Feeling Jolly?

This is awesome: Mentally ill are ‘jollied along’ rather than treated by psychiatrists. 36 psychiatrists write a letter to the British Journal of Psychiatry explaining exactly how the system’s currently failing patients.

Some highlights:

“If a GP suspected a patient had cancer, he wouldn’t dream of referring him to anybody other than a cancer specialist. A cancer patient might need jollying along, but what he really needs is the correct diagnosis and treatment. That’s what he gets from a specialist. But patients with mental illness are not automatically referred to psychiatrists. If they only see a social worker, there’s every chance that mental illness, or underlying physical illness, will be missed. Patients are getting a bum deal.”

and this:

Psychiatry, the group says, is the only medical speciality to adopt an approach that so distorts its original purpose. “For those with severe mental illness, to avoid medicalisation is at best confusing and at worst damaging or even life-threatening … these individuals are being let down by the current state of affairs.”

and this:

Professor Craddock and his co-signatories are not claiming that psychosocial treatments do not have a place, but they claim it is vital that patients are seen by a psychiatrist first. “Psychiatrists may not be the best people to deliver treatments, but they are the best to make assessments,” Professor Craddock said.

My experience in the mental health system was, up until this year, one of jumping through hoops in order to see psychiatrists and get onto medication. (Although I did see a psychiatrist fairly quickly after my initial referral, she was pretty much useless.) The first blood tests I had to rule out physical illness didn’t happen until I was put on Seroquel. So this pretty accurately describes how I feel about the system. It’s working for me now, but it sure took a while and I’m only getting the right treatment because I continually pushed for it over the course of a pretty horrible year.

Do nutritional supplements help with mental health? Part 2: Vitamins that do begin with a ‘B’

This is part two of my series of posts on nutritional supplements and mental health. Yesterday I looked at vitamins that don’t begin with a ‘B’ (see that post for my various caveats and disclaimers). Today I’m going to look at vitamins that do start with a ‘B’. Tomorrow: Those crunchy, crunchy minerals.

Vitamin B₁ (thiamin)

Thiamin’s an important vitamin. Deficiency can lead to a variety of neuro-degenerative disorders. Since alcoholism impairs the ability of the body to utilise thiamin, these conditions – Wernicke’s encephalopathy, Korsakoff’s psychosis, etc. – tend to be associated with alcoholism. There doesn’t seem to be much evidence linking thiamin to any mental disorders. Mostly I was only able to find case reports of schizophrenics with thiamin-deficiency as a result of poor diet or co-morbid alcohol disorders.

The one exception was this study from 1989, which added thiamin and a drug called acetazolamide (used to treat glaucoma, absence seizures and altitude sickness) to the drug regime of 24 schizophrenics. This apparently had positive results.

Acetazolamide, incidentally, has recently been investigated as a way to reverse anti-psychotic induced weight gain, and also as a treatment for bipolar disorder.

Vitamin B₂ (riboflavin)

This rather equivocal paper from 1992 made cautious links between depression, riboflavin deficiency and thyroxine levels: “The findings suggest that B2 (FAD) activity may serve as a sensitive marker of thyroxine status in certain female psychiatric inpatients and that B2 deficiency may play an etiological role in defects of the methylation pathways in a subset of mentally ill individuals.”

Aside from this, all I could turn up were a number of studies that used riboflavin as a marker to check medication compliance. Excess riboflavin is excreted by the body (turning urine bright yellow) and it glows under UV light. This means that if you combine riboflavin with your patients psychiatric drugs and then collect urine samples every day you can tell if they’ve actually been taking what you’ve prescribed them. This also means that large doses of riboflavin are pointless – the body just gets rid of it.

Vitamin B₃ (niacin)

Niacin (which is called niacin because calling it ‘nicotinic acid’ might make people think that cigarettes are full of healthy vitamins) was widely investigated for use in the treatment of schizophrenia in the 1960’s and early 1970’s. This never really added up to much, with one review of the literature concluding that “the data indicate that nicotinic acid has no therapeutic effect of schizophrenia.”.

More recently, the interest in niacin has turned towards its (possible) use as a test for schizophrenia. High doses of niacin cause a flush response of the skin; it turns out that this response is weaker and less often found in schizophrenics. Studies like this have found that the effect is not found in other mental illnesses like bipolar disorder and depression. Another study found that people experiencing their first psychotic episode exhibited the effect, but people who had experienced multiple episodes did not. While this is interesting (and could potentially lead to a test for schizophrenia) it’s not an argument for supplemental niacin.

The only recent paper I could find that did suggest supplemental niacin for mental illnesses was a 1995 paper from the Ukraine:

Participation of nicotinic acid and its derivates in the functioning of nervous system is considered basing on the data from literature. It is supposed that the favourable therapeutic effects of nicotinamide, nicotinic acid and their active biological form–NAD are realized due to the mechanisms of their functioning in the nervous system, for treating schizophrenia, epilepsy and other diseases of the nervous system.

