 10-minute appointment, there is no way we can squeeze in everything that needs to be done in one visit.
But the agenda for each appointment needs to be a joint decision, and if the patient is timid or unwilling to be honest, no one benefits.
I know it is common for patients to tell me what they think I want to hear, not realizing that what I really want and need to hear is how they actually feel. In this crazy modern world of ours, we have far too few opportunities to tell people what's really bothering us. Our families often live in distant locations, our friends have their own problems, and we don't want to worry our spouses and children. So, as my kids say, we suck it up.
But the doctor is the one person with whom you should be able to talk. Tell your doctor that you're feeling low, that you're not getting along with your spouse, that you were fired last week. Do not be embarrassed to pull out your list of concerns.
We can't always solve the problem, but we can listen, and perhaps you'd be surprised how much the doctor can help.

About the writer:
Michael Wilkes, M.D., is a professor of medicine at the University of California, Davis. Identifying characteristics of patients mentioned in his column are changed to protect their confidentiality. Reach him at drwilkes@sacbee.com
 
* * *
This is my experience exactly.  As soon as I ask questions or, worse yet, get assertive and start putting my health ahead of the doctor's ego, you can see the doctor shut down on me.  He doesn't like me because I've become one of those difficult patients.
 
They like me when I'm a good little patient who does what I'm told without questioning, but as soon as I say "I will not take these pills, I want something else", the doctor gets annoyed with me.  Even if I have a very good reason, like I tried them already with no results, or I've been told not to take anything in that family ever again due to an adverse reaction (one anti-depressant put me in a near-coma), it comes down to a stubborn match between the doctor stubbornlyclinging to his original prescription and me just as stubbornly insisting that I want the right pills for me, not the right pills for someone else.
 
Well, get this doctors: I do not give a damn about your ego.  The only thing that matters to me is my health.  Coddling your ego is not going to pay my bills the rest of my life.
 
Your professional responsibility is to be concerned primarily with my health.  If you can't deal with an educated, informed patient, maybe you should become a veterinarian ... horses don't ask questions.

Power-tripping at patients' expense

A woman who has been ill with CFS for years but without a diagnosis, even after she is diagnosed, is very vulnerable and this attracts doctors who need to control and blame the patient, who need this type of power for their egos.

Greenhalgh, S (2001). Under the medical gaze: facts and fictions of chronic pain. Berkeley: University of California Press.

http://www.amazon.com/Under_Medical_Gaze_Fictions_Chronic/dp/0756783488/ref=sr_1_2?ie=UTF8&s=books&qid=1199548364&sr=1_2

In this book, Dr. Greenhalgh, writing as a patient, discusses at length her treatment by a doctor whose treatments made her worse, eventually endangering her career. Publishers Weekly says "The author speculates at length about the role her female identity played in her willingness to accept the forceful and ultimately wrong advice of a male physician".

Library Journal observes that the book "convincingly exposes the limitations of the medical profession's "scientific" approach to illness. ... while physicians do not intend to deceive patients or cause harm, their use of the language and trappings of science can cause them and their patients to be blind to the possibility of personal biases and medical errors. She also draws on feminist psychology, theorizing that male physicians often dismiss the concerns of their female patients and that female patients do not advocate for themselves as they should, reverting instead to the societal expectation of trying to please a man by being "a good patient.""

The good news is Dr. Greenhalgh is now doing well under the care of a female physician.

That male physicians dismiss female patients is more than just theory; it’s been proven. One of the early CFS experts got the virologist who had identified AIDS to look at some of her CFS patients, in hopes of confirming her diagnosis that this was a virus. She sent a series of extremely ill women, all of whom returned with an erroneous psych diagnosis. Then she sent a man, whose symptoms were nowhere near as bad as those of the women she’d sent previously, and he was returned to her with the diagnosis of "a virus we don’t have a test for yet". It was obvious that the virologist had the prejudice that all female patients are mentally unstable but men are really sick.

He’s not alone: there is plenty of anecdotal evidence of female patients being called lazy, hysterical, whiner, hypochondriac ... and then a male patient with the same symptoms comes in and is taken seriously.

Almost every CFS patient can tell you horror stories about doctors who figure out ways to blame the patient either for the initial illness or for not recovering quickly enough (I was told that I "didn’t want to get well because then you’ll have to go back to work" when, in fact, the problem was that I was being given medication that researchers had proven totally useless against CFS – I started to recover when I finally got the right medication).

When I said that I did not have a prior PCP because I had not been sick enough to need a doctor in almost 10 years, I was accused of "not wanting me to get the records and find out you’re a hypochondriac". Unfortunately, as every debater knows, you can’t prove a negative; there was no way for me to prove that the only doctors I’d seen in years were the gynecologist and Urgent Care; he wanted to believe that I was a hypochondriac who developed these symptoms only after reading a magazine article and nothing would change his mind unless I produced non-existent records from my non-existent prior PCP. (In fact, it was my husband who read the article, recognized what he had been seeing for months, and dragged me to the ER in hopes that the article about Chronic Epstein Barr would result in a quick diagnosis and effective treatment; I hadn’t read the article myself because I was too sick to read.) Don’t confuse him with facts, his mind was already made up that all women are hypochondriacs and all women will fake illness to manipulate their husbands to allow them to quit work. His most telling quote "I’m not signing disability papers so you can get paid to sit home and watch soap operas", never mind that I hate soap operas, or that I was the primary breadwinner and knew that disability wasn’t enough to pay the bills. I wanted to get well and go back to supporting my family, but his prejudices about women blinded him to that.

The medical establishment has come up with many ways to blame the patient for CFS. Hillary Johnson observed "Many doctors have tried to find a causal link between CFS and personality traits that, in the case of any other illness, would be considered exemplary: blaming patients for having had a strong work ethic (calling them "overachievers") or exercising regularly (being "too driven")." One of the early theories about CFS – still not entirely abandoned – is that women bring it on themselves by trying to "have it all"; that it’s not really a virus, it’s just a woman who’s burned out from juggling a executive-level job, husband, children, housework, and that the problem will go away if she drops the stressful job. That young children who are only juggling play time, bath time and nap time also get CFS is swept under the carpet by that theory; "inconvenient truth" often is.

I am not the only female patient who has had male doctors say things to her face like "all women want to be housewives" or "you want me to help you get lifetime alimony so you don’t have to work". In one sense, this is understandable, since many women who don’t want to work target highly-paid men, like doctors, to become their husbands, so it may be the doctor’s personal experience that all the women who’ve chased him wanted to be a housewife and demanded massive alimony in the divorce, from which they extrapolate that this is the goal of every woman. But they would only have to look around and see their female colleagues who aren’t housewives, to see that there are some women who are more interested in a career than in scrubbing floors. But that would require examining their pre-conceptions, and it’s much easier to stubbornly cling to ingrained ideas.

My college had a large percentage of pre-med students, so I’ve observed the breed first-hand, at great length. Some of them wanted to be doctors only because of the money (such as one who shrugged "if I don’t get into med school, I’ll go to law school instead, the money is just as good"). Some wanted to be doctors for the power trip of being able to tell people what to do (I saw that one close-up in a boyfriend). Others, predominantly women, didn’t care about the money, they wanted to help people. The problem is, the ones who are only in it for the money don’t have a giant $ tattooed on their heads, and the control freaks don’t have a threatening fist tattooed on them, either.

It’s not always instantly obvious that you’re dealing with a doctor who needs to control women and boost his ego. I had one who seemed quite sincere in saying "I want to help you"; it was only after I "refused to get better" that his true naturestartedto come out: belittling me, verbally abusing me, blaming me for the illness, accusing me of anything he could think of to take the blame off himself for his failure to cure me. When I returned with the bad news that the most recent pill had not helped at all, he reacted as if this were a personal affront to him, like I intentionally didn’t get well in order to make him look bad. But even after that he still wouldn’t prescribe what I told him the experts recommended, nor refer me to a specialist. It became clear that his ego was at stake, and taking advice from someone else was not what he wanted to do.

A friend who, unbeknownst to me, was seeing the same doctor for a different condition, later reported the same treatment. Comparing notes, he accused her, too, in almost the same words, of wanting alimony, gave her the same verbal abuse for "refusing to get better because she didn’t want to work", and refused to listen to other medical professionals who advised that if she continued to work her condition would get worse and she would eventually lose the use of her hands. It never crossed his mind that she’s the owner of a successful million-dollar business, all he saw was a divorcee who wanted his help in fleecing her husband for lifetime alimony so she wouldn’t have to work. His ego got in the way of helping her, too.

Again, prejudice that women don’t want to work got in the way of his understanding that she and I were self-supporting professionals who didn’t want permanent disability, we desperately wanted and needed to get well and go back to work, but needed temporary disability to tide us over while we recuperated from being too sick to work.

Fortunately for her, the company changed medical insurance and she went to a new doctor, who immediately put her on temporary disability until she recovered. Unfortunately for me, by the time I finally found a doctor willing to give me the right pills, it was too late and I’ll never fully recover.

As far as the notion that women need to advocate for themselves more strongly, one of the original Incline Village patients, a man, has told me that some of the doctors who at first dismissed the disease later changed their minds (usually as a result of seeing someone they knew personally come down with it, someone they knew wasn’t given to faking, hysteria or hypochondria, as they’d accused previous patients). He, too, was told that the reason the doctors didn’t believe him (and other patients) was that they "didn’t advocate strongly enough". The question arises, how much more strongly could he have advocated? He did everything but slap the doctor upside the head.

Similarly, I know what symptoms differentiate CFS from depression and make sure to mention those whenever I see a new doctor; those symptoms don’t appear in my medical records, so apparently I need to take a deep breath and bellow those to make sure they are loud enough to get past the doctor’s selective deafness.

I was accompanied to my first appointment by my husband, who did most of the talking because I was too sick. His first-hand observations were disregarded, and the doctor eventually talked him around to believing that he didn’t see what he thought he saw, because there was nothing there to see. At a later appointment, I reported that "My boss says to tell you..." and my boss’s observations were also disregarded. The doctor wanted to see "nothing wrong" and didn’t want to believe that anyone else saw objective symptoms like fever/vomiting/diarrhea/fainting/weakness.