Niacin is dangerous at high doses, although some people seem to recommend it. The following case report shows why you shouldn’t believe everything you read on the internet (I include the stuff I’m writing in that, by the way – check it out for yourself):

A 56-year-old male with a history of schizophrenia presented to the emergency department after orally ingesting 11,000 mg of niacin. The patient cited an Internet resource that recommended high-dose niacin for therapy of schizophrenia as the reason for his ingestion. He stopped his psychiatric medications several weeks prior to his niacin overdose. At presentation, the patient was alert and normothermic. His pulse was 68 beats per minute and his blood pressure was initially 92/41 mmHg. Hypotension with a blood pressure of 58/40 developed over the next few hours and persisted despite intravenous infusion of over 4 liters of normal saline. The physical exam was otherwise unremarkable, specifically without signs of an allergic reaction or cutaneous flushing. He required intravenous dopamine infusion for 12 hours to support a mean arterial blood pressure greater than 60 mmHg. Evaluation for other etiologies of hypotension was unrevealing.

So, there’s very little evidence to suggest that niacin supplementation helps with any mental illnesses, and the high doses sometimes recommended by alternative medicine sites can be harmful.

Vitamin B₅ (pantothenic acid)

Pantothenic acid is everywhere. That’s what the word pantothenic means. It’s so prevalent that, to quote Wikipedia: “Pantothenic acid deficiency is exceptionally rare and has not been thoroughly studied. In the few cases where deficiency has been seen (victims of starvation and limited volunteer trials), nearly all symptoms can be reversed with the return of pantothenic acid.”

It looks like there were a couple of studies back in the dark ages of psychiatry about supplementing pantothenic acid for schizophrenia. For example, Partially favorable applications of pantothenic acid in schizophrenic subjects from 1953 or Treatment of chronic schizophrenia by a combination of electroshock, pantothenic acid and nicotinamide from 1954. There’s no details available on pubmed, so I have no idea what they found. I think it speaks for itself that nobody’s repeated them in the fifty years since.

Vitamin B₆ (pyridoxine, etc.)

There’s some reasonably good evidence that pyridoxine can help improve neuroleptic-induced tardive dyskinesia and akathasia. These kinds of studies have been going on for a while, but two recent studies from Israel seem to be the biggest and most comprehensive. The akathasia study compared pyridoxine to mianserin (an antidepressant) and a placebo in a group of sixty schizophrenic patients. They concluded that “results indicate that high doses of B(6) and a low dose of mianserin may be a useful addition to current treatments of NIA.” The tardive dyskinesia study involved fifty inpatients with schizophrenia or schizoaffective disorder and reported similarly positive results: “Vitamin B(6) appears to be effective in reducing symptoms of TD. The specific mechanisms by which vitamin B(6) attenuates symptoms of TD are not clear.” Note however, that the ‘high dose’ in both of these studies was 1200m. This is high enough to potentially cause sensory neuropathy. In other words, it’s probably not the kind of thing you want to be doing without medical supervision.

There is also research that suggests a link between low levels of pyridoxine and depression:

In 140 individuals, symptoms of depression were evaluated by the Major Depression Ir to examine whether treatment with vitamin Bnventory, and biochemical markers of vitamin B deficiency were measured. RESULTS: We found that 18 (13%) individuals were depressed. A low plasma level of PLP [pyridoxal phosphate] was significantly associated with the depression score … Our study suggests that a low level of plasma PLP is associated with symptoms of depression. Randomized trials are now justified and needed in orde6 may improve symptoms of depression.

Previous to this, there had been a rather unconvincing trial using pyridoxine to treat co-morbid minor-depression in schizophrenia patients. This involved 9 people in an open label study, of which two showed some improvement. This seems indistinguishable from placebo to me, even though the authors optimistically conclude that “A subgroup of schizophrenic patients with comorbid minor depression may benefit from pyridoxine addition to their on-going anti-psychotic treatment.” There doesn’t appear to have been any further investigation.

Finally, this paper from way back in 1982 that suggested that since oral contraceptives decrease serum levels of vitamin B6 and vitamin B6 is involved in tryptophan metabolism, which is implicated in depression, anxiety disorders and so on, that supplementation of small amounts of pyridoxine would relieve symptoms of these disorders in women taking oral contraceptives. No studies on this seem to have been carried out, though, so it’s pretty much just speculation. The lower serum levels of B6 are confirmed by this recent study however. As a quick tangent, the authors of that study conclude that “Since low vitamin B6 levels are independently associated with heightened risks for arterial and venous thromboembolism (TE), they could partly account for the increased TE risk of OC users.”