He eventually refused to see me again until I had a psych evaluation, but when I returned with the information that a professor of counseling had said my symptoms were those of physical illness, not depression (I lacked the emotional components required for that diagnosis), the doctor refused to accept that evaluation; it wasn’t what he wanted to hear. Thirteen years later, I ran into another doctor who was so sure that I was depressed that even two psych evaluations saying that I lacked the emotional components required for depression were not enough to convince him to shelve his ego and take the advice of experts. Both of them had to control the patient to the point of inflicting an erroneous, stigmatizing diagnosis; I was punished for daring to say "you’re wrong" and finding experts who backed me up that my problem was physical, not psychological.

One even punished me for my chutzpah by referring me to a doctor who treated nothing but AIDS. That doctor’s office called it "a sick joke", pointing out that Dr. Truax’s name in my medical records could mean nothing else, and the mere mention of his name in my records would stigmatize me for life because every future doctor would assume either that I had AIDS or that I was an irresponsible person who had engaged in enough drugs/unsafe sex to have concerns about AIDS. (Apparently, Dr. Truax had some meaningful dialoguewith thequack about ethics, because the copy of the records I got later didn’t have Truax’s name in them.)

I pay my bills by proofreading court transcripts, and have read several cases where the experts have testified that it’s abusive for the defendant to tell his victim to ignore her own feelings and observations and believe only what he tells her. Why is it not equally criminal for a doctor to abuse patients by telling them to ignore her own feelings and observations and believe him that she’s not really sick, doesn’t really have the objective symptoms she and her family/co-workers see?  "You'll feel better if you just stop thinking you're sick and go back to work" isn't helpful.

For that matter, why are doctors so adamant that no one be allowed to practice medicine without a license when so many of them are practicing psychiatry without a license? Only a licensed psych professional should be allowed to put diagnoses like depression and anxiety into a medical chart, to prevent these amateur psychologists from concluding that fatigue automatically means depression, and unwillingness to do what’s been proven to make your symptoms worse means anxiety, even without the emotional components required for those diagnoses.

But, as Dr. Bell observes, writing "depression" in the chart relieves the doctor of the obligation to do any further investigation. It may not help the patient to have an erroneous diagnosis, but it helps the doctor to wash his hands of a troublesome patient.

Dr. Bruno comments "In this new millennium, medicine must not be about doctor’s egos and their ability to "cure" disease." He urges doctors to change their thinking to simply helping chronically-ill patients to have the best possible quality of life. It should not be a blow to the doctor’s ego when he cannot effect a full cure of a disease for which there is no FDA-approved cure, but as one doctor asked me "what would it have hurt?" for my doctors to give me sleeping pills and/or pain pills so that I would have some quality of life instead of spending 12-15 hours tossing and turning in hopes of getting 2-3 hours sleep. Instead, they changed my diagnosis to something they could fix, and then became annoyed with me when I refused to be cured of what I didn’t have in the first place.

Now, that’s the ultimate in controlling behavior – trying to change the nature of a patient’s disease simply by changing the name.

The problem is, all the bullying, egoism and control-freak attitudes don’t do a thing to make the patients better and, in fact, often violate the medical credo of "first, do no harm" as the patient gets worse without proper treatment.

It is not the patients who are disturbed, it is the physicians who are psychologically disturbed because they ignore the data, and whatever data there is, they manipulate it to say what they want it to say. __ Muhammed B. Yunus, M.D.

Yet more on Vitamin D

Tackling vitamin D deficiency

Vitamin D deficiency is ~~very common~~ in the United States and often goes
unrecognized by primary care physicians.

This oversight is unfortunate, because vitamin D plays an important role in
bone development and muscle function. It also facilitates absorption of
calcium and phosphate from the gut and kidney, suppresses parathyroid
hormone (PTH), and acts on osteoblasts to stimulate bone formation.

Vitamin D deficiency is a risk factor for osteoporosis, osteomalacia, falls,
and fractures.

Other, less studied functions include roles in: muscle strength and in
prevention of autoimmune diseases (eg, type 1 diabetes, rheumatoid
arthritis, multiple sclerosis) and cancer (eg, prostate, colon).1

Sources of vitamin D

There are two sources of vitamin D: (1) synthesis in the skin from UV-B
sunlight xposure and (2) food. UV-B radiation converts 7-dehydrocholesterol,
a lipid in the epidermis, to previtamin D3. This rearranges to vitamin D3
within hours, binds with vitamin D-binding protein, and enters the
circulation.

Just 10 to 15 minutes of exposure to sunlight on face, hands, and arms each
day, 2 to 3 days a week, is required to synthesize sufficient amounts of
vitamin D.

Only a few natural foods, such as fatty fish, cod liver oil, and egg yolks,
contain vitamin D. Fortified foods are the major dietary source of vitamin D
and include milk, breakfast cereal, margarine, butter, and certain brands of
orange juice and yogurt. Ice cream and cheese are not fortified.

Recommendations for daily intake

The Food and Nutrition Board of the Institute of Medicine currently
recommends the following daily vitamin D intake levels: 200 international
units (IU) from birth to age 50 years, 400 IU from age 51 to 70 years, 600
IU for ages over 70 years, and 800 IU for patients who are homebound or
institutionalized.2

However, clinical studies3,4 indicate that these recommendations may be too
low and that the minimum intake of vitamin D for adults should be 800 to
1,000 IU per day.

Risk factors for vitamin D deficiency

There are many risk factors for vitamin D deficiency (table 1). The two most
commonly seen by primary care physicians are decreased skin synthesis and
inadequate dietary or supplemental intake.

Skin synthesis of vitamin D declines with age because of epidermal thinning,
loss of total lipid content, and decreased blood flow in the skin. It has
been shown that people aged 62 to 80 years have 25-hydroxyvitamin D3
(25[OH]D3) levels three times lower than people aged 22 to 30 years after
the same sunlight exposure.5 Although only short exposures to adequate
sunlight are sufficient to maintain a normal level of vitamin D, latitude
and time of year significantly influence skin synthesis.

In latitudes more than 35 degrees north of the equator (eg, Boston,
Seattle), vitamin D production does not take place from November through
February, regardless of the length of sun exposure.6 In lower latitudes (eg,
Los Angeles, Atlanta), vitamin D synthesis is adequate throughout the year.
Lack of sun exposure can also result from excessive use of sunscreen,
complete clothing coverage, skin pigmentation dark enough to block UV-B
transmission, and being homebound or institutionalized, all of which are
common causes of vitamin D deficiency.

Inadequate dietary intake of vitamin D is another common cause of vitamin D
deficiency. Fortified foods are the major source of dietary vitamin D, but
they are often unreliable, because they do not always contain the amount of
vitamin D listed on the label. Studies have found that up to 70% of milk
samples in North America do not contain the 400 IU per quart of vitamin D
that they advertise.7 Also, patients' dietary intake can vary enormously.
One study of 333 women showed that the intake of vitamin D varied from 20 IU
to 1,600 IU each day.8

***Decreased gastrointestinal absorption is another common cause of vitamin
D deficiency. Vitamin D absorption occurs in the proximal small bowel and is
facilitated by chylomicrons. Abnormalities of the hepatobiliary tree,
proximal small bowel, and pancreas can interfere with the absorption and
enterohepatic circulation of vitamin D. These abnormalities include
malabsorption syndromes, inflammatory bowel disease, celiac sprue, chronic
steatorrhea, cystic fibrosis, and pancreatic insufficiency. Bariatric
surgery, which is being performed more often because of the increasing
prevalence of obesity, is now becoming a more common cause of vitamin D
deficiency.

Measuring vitamin D

The serum 25(OH)D3 level best reflects the body's supply. Although
1,25-dihydroxyvitamin D3 (1,25[OH]2D3) is the biologically active form of
vitamin D, it is not a good measure of the body's storage supply and should
not be used. The laboratory definition of vitamin D deficiency is extremely
controversial. Reference ranges, based on population studies, vary
considerably among laboratories. The lack of standardization, in addition to
different measuring methods, has made it difficult to define the level of
deficiency.

Many experts think that vitamin D deficiency is the 25(OH)D3 level at which
the PTH concentration rises to maintain the serum calcium level at the
expense of the bone (secondary hyperpara-thyroidism).9 Population studies
have found this level to be about 31 ng/mL (77 nmol/L).10 However, the more
conventional level currently used in laboratories is in the range of 15 to
20 ng/mL (37 to 50 nmol/L).

Prevalence of vitamin D deficiency

The prevalence of vitamin D deficiency varies according to the population
studied. Age, latitude, season, race, and lifestyle all play important roles
in vitamin D status.

***Clearly, homebound or institutionalized persons have a high prevalence of
vitamin D deficiency. In one study, the prevalence ranged from 38% in
nursing home residents to 54% in housebound community dwellers.11

Less recognized is the frequency of vitamin D deficiency in healthy African
Americans, regardless of age, and in healthy adolescents and young adults.
The third National Health and Nutrition Examination Survey (NHANES III)
included more than 18,000 adolescents and adults living at latitudes of 32
or more degrees north and found that vitamin D insufficiency was very
common, although a severe deficiency was not.12 The lowest vitamin D levels
were in African Americans, most likely because of decreased skin synthesis
due to dark pigmentation. A study of 1,546 healthy African American and
1,426 white women between ages 15 and 49 years (participants in NHANES III)
showed that 42% and 4%, respectively, had a mild to moderate vitamin D
de-ficiency (<15 ng/mL [37 nmol/L]).13 Twelve percent of the African
American women and less than 1% of the white women had a severe deficiency
(<8 ng/mL [20 nmol/L]).

Reinforcing the observation that latitude and season play a role in vitamin
D deficiency, vitamin D levels were measured in healthy men and women living
in Boston at the end of summer and winter.14 Low vitamin D levels (<20 ng/mL
[50 nmol/L]) were found in 30% at the end of winter and in 11% at the end of
summer. Surprisingly, 32% of the youngest age-group (18 to 29 years) had
vitamin D insufficiency at the end of winter as compared with 16% in the
oldest age-group (>50 years). *This discrepancy may be because older persons
take a multivitamin that provides vitamin D.

Clinical presentation

**The clinical presentation of vitamin D deficiency depends on the severity.
People with a mild to moderate deficiency are asymptomatic, or may have
nonspecific, diffuse musculoskeletal pain.15

**Those with severe deficiency may have deep bone pain, diffuse muscle pain,
hip pain, proximal weakness, or fractures. They may report difficulty with
gait, walking up stairs, and getting out of a chair, in addition to falls.16

Treatment

Patients with vitamin D deficiency require high doses of the vitamin - until
their total body stores have been replenished. Subsequently, they should be
switched to a maintenance dose to prevent future deficiency.

The amount and form of vitamin D are dependent on the severity and mechanism
of the deficiency. Various forms of vitamin D are available for treatment
(table 2). Oral ergocalciferol (Calciferol, Drisdol) or cholecalciferol is
the treatment of choice in patients with normal renal and hepatic function.

*Calcium supplements should be recommended to bring the total elemental
calcium intake (diet and supplement) to 1,500 mg per day.

A patient with a mild to moderate vitamin D deficiency due to limited sun
exposure or poor oral intake should be replenished with 50,000 IU of
ergocalciferol a week for 6 to 8 weeks.

For a severe deficiency (<8 ng/mL [20 nmol/L]), it is reasonable to take
50,000 IU orally twice a week for 6 to 8 weeks. A patient with severe
malabsorption may require even higher weekly doses. Even patients with
significant malabsorption will absorb more than 60% of vitamin D in this
form.

Once the appropriate 25(OH)D3 level has been reached, the patient should be
switched to maintenance therapy. This dose can be quite variable, depending
on the patient's needs.

A patient with a vitamin D deficiency from inadequate sunlight or dietary
intake needs 1,000 IU daily, whereas a patient with significant
malabsorption from Crohn's disease may need 50,000 IU daily.

If a patient with severe malabsorption is unresponsive to a high dose of
ergocalciferol (or it is intolerable), the patient should be switched to the
oral form of calcitriol (1,25[OH]2D3) (Rocaltrol). If this is poorly
absorbed, then the injectable form of calcitriol (Calcijex) is indicated.

Vitamin D replacement in the form of calcitriol (oral or intravenous) is
often needed in patients with chronic renal disease. Vitamin D dosing in
this situation depends on the patient's calcium, phosphate, and PTH levels
and is beyond the scope of this article. Calcifediol (Calderol) is useful in
patients with severe liver disease and those taking medications that impair
metabolism of 25(OH)D3, such as phenytoin (Dilantin) and phenobarbital
(Bellatal, Luminal, Solfoton).

Laboratory monitoring

Once vitamin D deficiency has been confirmed, serum calcium and PTH levels
should be checked. If these levels are normal, the treatment goal is to
bring the vitamin D level into the higher end of the normal range. If serum
calcium and PTH levels are abnormal as seen with moderate to severe
deficiencies PTH, calcium, and 25(OH)D3 levels should be monitored
carefully, starting 6 to 8 weeks after initiating therapy. The goal is to
reach a 25(OH)D3 level at which both PTH and calcium normalize. The
patient's dose may need to be increased an additional 6 to 8 weeks to
achieve this goal.

-->It is important to avoid vitamin D toxicity, which can cause
hypercalcemia, hypercalciuria (nephrolithiasis), and accelerated bone
resorption. Toxic effects are uncommon and have been reported only in
patients taking high daily doses of ergocalciferol (†40,000 IU) for weeks
to months.4,17 However, experts recommend avoiding daily doses greater than
10,000 IU (in patients without malabsorption). Toxicity is more likely to
occur with calcitriol than with ergocalciferol. The costs of tests vary
among laboratories, but at our institution, a serum PTH test is $87.00 and a
25(OH)D3 test is $76.50.

Treatment benefits

Two randomized controlled trials18,19 have shown that vitamin D and calcium
supplements increase bone mineral density and reduce fracture rates in
elderly patients with marginal vitamin D status. A study of 1,400 ambulatory
women with a mean age of 84 years18 showed that those treated with 800 IU of
vitamin D and 1.2 g of calcium each day had 23% fewer hip fractures than
those receiving placebo after 36 months. The PTH and vitamin D levels had
normalized in the treated group but remained abnormal in the placebo group.
There is also evidence that vitamin D supplements can prevent falls in the
elderly. A meta-analysis of 1,237 persons20 showed that elderly patients
taking vitamin D supplements had a 22% decrease in falls compared with
patients receiving placebo, presumably because of the influence of vitamin D
on *muscle strength.

Prevention

Vitamin D deficiency can be prevented by recommending that all patients
maintain appropriate sunlight exposure or dietary intake. However, in
northern latitudes, where skin synthesis does not occur in the winter,
vitamin D requirements must be met through dietary intake or
supplementation. Experts recommend that adults get at least 800 IU of
dietary vitamin D each day.

Conclusion

-->Vitamin D deficiency is a common clinical problem in the United States.
Because most patients with mild deficiency are asymptomatic, physicians
should have a high index of suspicion in populations at highest risk for
deficiency.

-->Identification and treatment of patients with vitamin D deficiency is
important for optimal bone development and muscle strength.

by Heidi S. Powell, MD Deborah Greenberg, MD

Dr Powell is assistant professor, department of medicine, University of
Washington School of Medicine and General Internal Medicine Center, Seattle.
Dr Greenberg is associate professor, department of medicine, University of
Washington School of Medicine and General Internal Medicine Center, Seattle.
Correspondence: Heidi S. Powell, MD, University of Washington General
Internal Medicine Center, 4245 Roosevelt Way NE, Seattle, WA 98105. E-mail:
powell@u.washington.edu.

VOL 119 / NO 1 / JUNE-JULY 2006 / POSTGRADUATE MEDICINE
SYMPOSIUM ON OSTEOPOROSIS

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Holick MF, Shao Q, Liu WW, et al. The vitamin D content of fortified milk
and infant formula. N Engl J Med 1992; 326( 18): 1178-81
Krall EA, Sahyoun N, TannenbaumS, et al. Effect of vitamin D intake on
seasonal variations in parathyroid hormone secretion in postmenopausal
women. N Engl J Med 1989; 321( 26): 1777-83
Hollis BW. Circulating 25-hydroxyvitamin D levels indicative of vitamin D
sufficiency: implications for establishing a new effective dietary intake
recommendation for vitamin D. J Nutr 2005; 135( 2): 317-22
Chapuy MC, Preziosi P, Maamer M, et al. Prevalence of vitamin D
insufficiency in an adult normal population. Osteoporos Int 1997; 7( 5):
439-43
Gloth FM III, Gundberg CM, Hollis BW, et al. Vitamin D deficiency in
homebound elderly persons. JAMA 1995; 274( 21): 1683-6
Looker AC, Dawson-Hughes B, Calvo MS, et al. Serum 25-hydroxyvitamin D
status of adolescents and adults in two seasonal subpopulations from NHANES
III. Bone 2002; 30( 5): 771-7
Nesby-O'Dell S, Scanlon KS, Cogswell ME, et al. Hypovitaminosis D prevalence
and determinants among African American and white women of reproductive age:
third National Health and Nutrition Examination Survey, 1988-1994. Am J Clin
Nutr 2002; 76( 1): 187-92
Tangpricha V, Pearce EN, Chen TC, et al. Vitamin D insufficiency among
free-living healthy young adults. Am J Med 2002; 112( 8): 659-62
Plotnikoff GA, Quigley JM. Prevalence of severe hypovitaminosis D in
patients with persistent, nonspecific musculoskeletal pain. Mayo Clin Proc
2003; 78( 12): 1463-70
Pfeifer M, Begerow B, MinneH W. Vitamin D and muscle function. Osteoporos
Int 2002; 13( 3): 187-94
Breslau NA, Zerwekh JE. Pharmacology of vitamin D preparations. In:
FeldmanD, GlorieuxFH, PikeJW, eds. Vitamin D. New York: Academic Press,
1997: 607-18
Chapuy MC, Arlot ME, Delmas PD, et al. Effect of calcium and cholecalciferol
treatment for three years on hip fractures in elderly women. BMJ 1994;
308( 6936): 1081-2
Dawson-Hughes B, Harris SS, Krall EA, et al. Effect of calcium and vitamin D
supplementation on bone density in men and women 65 years of age or older. N
Engl J Med 1997; 337( 10): 670-6
Bischoff-FerrariH A, Dawson-Hughes B, Willet WC, et al. Effect of vitamin D
on falls: a meta-analysis. JAMA 2004; 291( 16): 1999-2006

* * *

Lara (our science expert) warns that Vitamin D overdose can be dangerous and therefore, high levels of Vitamin D supplementation should only be undertaken with close medical supervision.

More on the NICE Guidelines and Vitamin D

Help ME Circle

Editorship : j.van.roijen@chello.nl

Dear Readers / Friends,

An hour ago I awoke very sick, out of a sleep from Thursday 19 o'clock till Friday 21 o'clock, with a hard pounding heart, a terrible head age and shaking hands. And I'm yearning for sleep again.

Some of you may know, that I suffer from a severe writing-aphasia because of ME; so at the moment I can't explain why I couldn't (and can't) handle my bulletin *Help ME Circle*.

I hope that I will come back in the near future; probably with a much lower sequence. But my pc don't work; I have to reinstall XP, which is a hell of a job.

I just received a very interesting article written by Margaret Williams, which I can't resist to post.

It is not only important for the UK, but also for Europe (see for example the fraudulent report of the Dutch Health Council of The Netherlands - in which all the bio-medical research is completely omitted - http://www.gr.nl/pdf.php?ID=1169&p=1 - and of course the USA.

The CDC is slowly on busy to gear their politics to the ideas of the patron of the insurance- and war-industry Simon Wessely. With the "redefined" Reeves's guidelines the prevalence of *CFS* is from one day to the other 6- to 10-fold higher than before.

By mixing more and more psychological disorders into the FATIGUE-soup, as they already did in 1994 (Fukuda/UNUM-Sharpe) in which the hallmark of ME/ICD-CFS *post-exertional malaise* was NOT mandatory - that's the real reason, why findings in research are so inconsistent - the authentic, neurological, multi-systemic disease ME and ICD-CFS (which was of course based on *ME*-outbreaks in the USA) will completely disappear.