So, currently it looks like vitamin B6 supplementation could help with some of the serious side effects of anti-psychotics, though in doses that could cause other problems. Depressed people seem to have lower levels of pyridoxine in their blood, but it’s not clear whether supplemental B6 would help, nor what kind of dosages would be required if it did. Women taking oral contraceptives might benefit from taking a small dose of supplemental B6, though it’s more persuasive that this could reduce the risk of throboembolism than help with mental illness.

Vitamin B₇ (biotin; sometimes called Vitamin H)

To quote from Wikipedia:

Biotin deficiency rarely occurs among healthy people, since the daily requirement of biotin is low, many foods provide adequate amounts of it, intestinal bacteria synthesize small amounts of it, and the body effectively scavenges and recycles it from bodily waste. However, deficiencies can be caused by consuming raw egg whites over a period of months to years. Egg whites contain high levels of avidin, a protein that binds biotin strongly. When cooked, avidin is denatured and becomes entirely non-toxic.

The only relevant paper I could find was a case study of a patient who was gastrointestinally impaired and had been fed intravenously for months, which led to biotin deficiency and a cluster of symptoms which included severe depression. So, if you’re not being fed on a drip and you don’t eat raw egg whites all the time, you probably don’t need supplemental biotin.

Vitamin B₉ (folic acid / folate)

There’s been a lot of research into folate over the last decade or so, and plenty before then as well. There’s some fairly substantive evidence that folate deficiency is linked to depression and somewhat less for schizophrenia and bipolar disorder. It’s pretty well established that people with mental illnesses of various kinds tend to have lower serum levels of folate.

Let’s start with depression. A recent review concluded: “Depressed patients with both low and normal folate levels may benefit from augmenting a primary antidepressant medication either initially, at the onset of treatment, or later after some degree of treatment resistance has been recognized.”

Another paper, published last year, concluded that:

“… folate deficiencies may be caused by improper absorption and utilization, often due to genetic polymorphisms. Individuals, therefore, can have insufficient levels or lack needed forms of folate, despite adequate intake. Supplementation with the active form of folate, methyltetrahydrofolate, which is more readily absorbed, may be effective in the prevention and treatment of both depression and dementia.”

Or this paper from 2005:

There is now substantial evidence of a common decrease in serum/red blood cell folate, serum vitamin B12 and an increase in plasma homocysteine in depression. Furthermore, the MTHFR C677T polymorphism that impairs the homocysteine metabolism is shown to be overrepresented among depressive patients, which strengthens the association. On the basis of current data, we suggest that oral doses of both folic acid (800 microg daily) and vitamin B12 (1 mg daily) should be tried to improve treatment outcome in depression.

Lots of studies seem to have resulted in a positive effect. Research continues.

There isn’t quite this level of confidence with the schizophrenia research. A Korean study from 2006 reported that “findings suggest that folate supplement may be beneficial to some schizophrenic patients with homocysteinemia due to the genetic defect of methylenetetrahydrofolate reductase.” It wasn’t the only study from 2006 to reach this conclusion.

A review of the literature from the previous year was less positive, finding methodological flaws in previous studies and calling for further studies “to clarify the relationship between folate status and schizophrenia”. However the two studies from 2006 mentioned above strike me as enough to be cautiously positive.

Folate supplementation in bipolar disorder has, if anything, less evidence to back it up than in schizophrenia. The most recent study that I could find was from 1997. This measured the folate levels of 45 manic inpatients against a socio-economically matched control group. It concluded:

This indicated that the reduced red-cell folate in mania is associated with the illness and not due to reduced absorption or dietary deficiency of folate. Considering previous studies that showed reduced red-cell folate in depression, our findings suggest that reduced red-cell folate occurred in both phases of bipolar disorders.

Two studies looking at folate and lithium had rather different conclusions. One found that: “These results question the rationale of prescribing folic acid preparations for lithium-treated bipolar disorder patients, but the authors indicate that folate concentrations may be low in lithium-treated unipolar depressives.” While the other, conducted five years previously, went so far as to make this recommendation: “It is suggested that a daily supplement of 300-400 micrograms folic acid would be useful in long-term lithium prophylaxis.”

Here’s my own conclusions. Folate supplementation for people with depression – especially those who are taking anti-depressants – seems fairly well supported by the evidence as these things go. It’s definitely a promising area of investigation. For some people, taking folate may be a sensible decision, probably more so for people who don’t live in areas where foods are commonly enriched with it. The evidence for schizophrenia and bipolar disorder is much more limited, so using folate would be more speculative. However, it seems fairly well established that people with these conditions are more likely to have low folate levels, and since folate is both cheap and safe at the low-ish doses generally suggested, supplements of it may well be justifiable and possibly even sensible.