Jan van Roijen (about five hours later)

http://www.meactionuk.org.uk/Dangers_of_NICE_for_MECFS.htm

More potential dangers of the UK NICE Guideline on *CFS/ME* for people with ME/CFS?

Margaret Williams

Much has been written about the NICE Guideline on *CFS/ME* since its release on 22nd August 2007, mostly noting concern over the Guideline's recommendations that cognitive behavioural therapy and graded exercise therapy (CBT/GET) should the first-line (and only) management for "Chronic Fatigue Syndrome / Myalgic Encephalomyelitis" or *CFS/ME*. This concern is unsurprising, given the existence of numerous published papers which all conclude that CBT is of limited and non-lasting benefit, and given that at least four major surveys of over 3,200 patients with ME/CFS have clearly shown GET to be actively harmful.

*CFS/ME* is different from ME/CFS, the former being the psychiatric model which has no abnormal signs or laboratory findings (i.e. chronic somatisation disorder) proposed and favoured by Wessely School psychiatrists who advise Government Departments on *CFS/ME* and who are believed to exert control over the Medical Research Council's funding agenda, whilst the latter is a nosological neurological disorder (classified as such by the World Health Organisation) which exhibits distinct signs and has an abundance of abnormal laboratory findings, albeit no single, definitive test.

It is a matter of on-going concern that the psychiatric lobby continues to use the terms ME, CFS and chronic fatigue (CF) as if they were interchangeable, when such is not the case.

Virtually none of the peer-reviewed, published biomedical evidence seems to penetrate the consciousness of these psychiatrists and their supporters, who continue to dismiss or ignore the ever-mounting confirmation of abnormal laboratory investigations now known to exist in ME/CFS. What is so curious is that there is such an abundance of easily accessible evidence of abnormal laboratory findings in ME/CFS, so how -- without losing credibility -- can the psychiatric lobby keep asserting that none exists?

Not only is this evidence down-played, its very existence is repeatedly denied: in an in-press article to be published in Psychoneuroendocrinology, James Jones from the Division of Viral and Rickettsial Diseases at the US Centres for Disease Control also seems to ignore this body of biomedical evidence, claiming: "In the absence of overtly abnormal findings in a person with prolonged duration of illness, it is common for practitioners to consider a psychological explanation during clinical evaluation" (" An extended concept of altered self: Chronic fatigue and post-infection syndromes". James F Jones. Doi:10.1016/j.psyneuen.2007.11.007). For Jones to propose in his essay that:

(i) " the illnesses in question stem from responses to previous infections and not to ongoing viral or immunologic factors"

(ii) interoception is responsible for the illness behaviour exhibited by patients ( " the sensations and consequences of sickness behaviour are remembered")

(iii) " persistent illnesses such as CFS are due to maladaptive biological (interoceptive) signal recognition"

(iv) " It is of interest that CBT remains an effective therapy for CFS" and

(v) " Chronic illnesses, such as CFS, in the absence of evidence of standard mechanisms of pathogenesis, require new concepts of illness origin"

seems remarkable, given that in 1996 Jones was one of the authors of a paper that provided laboratory evidence for an autoimmune component in ME/CFS (see below).

Royal Society of Medicine meeting to support the NICE Guideline

It is a matter of acute concern that the Royal Society of Medicine is to host a meeting on 28th April 2008 on " CFS" (reference to " ME" is omitted, which is in keeping with the Wessely School's documented intention to eradicate the term) at which the psychiatric lobby is to provide most of the speakers; not only do those speakers include Professor Simon Wessely himself (famous for his trenchant belief that ME is a myth and that it does not exist except as an aberrant belief in the mind of those who think they suffer from it), but other devout believers in the psychosocial model of *CFS/ME* such as Professor Peter White; Dr Anthony Cleare; Professor Rona Moss-Morris and Professor Matthew Hotopf.

Professor Anthony Pinching is to chair Session Two. Pinching is widely-known for his belief that in ME/CFS, " over-investigation can [cause patients] to seek abnormal test results to validate their illness", that "fatigue [is] not related to ongoing exertion" and that " The essence of treatment is activity management and graded rehabilitation" (as set out in Prescribers' Journal 2000:40:2:99-196).

Sir Peter Spencer, CEO of the charity Action for ME, is to speak in Session Three (to be chaired by Professor Mansel Aylward, formerly Chief Medical Adviser to the DWP and now funded by the notorious medical insurance company UNUM). Another speaker is Professor Chris Dowrick from Liverpool, who, with Rona Moss-Morris is one of the authors of a study for which the MRC awarded ££459,707, the results of which were published in the British Journal of Psychiatry: 2007: December:191:536-542 (" Cluster randomised controlled trial of training practices in reattribution for medically unexplained symptoms"). The object of the study was to teach general practitioners that " reattribution" of symptoms provides a psychological explanation for medically unexplained symptoms in disorders such as *CFS/ME*.

Another danger of the NICE Guideline?

Given the wall-to-wall influence of the Wessely School lobby and the choice of members of the Guideline Development Group that produced the Guideline on *CFS/ME*, it is little wonder that NICE got things so wrong.

There can be no doubt that NICE ignored the international evidence that ME/CFS is a biomedical, not psychiatric, disorder, claiming that studying this evidence fell outwith its remit. Such a claim is mystifying, since knowledge of the existing evidence-base ought surely to be mandatory before producing a national Guideline on the management of any disorder, especially given that adherence to such a Guideline is obligatory throughout the NHS (and hence for affiliated agencies such as the Department for Work and Pensions and Social Services). Not only has the " evidence-base" upon which NICE relied for its recommended management interventions for ME/CFS been exposed as deeply flawed by virtue of the heterogeneous populations studied; the methodological inadequacy; the corrupted data; the high drop-out rates; the undeniable ineffectiveness of CBT/GET as shown by the outcomes measures, and the finding that the claimed benefits may have been illusory ( see: " Inadequacy of the York (2005) Systematic Review of the CFS/ME Medical Evidence Base" by Malcolm Hooper & Horace Reid at http://www.meactionuk.org.uk/FINAL_on_NICE_for_Gibson.html ) but, just as importantly, the proscribing by NICE of appropriate testing and its stipulation that any vitamin or mineral deficiency must not be corrected by prescription would seem to constitute a real and even life-threatening danger to people with ME/CFS - see below.

The proscribing by NICE of testing for Vitamin D status in patients with ME/CFS

This is particularly problematic in respect of vitamin D status which, according to clinicians who specialise in ME/CFS, is known to be frequently deficient in patients with true ME/CFS. If serum vitamin D levels are low, one might expect the serum calcium level to be low and the alkaline phosphate (ATP) level to be high, but in ME/CFS this seems not to be so. Normal screening rules simply do not apply in this disorder.

It seems that some doctors still believe that vitamin D relates just to the health of bones, and that a lack of vitamin D solely results in osteomalacia or in osteoporosis (a thinning of the bone predisposing to multiple fractures).

Whilst this is indeed so, nothing could be further from the whole truth.

Vitamin D is a misnomer because it is now known that it is more than just a vitamin - it is a precursor of a steroid hormone that affects the entire body. Receptors that respond to vitamin D have been found in almost every type of human cell from brain to bone ( see: www.mercola.com ).

It should be noted that whilst this website (run by Dr Joseph Mercola MD) is useful and informative in many ways, it is essentially an advertising website and contains some information which some clinicians might challenge.

Vitamin D represents D2 or D3. The former is known as ergocalciferol and the latter as cholecalciferol.

Whilst vitamin D2 occurs naturally in fungal form (usually mushroom), medically prescribed vitamin D2 is usually a synthetic form, which according to some sources has been shown to cause toxicity and to have greater potential for harm (see " Test Values and Treatment for Vitamin D Deficiency" at www.mercola.com ).

Vitamin D3 is the natural form (i.e. the same vitamin D that the body makes when exposed to sunshine).

Vitamin D3 is converted 500% faster than vitamin D2.

Currently there is much debate as to whether recommended levels of vitamin D in the diet are sufficient for people living in northern latitudes, but over-supplementation is dangerous and can lead to vomiting, kidney failure and calcification of the arteries ( see www.mercola.com ) and it is essential to consult a doctor specialising in the field.

With regard to supplementation, it is perhaps worth mentioning that one GP who specialises in ME/CFS (Dr Sarah Myhill, a leading member of the British Society for Allergy & Environmental Medicine / BSAEM) apparently prescribes 0.5 micrograms of calcitriol (ie. the active form of 1,25 dihydroxyvitamin D - see below) for patients with depleted vitamin D levels, which is manufactured by a company called Teva Ltd (0113 - 238 - 0099).

The Medical Information department of this company has confirmed that they use wholly synthetic products in the manufacture and that in addition to the active (synthetic) ingredient, their calcitriol contains butylated hydroxyanisol (E321, a " red" or dangerous substance [BHA/BHT] to which people with ME/CFS who have hypersensitivities might react badly: BHA has a benzene / phenol ring and was developed to protect petroleum from oxidative gumming, whilst BHT [toluene] is methylbenzene derived from petroleum; it is used as a solvent in aircraft fuels); coconut oil; gelatine for the capsule from a mixture of both porcine and bovine sources; glycerol; sorbitol; titanium dioxide (E171); quinoline yellow (E104, another " red" or dangerous substance and a coal tar dye that has been banned in the US, in Australia, in Norway and in Japan, but not in the UK, even though the UK Committee on Toxicity acknowledged the evidence that it inhibits cholinesterase activity in in vitro human red blood cells and plasma, and assays have shown that quinoline yellow is genotoxic); patent blue (E131, another " red" coal tar dye and a dangerous substance). In addition, each capsule contains refined shellac and black oxide used in the printing ink.

Ranges of Vitamin D

Vitamin D from the skin and diet is metabolised in the liver to 25-hydroxyvitamin D (25 (OH)D), known as calcidiol. It is this that is used to determine vitamin D status. 25(OH)D is in turn metabolised in the kidney to its active form of 1,25 dihydroxyvitamin D (1,25(OH)2D, known as calcitriol).

Optimal range is now considered by world experts to be 45-50 ng/ml (nanograms per millilitre). Twenty-five nanograms equates to one International Unit (the measure in which supplementation is usually prescribed).