Vitamin B₁₂ (cobalamins)

Cobalmin is often studied together with pyridoxine (B₆) and folic acid, mostly because all three are involved in homocysteine metabolism. Deficiencies can lead to raised levels of homocysteine, which has been suggested as a risk factor for a variety of mental illnesses. Like those other two vitamins, there’s a long history of research into cobalmin as a treatment for depression.

A number of studies have found that people with mental illness tend to have low cobalmin levels. For example, this Israeli study from 2000 looked at the cobalmin levels of 644 psychiatric in-patients: “Vitamin B12 deficiency is common in chronically ill psychotic patients with adequate nutrition and is not readily detected by routine hematology tests.”

The evidence that low cobalmin levels can impair treatment of mental illnesses is contradictory. While this study concluded that cobalmin levels were more important than folate levels in predicting response to treatment in people suffering from major depressive disorder, this study found almost exactly the opposite. The second study was looking specifically at people with treatment-resistant depression, which could conceivably account for this difference, though it doesn’t seem especially likely to me.

As I noted in the section on folic acid, some researchers are already recommending supplementation of cobalmin: “On the basis of current data, we suggest that oral doses of both folic acid (800 microg daily) and vitamin B12 (1 mg daily) should be tried to improve treatment outcome in depression.”

The evidence for cobalmin supplementation seems less convincing to me than the evidence for folate. There don’t appear to be any studies that show a benefit from additional cobalmin. It may be worth noting that folic acid supplementation can mask the symptoms of cobalmin deficiency, so it may be prudent for people who are at risk of b12 deficiency (eg. the elderly, alcoholics, elderly alcoholics, etc.) who are taking folic acid supplements to also take a cobalmnin supplement.

Conclusions

The substance of real interest here is vitamin B₉ (folic acid). The evidence isn’t absolutely convincing, but it is persuasive, particularly for its use as an adjunct to anti-depressants. There haven’t been any studies that actually use it for bipolar disorder, but it doesn’t seem unreasonable – given the similarly low levels that have been found in manic patients – to provisionally assume that it may help. I’m equivocating here. Folic acid’s dirt cheap and safe enough that various countries fortify bread and cereal products with it. And it looks like a good enough idea that I’m going to start taking it myself.

Do nutritional supplements help with mental health? Part 1: Vitamins that don’t begin with a ‘B’.

I’ve been looking into nutritional treatments for bipolar disorder recently. I was taking a multi-vitamin up until a while ago (ironically enough I stopped taking it because I got depressed and couldn’t be bothered). There’s products available like EmPowerPlus that look a lot like really expensive multi-vitamins to me (with some other stuff thrown in, admittedly). So I decided to take a stroll through pubmed and see what kind of evidence there are for various vitamins, minerals and other ‘nutritional supplements’.

First some notes.

My only qualification for doing this is that I’m reasonably scientifically literate and I find this kind of stuff fairly interesting. Anyone with access to the internet could do the same thing. I generally haven’t seen anything more than the abstracts of the papers I’ve linked to (I don’t have access to a university library and I’m not going to pay for them). To be honest, I probably wouldn’t be able to evaluate their reliability or the effectiveness of their methods even if I did read the whole things.

I’m specifically looking at the role of these substances in (some) mental illness – vitamins and minerals may be wonderful for other things. I don’t know – I haven’t looked. Also, I’ve focused on depression, bipolar disorder and schizophrenia.

This is part one, in which we look at all the vitamins that aren’t one of the B vitamins. Part two, which I’ll hopefully post tomorrow, will be for the eight B vitamins. Parts three and four will be for minerals and other stuff, respectively.

Anyway, without further waffling:

Vitamin A (Retinol)

One schizophrenia researcher has written a couple of papers that suggest that retinoids (which are chemicals the body makes from Vitamin A) may be implicated in schizophrenia. I wasn’t able to find anything to suggest that Vitamin A supplementation could help with any mental illnesses. Vitamin A deficiency isn’t really a problem in developed nations anyway.

Recently a big meta-study in the UK looked at a number of different supplements. Vitamin A supplementation (as well as beta-carotene supplementation, which is essentially the same thing) appears to increase mortality. There’s an increased risk of lung-cancer, particularly for smokers.

So, to sum up, there’s no clear benefit to taking additional vitamin A, deficiency in developed nations is rare and vitamin A supplements may have harmful effects.

Vitamin C (Ascorbic Acid)

There’s some research from the 1980’s that showed raised levels of the element vanadium in people who have manic depression. Some of this work speculated (not very convincingly) that these high levels of vanadium cause manic depression. Vitamin C increases the rate at which vanadium is excreted via the kidneys. There was at least one study that compared vitamin C to the then standard drug used in treating manic depression:

There was no significant difference between the response of depressed patients to amitriptyline or ascorbic acid and EDTA. Manic patients responded significantly better to lithium than to ascorbic acid and EDTA. These results are in keeping with the suggestion that vanadium may be of aetiological importance in depressive psychosis, but do not support such a suggestion for mania.