Below 40 ng/ml is considered sub-optimal; below 30 ng/ml is deficient; below 20 ng/ml is now considered seriously deficient, and below 10 ng/ml places the patient at real risk, requiring prompt intervention. Experts recommend that, ideally, the vitamin D level should never be below 32 ng/ml ( see www.mercola.com ).

In ME/CFS, levels as low as 8.3 ng/ml have been recorded.

The NICE Guideline on *CFS/ME*, however, is categoric: not only is testing for vitamin D status proscribed, but the prescribing of vitamin supplements to rectify any deficiency is specifically forbidden: the Guideline states that supplements to correct any vitamin or mineral deficiency " should not be prescribed for treating the symptoms of the condition" (see the 52 page version of the Guideline, page 24, paragraph 1.4.7.2).

Quite how cognitive behavioural therapy and graded exercise can raise deficient levels of this vital and life-saving hormone that are found in ME/CFS patients is not explained by NICE.

Effects of deficiency of Vitamin D

Deficiency results in chronic illnesses, specifically in symptoms that occur in ME/CFS: deficiency impacts on muscle function (with muscle pain and weakness) and is a risk factor for cardiovascular disease (CVD risk is documented in the ME/CFS literature and was the subject of keynote lectures at the international research conference hosted on 25th May 2007 by ME Research UK in Edinburgh). A deficient vitamin D status is known to result in high blood pressure, with the consequent dangers of heart attack or stroke (see " Vitamin D Deficiency". Michael F Holick MD PhD; NEJM 2007:357:266-281; see also " Ultraviolet B and blood pressure". Rolfdieter Krause, Michael Holick et al. Lancet 1998:352:709-710), and in raised triglycerides (see " Prevalence of Cardiovascular Risk Factors and the Serum Levels of 25-Hydroxyvitamin D in the United States". David Martins et al. Arch Intern Med: 2007:167:1159-1165).

Vitamin D is an essential part of the endocrine system (which is well-documented as being disrupted in ME/CFS) and it controls several of the adrenal hormones, production of enzymes and the growth of cells ( www.mercola.com: interview with William B Grant PhD of the Sunlight, Nutrition and Health Research Centre, one of the top vitamin D researchers).

Deficiency of vitamin D has also been implicated in inflammatory disorders such as ME/CFS is increasingly being demonstrated to be (see " Higher serum vitamin D concentrations are associated with longer leukocyte telomere length in women". T Spector et al. The American Journal of Clinical Nutrition, 8th November 2007) and in autoimmune disorders such as multiple sclerosis, rheumatoid arthritis and diabetes (see " Vitamin D Deficiency". Michael Holick MD, PhD: NEJM 2007:357:266-281).

It will be recalled that some experienced ME/CFS researchers - including Professor Kenny De Meirleir from Belgium -- now hold ME/CFS to be an autoimmune disease and that evidence of autoimmunity was presented at the fifth AACFS International Research and Clinical Conference held in 2001 in Seattle. This was a major multi-centre study looking at the presence of autoantibodies to a cellular protein expressed primarily in neuronal cells (MAP2). Initial studies with immunohistochemistry showed a high percentage of (ME)CFS sera reactive to centrosomes and that other proteins besides MAP2 might also be target antigens in (ME)CFS autoimmunity (see " A multi-centre study of autoimmunity in (ME)CFS". K Sugiura, A Komaroff, E Tan et al. AACFS #037).

Previously, a 1996 paper demonstrated the occurrence of autoantibodies to a conserved intracellular protein (lamin B1), which provides laboratory evidence for an autoimmune component in ME/CFS. The authors found that 52% of patients with ME/CFS develop autoantibodies to components of the nuclear envelope (NE), mainly nuclear lamins, suggesting that in addition to the other documented disturbances of the immune system, humoral autoimmunity against polypeptides of the NE is a prominent immune derangement in ME/CFS. 67% of ME/CFS patients were positive for NE reactivity compared with 10% of normal subjects. No patients with either depression or atopy showed reactivity to NE proteins. Autoantibodies to NE proteins are relatively infrequent and most fall into the category of an unusual connective tissue disease subset characterised by brain or skin vasculitis (see " Autoantibodies to Nuclear Envelope Antigens in Chronic Fatigue Syndrome". K Konstantinov, James Jones, Eng Tan et al. J Clin Invest 1996:98:8:1888-1896). Many patients with ME/CFS report a vasculitic-type headache which has become known as " the ME headache". The paper concluded that such activation " could be the result of various triggering agents, such as infections or environmental toxins". It recommended that: "Future work should be directed at a better understanding of the autoimmune response of CFS patients to other NE antigens".

This important paper has been widely cited in, for example: American Journal of Psychiatry:2003:160(2):221-236 (N Afari and D Buchwald); Clin Vaccine Immunol: 2002:9(4):747-752 (BH Natelson et al); Brain 2001:124(9):1821-1831 (RK Gherardi et al); Rheumatology: 2001:40(7):806-810 (M Nishikai et al) and Journal Watch:1997:314:4.

It therefore surprising that one of the authors (James Jones) now seems to regard ME/CFS as maladaptive interoceptive signal recognition.

Not only is deficient vitamin D implicated in autoimmune disorders, it is also known to be implicated in at least 16 different types of cancer, especially pancreatic, lung, breast, ovarian, prostate and colon cancers ( see www.mercola.com ). A landmark study from the Moores Cancer Centre at the University of California found that some 600,000 cases of breast and colorectal cancer could be prevented each year, if only vitamin D3 levels were increased.

Quite apart from being implicated in pancreatic cancer, low vitamin D is also known to affect pancreatic function, and pancreatic dysfunction is well-documented in ME/CFS.

As well as being implicated in common cancers, autoimmune diseases and cardiovascular disease, there is evidence that deficient vitamin D levels are implicated in infections: vitamin D can increase the body's production of naturally occurring antimicrobial peptides which destroy the cell wall of viruses and bacteria (see www.mercola.com; see also "Vitamin D Deficiency". Michael F Holick as above) and a deficiency is also implicated in seizures (see http://news.bbc.co.uk/1/hi/health/7161458.stm ).

Holick, a world expert on vitamin D, states that 1,25 dihydroxyvitamin D controls more than 200 genes, including genes responsible for the regulation of cellular proliferation, differentiation, apoptosis and angiogenesis, and that it is also a potent immunomodulator, as well as increasing insulin production and myocardial contactability. Vitamin D deficiency is associated with congestive cardiac failure and blood levels of inflammatory factors including C-reactive protein and interleukin-10.

Conclusion

Given the immense importance of vitamin D, and given the fact that people with ME/CFS are known sometimes to have inordinately low levels, and given the protean symptomatology arising from a deficiency, it is disturbing that NICE precludes both testing for it and the prescribing of supplements to raise the level if necessary for patients with ME/CFS.

It would seem to be imperative that patients suffering from ME/CFS take charge of their own management and either persuade their GP to act against the NICE Guideline and check their vitamin D status (which in the UK, may mean sending blood to a specialist laboratory in Manchester and is expensive to do) or consult a private clinician specialising in ME/CFS.

For people within travelling distance of London, one such clinician is Dr William Weir, whose details are on the Co-Cure UK Good Doctor List ( http://www.co-cure.org/Good-Doc.htm ). Dr Weir works part-time as a Consultant Physician in the NHS but he also runs a private ME/CFS Clinic at 10, Harley Street, London W1G 9PF (telephone: 0207 - 467 - 8478) and he now routinely checks vitamin D levels in all his ME/CFS patients.

The Doctors' Laboratory (55 Wimpole Street, London W1G 8YL, telephone 0207 - 460 - 4800) also carries out the 25 (OH)D test. A referral from a medical practitioner is required, but blood can be sent by post in a serum tube and must arrive within two days. If sent by post by a medical practitioner, the cost is £40, but if a patient is referred and attends in person to have blood taken, there is an additional service cost of £29.

There are numerous sources of vitamin D3 supplements that do not contain excipients; one such company is Biocare (telephone 0121 - 433 - 3727), whose supplement contains only lanolin (the source of D3) in extra virgin olive oil (but some people with ME/CFS may be unable to tolerate lanolin). There are different strengths of the supplement.

A more efficient way of increasing vitamin D levels may be by using a lamp specifically made for the purpose. One such lamp is the Xiris. It is made in Italy and can be obtained from Allergy Matters (telephone 0208 - 339 - 0029). It comes with full instructions and costs £225.

Alternatively, provided that the support of clinicians can be obtained and for those fortunate enough to have access to an NHS phototherapy unit (within a Dermatology Department), personalised, carefully titrated and monitored phototherapy is available on the NHS.

The NICE Guideline on *CFS/ME*, however, may prove to be a barrier impossible to surmount.

Tags: , , ,

Did the Princess and the Pea have Fibromyalgia?


Did 'The Princess on the Pea' suffer from fibromyalgia syndrome? The
influence on sleep and the effects of acupuncture.

Acupunct Med. 2007 Dec;25(4):184-97.

Lundeberg T, Lund I.

PMID: 18160929


Fibromyalgia syndrome (FMS) is a chronic pain syndrome characterised
by central sensitisation resulting in hypersentivity of the skin and
deeper tissues as well as fatigue. Possibly the princess in Hans
Christian Andersen's 'The Princess and the Pea' suffered from FMS
since chronic sleep disturbances are typical in FMS. These sleep
disturbances have been attributed to a dysfunction in the systems
regulating sleep and wakefulness resulting in loss of deep sleep. In
addition, many patients with FMS experience cognitive dysfunction,
characterised by impaired concentration and short term memory
consolidation, a complaint also commonly reported in other sleep disorders.

In recent reviews evaluating the efficacy of acupuncture in FMS it
has been concluded that acupuncture has no specific effect. A
prerequisite for this conclusion is that all the major symptoms in
the syndrome have been assessed. However, previous studies have
generally focused on the pain alleviating effect of acupuncture in
FMS. We have observed that not only pain but also sleep and cognitive
dysfunction may be ameliorated in response to acupuncture, suggesting
that these variables should be taken into account when evaluating the
effects of acupuncture in FMS.