Recently, vanadium has started to be sold as a supplement and has been (so far fairly inconclusively) investigated as a treatment for type II diabetes. Neither the people in these studies, nor those taking it in the form of commercially available supplements appear to report depression or mania as a side-effect. In other words, the evidence is very limited and the limited evidence that there is seems contradictory.

Vitamin D (ergocalciferol, cholecalciferol, etc.)

Over the last ten years, there’s been a growing amount of work linking vitamin D to schizophrenia. It looks like your mother not getting enough vitamin D while she was pregnant could increase your risk of developing schizophrenia.

The connection seems to have initially been made in 1999 by McGrath:

The central nervous system is increasingly being recognised as a target organ for vitamin D via its wide-ranging steroid hormonal effects and via the induction of various proteins such as nerve growth factor. This paper proposes that low maternal vitamin D may impact adversely on the developing foetal brain, leaving the affected offspring at increased risk of adult-onset schizophrenia. The hypothesis can parsimoniously explain diverse epidemiological features of schizophrenia, such as the excess of winter births, increased rates of schizophrenia in dark-skinned migrants to cold climates, the increased rate of schizophrenia births in urban versus rural setting, and the association between prenatal famine and schizophrenia.

This small study looked at a family with a high prevalence of psychiatric disorders and a hereditary defect in the vitamin D receptor gene. It only involved 40 people, 18 of whom had relevant psychiatric disorders and conluded that there was no link between vitamin D and psychotic illness.

However, a much larger study from Finland (a cohort study of just over 9000 people) found that “Vitamin D supplementation during the first year of life is associated with a reduced risk of schizophrenia in males. Preventing hypovitaminosis D during early life may reduce the incidence of schizophrenia.” Recent studies using rats and mice are also quite persausive.

So although I didn’t find any studies that showed taking vitamin D could help with your own mental illness, if you’re pregnant getting enough vitamin D could reduce your child’s risk of developing schizophrenia. This is likely to be more important if you live somewhere it’s not very sunny and have dark skin.

Vitamin E (tocopherols and tocotrienols)

Like vitamins A and C, vitamin E is an antioxidant. There’s a theory that schizophrenia may be caused by oxidative stress, which vitamin E may protect from. There’s been a couple of recent studies using vitamin E in combination with vitamin C and Omega-3 fatty acids as an adjunct to anti-psychotics. While both reported positive results, they were both small studies with only 50 subjects combined and neither provided a control group. As the first of these said: “Future studies need be done in placebo-controlled trials and also with a comparison group supplemented with fatty acids alone in a larger number of patients, both chronic as well as never medicated, and for a longer duration of treatment while the dietary intake is monitored.”

There’s also been research into whether vitamin E (possibly combined with vitamin C) can protect against tardive dyskinesia and neuroleptic-induced parkinsonism. While some of these individual studies have reported positive results, a Cochrane review of Vitamin E for neuroleptic-induced tardive dyskinesia found that “Small trials with uncertain quality of randomisation indicate that vitamin E protects against deterioration of TD but there is no evidence that vitamin E improves symptoms of TD.”

Another study linked low plama levels of vitamin E to major depression, but concluded that ” plasma levels of alpha-tocopherol are lower in depression, but this is not likely to be the result of inability to meet recommended dietary intake.” This doesn’t contribute to a case for taking supplemental vitamin E.

On balance, the current evidence is that if you’re taking an anti-psychotic, vitamin E supplementation might help stop you developing tardive dyskinesia or keep your tardive dyskinesia from getting worse. It won’t make it get better, though. Remember though, there’s also evidence that taking vitamin E and C supplements can increase mortality.

Vitamin K (phylloquinone, menaquinone, etc.)

Vitamin K is a group of chemicals that are mostly used in blood coagulation. There doesn’t seem to be any research into any possible connection with mental illnesses, although this case report from earlier this year seems interesting:

We report the case of a 26-year-old woman suffering from borderline personality disorder (BPD), major depression and bulimia nervosa according to DSM-IV who showed unexplained impairment of the vitamin K-dependent coagulation pathway. Subsequently we discuss different manifestations of self damaging behaviour and comorbidities, as well as psychosocial issues potentially leading to coagulation abnormalities or complications in patients with BPD.

Conclusions

There appears to be very little evidence that taking any of these vitamins will improve your mental health, although there’s at least some evidence that if your mother got enough vitamin D while she was pregant, you’ll be at a slightly reduced risk of contracting schizophrenia. If you’re taking neuroleptics and have tardive dyskinesia, there’s some limited evidence to suggest that vitamin E may stop it symptoms from getting any worse, but that’s something you should probably speak to your doctor about. In general, I don’t see any reason for most people to take supplements of any of these for mental health purposes.