Furthermore, the results demonstrated great individual variability
apart from the systematic effects related to the group, indicating
that individually performed treatment strategies are required. Our
suggestion is supported by experimental and clinical studies showing
that acupuncture may affect insomnia and alertness, and that there
may be neurophysiologic bases for these specific effects.

* * *

"Princess and the Pea" is a good analogy that helps people understand WHY I go to bed and can't sleep.

When the fibro is really acting up, the smallest wrinkle in the sheet feels like I'm laying on a log.

Tramadol has been scientifically proven useful, and it's the only thing that I've found that eases the pain enough to let me sleep (as opposed to sleeping pills that have to be strong enough to dope me up well into the next day).

Blame the Patient

CDC'S JIM JONES BLAME-THE-PATIENT RHETORIC:

THE SHAPE OF THINGS TO COME?

Clara Valverde RN, BSc

Aquo Health Professionals Training Team

formacionsalud@hotmail.com

Even though CDC's Dr James Jones' article "An extended concept of altered self: chronic fatigue and post-infection syndromes" is not a scientific article (mixing, as he does so esoterically, in the same sentence, "cytokines" with "philosophical self"), it is a very important piece of warning to anyone attempting to do serious scientific work in CFS and to PWCFS (people with CFS) about the direction that agencies and other goverment bodies are taking in order to dilute this bothersome and expensive illness.

Jones' blame-the-patient rhetoric is, to the untrained reader, well camouflaged under the pretense of being "psychoneuroendocrinology" with an extensive bibliography of other metanarrative builders like himself with blame-the-patient topics such as "the neurobiology of aggression and rage: role of cytokines". No one with any serious training in psychology, philosophy or immunology will think twice about this piece of rhetoric, unless they are concerned about the fact that the author, a virologist turned self-made-psychoanalyst, works for the CDC, payed by American tax-payers.

The whole article can be easily summarized in three points:

- CFS is not a disease.

- PWCFS make themselves sick.

- PWCFS bother those around them with their irritable behaviour.

To go into more detail, Jones says that "the current CFS case definition relies on self-reported symptoms and disability and specifies no standard measures". If Dr. Jones was not so busy playing philospher and psychologist, perhaps he could use some of his time at the CDC more usefully and do what many doctors with almost no budgets are trying to do: compile immune dysfunction and active viral infections amongst PWCFS with which to write up a proper case definition.

Jones says that the research findings have not been consistent on a possible ongoing cause and effect relationship between the syndrome and immunological processes. Actually, what have not been consistent are the studies. If long-term immunological studies were done, we surely would find some very interesting and useful information. But the more important question is: why are these studies not done after so many years of knowing that CFS is mostly an immunological alteration?

Dr Jones also seems very concerned by "sickness behaviour". This and his confused yet intense preocupation with what he calls the "unconscious" (it is "subconscious", Dr Jones,- do read Jacques Lacan, please) take him to the following interesting affirmation: "Most adults can conjure up the feeling and sensations they experienced when having an influenza infection, infeccious mononucleosis, or other systemic virus infection. Since infections and immunizations begin in early childhood, it is possible that such memories (conscious and unconscious) are stired indefinetly". This pathetic attempt to summarize the workings of the subconscious does little justice to Dr Freud and to PWCFS.

Jones, also in his article, repeats several times (a sign that his subconscious wants to say something) that a person with CFS's "physical and mental inactivity may be associated with irritability and aggressive behaviour leading to isolation from others". Here philosopher Jones's logic fails somewhat as it is usually the reverse: the isolation that the PWCFS suffers lead him or her to irritability (an even more if he or she spends his or her time reading "the experts").

Seeing as Dr Jones takes the liberty to psychoanalyze PWCFS, we feel a certain liberty to analyze what he is projecting himself.

Without going into details, one can clearly see that Dr Jones is suffering from the type of chronicity and frustration shown by many doctors who went into medicine with the idea of "curing" ("caring" they leave to nurses so as not to have to involve themselves with those uncomfortable parts of the human being which deal with the patient's own experience of disease). The lineal medical symptom-diagnosis-treatment-cure paradigm is challenged deeply by CFS and this frustration is projected by many doctors onto the patients (Absbring and Navaren 2002, Ware 1999). As Arthur Kleinman wrote: "The medical profession is dangerous for chronic patients".

Dr Jones' inability to deal with suffering is projected in his reiterated statements about the impact of the PWCFS' "behaviours" on "surrounding individuals". I.e. He is fed-up with PWCFS and he needs to discredit them (Alonzo and Reynolds 1995, Goffman 1963).

If Dr Jones' is fed up with PWCFS lack of "normal positive dynamic self-constraint", why does not he dedicate his career to other diseases?

We can only guess (the same way he does with PWCFS behaviours). But we see that in emerging diseases like CFS, there is a dangerous void which can easily be filled by an abuse of medical power and to deligitimize patients (Wendell 1996).

Doctors such as Jones, think that it is their role to define patients and their behaviour and they censor the patients' right to their definition, to their own narrative (Kleinman 1988), while they spout and publish rhetorics of domination, "professionality" and coercion. And they take things which are only probable and try to pass them as definitely true (Locke 1992).

CFS is a hard disease to work with. It takes a very skilled immunologist to work with dedication all the alterations that this disease creates. It is not a disease for those who have narrow and reductionist values (Ware and Kleinman 1992). Faced with the doubts and fears which are part of working with CFS, doctors like Jim Jones hide behind a shield of invicibility and forget that it is only a shield. Their views speak beyond the scientific evidence and grant themselves the status of a new priesthood (Raymond 1982). The fact that CFS is predominatly a woman's illness is not a small matter. A woman who has been ill with CFS for years but without a diagnosis, even after she is diagnosed, is very vulnerable and this attracts doctors who need to control and blame the patient, who need this type of power for their egos (Greenhalgh 2001).

This article is a warning. When virologists and the CDC start to "philosophyze" and to "psychoanalyze" CFS, we know that they are fullfilling any goverment's dream-come-true: to dilute this expensive disease and have it disappear by the magic of rhetoric. This is so needed by European and North American countries which are in a neo-liberal frenzy of privatizing any health care services which might still be public and accessible. These goverments know that increased immune-related emergent illnesses threaten their budgets and they will welcome Dr Jones' ideas and those of the pro-psy lobby in the UK and in other countries.

Today Dr Jones of the CDC is ranting on about PWCFS behaviour and tomorrow CFS is "a psychologial illness" and PWCFS will be in CBT groups working out their "sickness behaviour", while their Th1 and Th2 get more out of balance and their EBV, CMV and HHV6 skyrocket. The shape of things to come?

Perhaps Dr Jones and others at the CDC should know that PWCFS are watching them closely. Thousands of people with CFS who are ex (or not so ex) health workers, researchers, philosophers, psychoanalysts, policy makers, etc, and are not ready to accept this kind of article and will continue to denounce the coercion and incompetence of the likes of Jones.

PWCFS are ill, day after day, with very faulty immune systems, untreated infections, outrageously low aminoacid levels and other dysfunctions which Dr Jones does not care about (or is too busy with some useful activity, on tax-payers' time, such as trying to psychoanalyze the high levels of cytokines).

Patients are now turning away from these so-called "experts" who are only interested in the next congress to show off their cooked-up numbers, and instead, patients are collaborating with doctors who humbly work with micro-immunity, antivirals, etc, in order to stop the deterioration of the PWCFS.

And it is up to us, interested health workers, respectful health workers, informed health workers, who reject the coercion and labelling patient's behaviours and up to us, PWCFS to keep uniting and denouncing rhetoric and building networks of patients and health workers for truly scientific, respectful and efficient health services for CFS.

References

Ainsworth-Vaughn, N. (1995). Claiming power in the medical encounter: The whirlpool discourse. Qualitative Health Research, 5(3), 270-291.

Alonzo, AA, Reynolds NR (1995). Stigma, HIV and AIDS: An exploration and elaboration of a stigma trajectory. Social Science and Medicine, 41, 303-315.

Brown, Phil. 2000. Perspectives in Medical Sociology. Third Edition. Prospect Heights, Ill: Waveland Press.

Clark, J. A., & Mishler, E.G. (1992). Attending to patients' stories: reframing the clinical task. Sociology of Health & Illness, 14(3), 344-371.

Conrad, Peter. Editor. 2005. The Sociology of Health and Illness: Critical Perspectives. Seventh Edition. New York: Worth Publishers.

Goffman E. (1963). Stigma. Notes on the management of spoiled identity. London: Penguin.

Greenhalgh, S (2001). Under the medical gaze: facts and fictions of chronic pain. Berkeley: University of California Press.

Kleinman, A (1988). The Illness Narratives: Suffering, Healing and the Human Condition. New York: Basic Books.

Lane, V. & Lawler, J. (1997). Pap smear brochures, misogyny and language: adiscourse analysis and feminist critique. Nursing Inquiry, 4(4), 262-267.

Lupton, D. (1992). Discourse analysis: a new methodology for understanding the ideologies of health and illness. Australian Journal of Public Health, 16(2), 145-149.

Murray, Michael, (1997) Narrative health psychology, Massey University, Palmerston North, Dept. of Psychology. Visiting scholar series; no. 7.

Nessa, J., & Malterud, K. (1990). Discourse analysis in general practice: A sociolinguistic approach. Family Practice, 7(2), 77-83.

Reynolds, J. M. 1973. "The medical institution." In L. T. Reynolds & J. M. Henslin (Eds.), American society: A critical analysis. New York: David McKay, p. 200.

Potter, J. and Wetherell, M. (1987). Discourse and social psychology: Beyond attitudes and behaviour. London: Sage. Parenti, M. 1988. Democracy for the few. New York: St. Martin's Press, pp. 150-151.

Sherwin, Susan Diagnosis: Difference: The Moral Authority of Medicine (review) Hypatia - Volume 16, Number 3, Summer 2001, pp. 172-176

Ware, NC (1999). Towards a model of social course in chronic illness: The example of chronic fatigue syndrome. Culture, Medicine and Psychiatry, 23, 303-331.

Ware, NC (1992). Culture and somatic experience: The social course of illness in neurasthenia and chronic fatigue syndrome. Psychosomatic Medicine, 54, 546-560.