Does anyone in the UK actually get help from the mental health services?

Here’s a comment from Alison, which was originally in response to an earlier post of mine, called 90 Days. I’m quoting it in full, because it highlights the difficulty that I and others seem to have getting anywhere (hope you don’t mind me doing this Alison):

Reading your story is a little like my own. I too have suffered with periods of depression and self harm for a number of years, focussing on the past 4 years which resulted in time off work and endless appointments with my GP. I was referred to someone at the GP surgery who have two visits sent me to a CPN, I waited about 4 months for an appointment with this woman! I saw her twice and was discharged, I too do a good impression of often hiding how I really am, it would seem when I see these people they think I am perfectly normal!

She told me I could self refer and in the new year of 2007 after being back at work about 6 week I realised I was not coping and telephoned her, she asked me to keep a mood diary for a month and phone her back. During that time I had several bouts of wanting to die but did what she asked and called her back. She made me an appointment for the following week, she asked me to see my GP to go back on antidepressants and I did the next day, I was given Mirtazapine.

Days after starting this I went into rapid cycling and knowing the signs I went back to my GP and told him, I felt uncomfortable in the appointment as he had a student with him and when he asked me if I was suicidal I said yes but that I would not act on it. 3 hours later in my lunch break I nearly walked in front of a police car. I went back to work and spend the rest of the afternoon in a daze. My closest friend begged me to go to the hospital but I refused and kept repeating I would be fine.

The next morning a Friday {March 9th a day I won’t forget} on the way to work I couldn’t get the thoughts out of my head that I needed to end the hell I was living in, I went to work dazed and confused and it was during a call {I worked in the council call centre} with a customer that I exploded and lost my temper not only with the customer on the phone but with a manager. The tears came and I walked or rather ran from the building ringing my GP surgery to see someone I needed help and now.

I was chased by the department manager who encouraged me to talk to her and I explained how I was feeling, she drove me to the doctors. My GP seeing the state I was in telephoned the Crisis Team and later that afternoon I was visited by two CPN’s who both mentioned Bipolar. I have suspected I was Bipolar for around 3 years but I didn’t want to admit I was ill. On that day the biggest break through I made was telling my mother what I was feeling, it was the first time I admitted what I was thinking and whilst she has given me some support I still don’t open up and tell her everything.

I was referred to a Psychiatrist {a trainee} who I saw 6 weeks later. I felt patronised and he told me I was Bipolar only because I had read about it on the internet! He was rude and ignorant and didn’t listen to me or anything I mentioned. I left determined to go Private but my friend said she would come with me to my next appointment 12 weeks later. That too was useless he told me I had Bipolar traits but would need to discuss me with the consultant and see me in 8 weeks.

8 weeks turned into 12 and that was 2 weeks ago and I saw someone else, who didn’t seem to know anything about what had gone on and gave me the option of seeing them again or being discharged! I choose to be discharged and am thinking of going back to the CPN who I found partly helpful this year.

I resigned from my job in August after the pressure to return and now I just feel in limbo, no definite diagnosis and no suitable medication. I am and have been sinking into depression again the past few weeks, reluctant to go on AD’s because I hate the way they make the mood swings worse but at the same time I am scared to hit the low points again.

There is not a day goes by I don’t think of death and ways to end how I feel like you I also think the last thing I would do again would cry for help especially when help is usually a waste of space.

Well that’s my story, sorry to bore you!

And then there’s this interesting post, from Fighting The Urge:

The CMHT rang me earlier, they’re not sure if I fit their referral criteria as they are not sure that I am suffering from a “severe and enduring mental illness”.

I told them that my GP wants me to be referred. They said that they cannot accept all GP referrals. I then said that I wasn’t initially referred by my GP, I was initially referred by the duty psych at UCH because I attended A&E. They said that said duty psych refers a lot to ease their conscience.

I asked what would happen now… they said they didn’t know but they would be in touch, but in the meantime to keep the appointment with my GP on Friday and to keep taking my medication.

I said I wasn’t on any medication because my GP wanting me to be assessed by the CMHT and get their opinion before re-prescribing anything.

They said that if I wasn’t taking any medications then I couldn’t be that ill and therefore didn’t require CMHT intervention. I put phone down.

*Slams head against wall*

Ruth

PS. Someone found this site yesterday by searching for “depression cmht cpn” – please don’t use the above post as any indication for yourself!

Regular readers will know my own story, which starts off with me walking into A+E with cuts on my arm and the acute mental health team refusing to see me. I found little help from the psychiatrist I saw, being prescribed citalopram by my GP and ending up in hospital after severing a tendon in my wrist. And currently being pretty much back where I was in January, waiting to see another psychiatrist.