Wendell, S (1996). The rejected body: feminist philosophical reflections on disability. New York: Routledge.

Zola, I. 1986. "Medicine as an institution of social control." In P. Conrad & R. Kern (Eds.), The sociology of health and illness. New York: St. Martin's Press.

* * *

One thing the detractors forget is that we have a lot of patients who used to be doctors and nurses. Whereas most patients just read the plain-English conclusion of research studies, there are those who can understand every word and point out the fictions (e.g., the researchers who load patient pools with depressed people who don’t meet CFS diagnostic criteria in order to prove CFS=depression) and lapses in logic.

Thank God for these medical experts within the CFS community who debunk the detractors’ prejudices with solid medical evidence and logic.

Friday, January 4, 2008

More potential dangers of NICE Guidelines

Permission to Repost

http://www.meactionuk.org.uk/Dangers_of_NICE_for_MECFS.htm

More potential dangers of the UK NICE Guideline on "CFS/ME" for people with
ME/CFS?

Margaret Williams

2nd January 2008

Much has been written about the NICE Guideline on "CFS/ME" since its release
on 22nd August 2007, mostly noting concern over the Guideline's
recommendations that cognitive behavioural therapy and graded exercise
therapy (CBT/GET) should the first-line (and only) management for "Chronic
Fatigue Syndrome / Myalgic Encephalomyelitis" or "CFS/ME".  This concern is
unsurprising, given the existence of numerous published papers which all conclude that CBT is of limited and non-lasting benefit, and given that at least four major surveys of over 3,200 patients with ME/CFS have clearly shown GET to be actively harmful.

"CFS/ME" is different from ME/CFS, the former being the psychiatric model
which has no abnormal signs or laboratory findings (i.e. chronic
somatisation disorder) proposed and favoured by Wessely School psychiatrists
who advise Government Departments on "CFS/ME" and who are believed to exert
control over the Medical Research Council's funding agenda, whilst the
latter is a nosological neurological disorder (classified as such by the
World Health Organisation) which exhibits distinct signs and has an
abundance of abnormal laboratory findings
, albeit no single, definitive
test.

It is a matter of on-going concern that the psychiatric lobby continues to use the terms ME, CFS and chronic fatigue (CF) as if they were interchangeable, when such is not the case.

Virtually none of the peer-reviewed, published biomedical evidence seems to
penetrate the consciousness of these psychiatrists and their supporters, who
continue to dismiss or ignore the ever-mounting confirmation of abnormal
laboratory investigations now known to exist in ME/CFS.  What is so curious
is that there is such an abundance of easily accessible evidence of abnormal
laboratory findings in ME/CFS, so how  -- without losing credibility -- can
the psychiatric lobby keep asserting that none exists?

Not only is this evidence down-played, its very existence is repeatedly
denied:
in an in-press article to be published in Psychoneuroendocrinology,
James Jones from the Division of Viral and Rickettsial Diseases at the US
Centres for Disease Control also seems to ignore this body of biomedical
evidence, claiming: "In the absence of overtly abnormal findings in a person
with prolonged duration of illness, it is common for practitioners to
consider a psychological explanation during clinical evaluation"  ("An
extended concept of altered self: Chronic fatigue and post-infection
syndromes". James F Jones. Doi:10.1016/j.psyneuen.2007.11.007).

For Jones to propose in his essay that:

(i)  "the illnesses in question stem from responses to previous infections
and not to ongoing viral or immunologic factors"

(ii) interoception is responsible for the illness behaviour exhibited by
patients ( "the sensations and consequences of sickness behaviour are
remembered")

(iii) "persistent illnesses such as CFS are due to maladaptive biological
(interoceptive) signal recognition"

(iv) "It is of interest that CBT remains an effective therapy for CFS"
and

(v) "Chronic illnesses, such as CFS, in the absence of evidence of standard
mechanisms of pathogenesis, require new concepts of illness origin" seems
remarkable, given that in 1996 Jones was one of the authors of a paper that
provided laboratory evidence for an autoimmune component in ME/CFS (see
below).

Royal Society of Medicine meeting to support the NICE Guideline

It is a matter of acute concern that the Royal Society of Medicine is to
host a meeting on 28th April 2008 on "CFS" (reference to "ME" is omitted,
which is in keeping with the Wessely School's documented intention  to
eradicate the term) at which the psychiatric lobby is to provide most of the
speakers; not only do those speakers include Professor Simon Wessely himself
(famous for his trenchant belief that ME is a myth and that it does not
exist except as an aberrant belief in the mind of those who think they
suffer from it), but other devout believers in the psychosocial model of
"CFS/ME" such as Professor Peter White; Dr Anthony Cleare; Professor Rona
Moss-Morris and Professor Matthew Hotopf.

Professor Anthony Pinching is to chair Session Two.  Pinching is
widely-known for his belief that in ME/CFS, "over-investigation can [cause
patients] to seek abnormal test results to validate their illness", that
"fatigue [is] not related to ongoing exertion" and that "The essence of
treatment is activity management and graded rehabilitation" (as set out in
Prescribers' Journal 2000:40:2:99-196).  Sir Peter Spencer, CEO of the
charity Action for ME, is to speak in Session Three (to be chaired by
Professor Mansel Aylward, formerly Chief Medical Adviser to the DWP and now
funded by the notorious medical insurance company UNUM). Another speaker is
Professor Chris Dowrick from Liverpool, who, with Rona Moss-Morris is one of
the authors of a study for which the MRC awarded £459,707, the results of
which were published in the British Journal of Psychiatry: 2007:
December:191:536-542 ("Cluster randomised controlled trial of training
practices in reattribution for medically unexplained symptoms").  The object
of the study was to teach general practitioners that "reattribution" of
symptoms provides a psychological explanation for medically unexplained
symptoms in disorders such as "CFS/ME".

Another danger of the NICE Guideline?

Given the wall-to-wall influence of the Wessely School lobby and the choice
of members of the Guideline Development Group that produced the Guideline on
"CFS/ME", it is little wonder that NICE got things so wrong.

There can be no doubt that NICE ignored the international evidence that ME/CFS is a biomedical, not psychiatric, disorder, claiming that studying this evidence fell outwith its remit.  Such a claim is mystifying, since knowledge of the existing evidence-base ought surely to be mandatory before
producing a national Guideline on the management of any disorder, especially
given that adherence to such a Guideline is obligatory throughout the NHS
(and hence for affiliated agencies such as the Department for Work and
Pensions and Social Services).

Not only has the "evidence-base" upon which NICE relied for its recommended
management interventions  for ME/CFS been exposed as deeply flawed by virtue
of the heterogeneous populations studied; the methodological inadequacy; the
corrupted data; the high drop-out rates; the undeniable ineffectiveness of
CBT/GET as shown by the outcomes measures, and the finding that the claimed
benefits may have been illusory ( see: "Inadequacy of the York (2005)
Systematic Review of the CFS/ME Medical Evidence Base" by Malcolm Hooper &
Horace Reid at http://www.meactionuk.org.uk/FINAL_on_NICE_for_Gibson.html )
but, just as importantly, the proscribing by NICE of appropriate testing and
its stipulation that any vitamin or mineral deficiency must not be corrected
by prescription would seem to constitute a real and even life-threatening
danger to people with ME/CFS - see below.

The proscribing by NICE of testing for Vitamin D status in patients with
ME/CFS

This is particularly problematic in respect of vitamin D status which,
according to clinicians who specialise in ME/CFS, is known to be frequently
deficient in patients with true ME/CFS. 
  If serum vitamin D levels are low,
one might expect the serum calcium level to be low and the alkaline
phosphate (ATP) level to be high, but in ME/CFS this seems not to be so.
Normal screening rules simply do not apply in this disorder.

It seems that some doctors still believe that vitamin D relates just to the
health of bones, and that a lack of vitamin D solely results in osteomalacia
or in osteoporosis (a thinning of the bone predisposing to multiple
fractures). Whilst this is indeed so, nothing could be further from the whole truth.

Vitamin D is a misnomer because it is now known that it is more than just a
vitamin - it is a precursor of a steroid hormone that affects the entire
body.  Receptors that respond to vitamin D have been found in almost every
type of human cell from brain to bone  ( see: www.mercola.com ).

It should be noted that whilst this website (run by Dr Joseph Mercola MD) is
useful and informative in many ways, it is essentially an advertising
website and contains some information which some clinicians might challenge.

Vitamin D represents D2 or D3.  The former is known as ergocalciferol and
the latter as cholecalciferol.

Whilst vitamin D2 occurs naturally in fungal form (usually mushroom),
medically prescribed vitamin D2 is usually a synthetic form, which according
to some sources has been shown to cause toxicity and tohave greater
potential for harm (see "Test Values and Treatment for Vitamin D Deficiency"
at  www.mercola.com ).

Vitamin D3  is the natural form (i.e. the same vitamin D that the body makes
when exposed to sunshine).

Vitamin D3 is converted 500% faster than vitamin D2.

Currently there is much debate as to whether recommended levels of vitamin D
in the diet are sufficient for people living in northern latitudes, but
over-supplementation is dangerous and can lead to vomiting, kidney failure
and calcification of the arteries ( see www.mercola.com ) and it is
essential to consult a doctor specialising in the field.

With regard to supplementation, it is perhaps worth mentioning that one GP
who specialises in ME/CFS (Dr Sarah Myhill, a leading member of the British
Society for Allergy & Environmental Medicine / BSAEM) apparently prescribes
0.5 micrograms of calcitriol (ie. the active form of 1,25 dihydroxyvitamin
D - see below) for patients with depleted vitamin D levels, which is
manufactured by a company called Teva Ltd  (0113 - 238 - 0099).

The Medical Information department of this company has confirmed that they
use wholly synthetic products in the manufacture and that in addition to the
active (synthetic) ingredient, their calcitriol contains butylated
hydroxyanisol (E321, a "red" or dangerous substance [BHA/BHT] to which
people with ME/CFS who have hypersensitivities might react badly: BHA has a
benzene / phenol ring and was developed to protect petroleum from oxidative
gumming, whilst BHT [toluene] is methylbenzene derived from petroleum; it is
used as a solvent in aircraft fuels); coconut oil; gelatine for the capsule
from a mixture of both porcine and bovine sources; glycerol; sorbitol;
titanium dioxide (E171); quinoline yellow (E104, another "red"  or dangerous
substance and a coal tar dye that has been banned in the US, in Australia,
in Norway and in Japan, but not in the UK, even though the UK Committee on
Toxicity acknowledged the evidence that it inhibits cholinesterase activity
in in vitro human red blood cells and plasma, and assays have shown that
quinoline yellow is genotoxic); patent blue (E131, another "red" coal tar
dye and a dangerous substance).  In addition, each capsule contains refined
shellac and black oxide used in the printing ink.

Ranges of Vitamin D

Vitamin D from the skin and diet is metabolised in the liver to
25-hydroxyvitamin D (25 (OH)D), known as calcidiol. It is this that is used
to determine vitamin D status.  25(OH)D is in turn metabolised in the kidney
to its active form of 1,25 dihydroxyvitamin D (1,25(OH)2D, known as
calcitriol).

Optimal range is now considered by world experts to be 45-50 ng/ml
(nanograms per millilitre).  Twenty-five nanograms equates to one
International Unit (the measure in which supplementation is usually
prescribed).

Below 40 ng/ml is considered sub-optimal; below 30 ng/ml is deficient; below
20 ng/ml is now considered seriously deficient, and below 10 ng/ml places
the patient at real risk, requiring prompt intervention. Experts recommend
that, ideally, the vitamin D level should never be below 32 ng/ml ( see
www.mercola.com ).

In ME/CFS, levels as low as 8.3 ng/ml have been recorded.

The NICE Guideline on "CFS/ME", however, is categoric: not only is testing
for vitamin D status proscribed, but the prescribing of vitamin supplements
to rectify any deficiency is specifically forbidden:  the Guideline states
that supplements to correct any vitamin or mineral deficiency  "should not
be prescribed for treating the symptoms of the condition"  (see the 52 page
version of the Guideline, page 24, paragraph 1.4.7.2).

Quite how cognitive behavioural therapy and graded exercise can raise
deficient levels of this vital and life-saving hormone that are found in
ME/CFS patients is not explained by NICE.


Effects of deficiency of Vitamin D

Deficiency results in chronic illnesses, specifically in symptoms that occur
in ME/CFS: deficiency impacts on muscle function (with muscle pain and
weakness) and is a risk factor for cardiovascular disease  (CVD risk is
documented in the ME/CFS literature and was the subject of keynote lectures
at the international research conference hosted on 25th May 2007 by ME
Research UK in Edinburgh).  A deficient vitamin D status is known to result
in high blood pressure, with the consequent dangers of heart attack or
stroke (see "Vitamin D Deficiency".  Michael F Holick MD PhD; NEJM
2007:357:266-281; see also "Ultraviolet B and blood pressure". Rolfdieter
Krause, Michael Holick et al. Lancet 1998:352:709-710), and in raised
triglycerides (see "Prevalence of Cardiovascular Risk Factors and the Serum
Levels of 25-Hydroxyvitamin D in the United States". David Martins et al.
Arch Intern Med: 2007:167:1159-1165).

Vitamin D is an essential part of the endocrine system (which is
well-documented as being disrupted in ME/CFS) and it controls several of the
adrenal hormones, production of enzymes and the growth of cells (
www.mercola.com: interview with William B Grant PhD of the Sunlight,
Nutrition and Health Research Centre, one of the top vitamin D researchers).

Deficiency of vitamin D has also been implicated in inflammatory disorders
such as ME/CFS is increasingly being demonstrated to be (see "Higher serum
vitamin D concentrations are associated with longer leukocyte telomere
length in women".  T Spector et al. The American Journal of Clinical
Nutrition, 8th November 2007) and in autoimmune disorders such as multiple
sclerosis, rheumatoid arthritis and diabetes (see  "Vitamin D Deficiency".
Michael Holick MD, PhD: NEJM 2007:357:266-281).

It will be recalled that some experienced ME/CFS researchers - including
Professor Kenny De Meirleir from Belgium -- now hold ME/CFS to be an
autoimmune disease and that evidence of autoimmunity was presented at the
fifth AACFS International Research and Clinical Conference held in 2001 in
Seattle.
This was a major multi-centre study looking at the presence of
autoantibodies to a cellular protein expressed primarily in neuronal cells
(MAP2).  Initial studies with immunohistochemistry showed a high percentage
of (ME)CFS sera reactive to centrosomes and that other proteins besides MAP2
might also be target antigens in (ME)CFS autoimmunity (see "A multi-centre
study of autoimmunity in (ME)CFS".  K Sugiura, A Komaroff, E Tan et al.
AACFS #037).

Previously, a 1996 paper demonstrated the occurrence of autoantibodies to a
conserved  intracellular protein (lamin B1), which provides laboratory
evidence for an autoimmune component in ME/CFS.  The authors found that 52%
of patients with ME/CFS develop autoantibodies to components of the nuclear
envelope (NE), mainly nuclear lamins, suggesting that in addition to the
other documented disturbances of the immune system, humoral autoimmunity
against polypeptides of the NE is a prominent immune derangement in ME/CFS.
67% of ME/CFS patients were positive for NE reactivity compared with 10% of
normal subjects. No patients with either depression or atopy showed
reactivity to NE proteins.

Autoantibodies to NE proteins are relatively infrequent and most fall into
the category of an unusual connective tissue disease subset characterised by
brain or skin vasculitis (see "Autoantibodies to Nuclear Envelope Antigens
in Chronic Fatigue Syndrome".  K Konstantinov, James Jones, Eng Tan et al.
J Clin Invest 1996:98:8:1888-1896).  Many patients with ME/CFS report a
vasculitic-type headache which has become known as "the ME headache".

The paper concluded that such activation "could be the result of various
triggering agents, such as infections or environmental toxins".  It
recommended that: "Future work should be directed at a better understanding
of the autoimmune response of CFS patients to other NE antigens".

This important paper has been widely cited in, for example: American Journal
of Psychiatry:2003:160(2):221-236 (N Afari and D Buchwald); Clin Vaccine
Immunol: 2002:9(4):747-752 (BH Natelson et al);  Brain 2001:124(9):1821-1831
(RK Gherardi et al); Rheumatology: 2001:40(7):806-810 (M Nishikai et al) and
Journal Watch:1997:314:4.

It therefore surprising that one of the authors (James Jones) now seems to
regard ME/CFS as maladaptive interoceptive signal recognition.

Not only is deficient vitamin D implicated in autoimmune disorders, it is
also known to be implicated in at least 16 different types of cancer,
especially pancreatic, lung, breast, ovarian, prostate and colon cancers (
see www.mercola.com ).  A landmark study from the Moores Cancer Centre at
the University of California found that some 600,000 cases of breast and
colorectal cancer could be prevented each year, if only vitamin D3 levels
were increased.

Quite apart from being implicated in pancreatic cancer, low vitamin D is
also known to affect pancreatic function, and pancreatic dysfunction is
well-documented in ME/CFS.

As well as being implicated in common cancers, autoimmune diseases and
cardiovascular disease, there is evidence that
deficient vitamin D levels are implicated in infections: vitamin D can
increase the body's production of naturally occurring antimicrobial peptides
which destroy the cell wall of viruses and bacteria (see www.mercola.com;
see also "Vitamin D Deficiency". Michael F Holick as above) and a deficiency
is also implicated in seizures (see
http://news.bbc.co.uk/1/hi/health/7161458.stm ).

Holick, a world expert on vitamin D, states that 1,25 dihydroxyvitamin D
controls more than 200 genes, including genes responsible for the regulation
of cellular proliferation, differentiation, apoptosis and angiogenesis, and
that it is also a potent immunomodulator, as well as increasing insulin
production and myocardial contactability.  Vitamin D deficiency is
associated with congestive cardiac failure and blood levels of inflammatory
factors including C-reactive protein and interleukin-10.

Conclusion

Given the immense importance of vitamin D, and given the fact that people
with ME/CFS are known sometimes to have inordinately low levels, and given
the protean symptomatology arising from a deficiency, it is disturbing that
NICE precludes both testing for it and the prescribing of supplements to
raise the level if necessary for patients with ME/CFS.
It would seem to be imperative that patients suffering from ME/CFS take
charge of their own management and either persuade their GP to act against
the NICE Guideline and check their vitamin D status (which in the UK, may
mean sending blood to a specialist laboratory in Manchester and is expensive
to do) or consult a private clinician specialising in ME/CFS.
For people within travelling distance of London, one such clinician is Dr
William Weir, whose details are on the Co-Cure UK Good Doctor List
(http://www.co-cure.org/Good-Doc.htm ).  Dr Weir works part-time as a
Consultant Physician in the NHS but he also runs a private ME/CFS Clinic at
10, Harley Street, London W1G 9PF (telephone: 0207 - 467 - 8478) and he now
routinely checks vitamin D levels in all his ME/CFS patients.

The Doctors' Laboratory (55 Wimpole Street, London W1G 8YL, telephone 0207 -
460 - 4800) also carries out the 25 (OH)D test.  A referral from a medical
practitioner is required, but blood can be sent by post in a serum tube and
must arrive within two days.  If sent by post by a medical practitioner, the
cost is £40, but if a patient is referred and attends in person to have
blood taken, there is an additional service cost of £29.

There are numerous sources of vitamin D3 supplements that do not contain
excipients; one such company is Biocare  (telephone 0121 - 433 - 3727),
whose supplement contains only lanolin (the source of D3) in extra virgin
olive oil (but some people with ME/CFS may be unable to tolerate lanolin).
There are different strengths of the supplement.

A more efficient way of increasing vitamin D levels may be by using a lamp
specifically made for the purpose.  One such lamp is the Xiris.  It is made
in Italy and can be obtained from Allergy Matters (telephone 0208 - 339 -
0029).  It comes with full instructions and costs £225.

Alternatively, provided that the support of clinicians can be obtained and
for those fortunate enough to have access to an NHS phototherapy unit
(within a Dermatology Department), personalised, carefully titrated and
monitored phototherapy is available on the NHS.

The NICE Guideline on "CFS/ME", however, may prove to be a barrier
impossible to surmount.