So is there anyone in the UK who does find that the mental health services work at all? Why are these services so useless? I mean, most first-world mental health services are underfunded and understaffed, but they still seem to offer at least some help within a reasonable timeframe. In the UK it seems like these services are just there to scoop people up when they’re making a public enough fuss. Anyone who doesn’t actually have a knife pressed against their own, or someone else’s throat, is presented with delays, refusals and apathy.

Has it always been like this, or have things got worse? How many people die through lack of treatment and care?

Looking at MIND‘s website, (MIND describes itself as “the leading mental health charity in England and Wales”), I see their current list of campaigns includes access to justice, “Ecotherapy – the green agenda for mental health”, independent living, a campaign against budget cuts, improved access to talking therapies. All important issues, but where’s the outrage about what seems to be the actively hostile stance of the mental health system towards would-be service users?

AstraZeneca and Wikipedia: More Edits Uncovered

[Since I’m getting a lot of hits from the Bad Science Blog, I wonder if I can point out this amusing edit from somewhere within the Pfizer network. Clearly Ben Goldacre has fans in Big Pharma.]

So the AstraZeneca edits to Seroquel page on Wikipedia have become a controversy. Turns out there’s more, covering a large number of antipsychotics. We start, however, with PPI’s.

Proton Pump Inhibitors and AstraZeneca

You’d take a PPI if you had gastric reflux or a similar condition. They stop the stomach producing so much acid. AstraZeneca produce a drug called Nexium (esomeprazole) for this. This replaced Losec (omeprazole). Those names sound similar because they’re pretty much the same drug. Chemicals can be right handed or left handed. Omeprazole is what they call a ‘racemic mixture’ – it’s made up of a mixture of left-handed and right-handed omeprazole molecules. Esomeprazole is the left-handed omeprazole molecule: It’s omeprazole with all the right-handed bits removed.

[Note for chemists: Yes, I know this is a simplification.]

Why produce such a thing? The patent on omeprazole expired, allowing other companies to make it. It’s a lot easier (and cheaper) to develop a new drug for market when you’re pretty much already making it.

The other drug in this story is Prevacid (Lansoprazole), already generic in some markets. All three drugs, omeprazole, esomeprazole and lansoprazole are PPIs. They do the same kind of thing. Since omeprazole went generic, they’re all competitors for the same market.

Anonymous Edits to various PPIs by a computer that seems to be on AstraZeneca’s network

Our story starts on the 15th September 2006. Someone using a computer on AstraZeneca’s network (or making it look as if they’re doing so – which would be difficult and without any immediate purpose) takes it upon themselves to make some edits to the pages of these PPIs.

At 02:18, they edit the Esomeprazole page, adding in plenty of information about how it compares favourably to other PPIs.

Eight minutes later, they edit the Lansoprazole page, mentioning that Nexium – the AstraZeneca drug – is better: “Available data comparing the effect of esomeprazole 40 mg and lansoprazole 30 mg once daily on intragastric pH found that esomeprazole provided significantly more effective acid control than lansoprazole.”

Another three minutes pass and they hit the omeprazole page, adding in that: “Esomeprazole 40 mg once daily has been shown to have statistically significantly higher rates of healing EE compared to omeprazole (Prilosec) 20 mg once daily, at both 4 and 8 weeks. Esomeprazole also provided more rapid healing and heartburn control compared to omeprazole.” Remember, omeprazole is generic and doesn’t make much money now, while esomeprazole is still nicely under patent and does.

Wikipedia being what it is, it doesn’t take its more benign users very long to fix things, so all of the edits that AstraZeneca (or the person pretending to be from AstraZeneca) made get reverted. This can’t have pleased our pharmaceutical editor, because they come back to the Lansoprazole page at 18:46, probably the next working day, and put all their information back in. This gets fixed pretty soon afterwards, too.

Things go quiet for a month, then on the 26th October, our user who seems to be from AstraZeneca is back. The esomeprazole page gets touched up again. But things keep getting reverted – maybe these anonymous edits are arousing suspicion.

chrisgaffneymd, come on down!

We move slightly out of the realms of the factual now, to some slight speculation. We focus on a user of Wikipedia calling themselves ‘chrisgaffneymd’.

You can see a list of chrissgaffneymd’s edits here. His first edit, on 12 September was to the Lansoprazole article. Of more interest are the edits, on the same day, to Esomeprazole, in which he adds very similar information to the anonymous user who seems to be from AstraZeneca. We’ll take a look at some of his other edits in due course.

But take a look at his User:Talk page. On Wikipedia, every registered user has a ‘talk’ page, which anyone can edit. It’s a bit like email and a bit like a forum. On this page we see that chrisgaffneymd was blocked from editing on the 15th September, because of edits to the Omeprazole page:

You have been temporarily blocked from editing: see [3], which appears to have been copied from a medical journal. If you wish to make useful contributions, you may come back after the block expires.– The Anome 00:10, 15 September 2006 (UTC)

The anonymous user who seems to be from AstraZeneca turned up, editing the same page (and others) on the 15th September, adding exactly the same information as chrisgaffneymd. Also note the following comments on the talk page from 28th October 2006:

I have explained this before on the lansoprazole talk page to 156.70.222.27 (I believe this is you, as edits by yourself and this IP are nearly identical – if not, I apologize): referencing articles and papers is one thing, adding their content verbatim is another. You are welcome to add relevant, verifiable content in your own words, rather than simply copying content from prescribing information or package inserts (I will gladly provide evidence of this if you wish). Some of your edits have also removed relevant contributions previously added by other editors, while adding unnecessary or overly technical information. If you look closely at my reversion of your last edit to Lansoprazole, you will notice I kept useful additions, such as CYP isozymes involved in the metabolism of lansoprazole and some drug interactions. I hope you understand my reasons for reverting your edits.

On another note, please sign your posts on talk pages by typing four tildes (~~~~) before saving. This prevents confusion as to who said what. Fvasconcellos 00:29, 28 October 2006 (UTC)

Fvasconcellos,

Ahhh … now I understand. However, many of the edits that I provided under the esomeprazole page were valid and not copied (although some – including dosage/indications were derived from the prescribing information … is this information not within the public domain??).

I think we can conclude, with very little doubt that chrissgaffneymd is the anonymous user who appears to be from AstraZeneca.

Disturbing Edits

13th September: A significant edit to Bipolar Spectrum

13th September: A significant edit to Bipolar Disorder

14th September: Rewrites to the Quetiapine (Seroquel) article).

Highlights of this edit include:

Original:

Two rare but serious side effects from quetiapine are neuroleptic malignant syndrome and tardive dyskinesia. However, quetiapine is believed to be less likely to cause [[extrapyramidal system|extrapyramidal]] side effects and tardive dyskinesia than typical antipsychotics.

Changed:

Two rare but serious side effects of atypical antipsychotics are neuroleptic malignant syndrome and tardive dyskinesia. However, Seroquel is the only atypical antipsychotic with an EPS profile that does not differ from placebo. In addition, NMS has never been reported through the AERS reporting system (FDA)

Original:

Weight gain can be a problem for some patients using quetiapine, by causing the patient’s appetite to persist even after meals. However, this effect may occur to a lesser degree compared to some other atypical antipsychotics such as olanzapine or clozapine. Like other atypical antipsychotics, there is some evidence suggesting a link to the development of diabetes, however this remains unclear and controversial.

Changed:

Weight gain can be a problem for some patients using quetiapine, by causing the patient’s appetite to persist even after meals. However, in pivotal clinical trials this effect was (on average) = 1.9kg. Additionally, this effect may occur to a lesser degree compared to some other atypical antipsychotics such as olanzapine or clozapine. Like other atypical antipsychotics, there is some evidence suggesting a link to the development of diabetes, however this remains unclear and controversial.

Original:

There is no reliable data to date regarding abuse of the drug. However, it seems that quetiapine has the potential for misuse due to its sedative effects. Users may crush the pill and insufflate the substance for rapid onset, or ingest multiple times the recommended dose. As individuals react to medicines differently small doses of quetiapine, 50 mg or less, may still cause severe sedation.

Changed:

Based on current prescribing information for Quetiapine Fumerate, this drug does not have the ability to cause chemical dependancy.

14th September: Adds negative information to Apiprazole.

Apiprazole is better known as Abilify. It’s an atypical antipsychotic and a competitor to AstraZeneca’s Seroquel.

Original:

Adverse events reported in the package insert for aripiprazole include headache, nausea, vomiting, somnolence, insomnia, and akathisia. It appears that aripiprazole has a very low incidence of EPS (extrapyramidal side effects). The risk of tardive dyskinesia with prolonged aripiprazole use is unclear.

Changed:

Adverse events reported in the package insert for aripiprazole include headache, nausea, vomiting, somnolence, insomnia, and akathisia. Of particular note is the high incidence of treatment-emergent EPS (notably, akathisia) that occurs with aripiprazole. Recent studies have been able to correlate a high incidence of akathisia to an increased risk for tardive dyskinesia. However, to date, the risk of tardive dyskinesia with prolonged aripiprazole use is unclear.

14th September: Adds negative information to Risperidone

Risperidone (Risperdal) is another competitor of Seroquel.

Original:

Like all antipsychotics, Risperidone can potentially cause tardive dyskinesia (TD), extrapyramidal symptoms (EPS), and neuroleptic malignant syndrome (NMS), although the risk is generally less than for the older typical antipsychotics.

Changed:

Risperidone can potentially cause tardive dyskinesia (TD) and neuroleptic malignant syndrome (NMS), although the risk is generally less than for the older typical antipsychotics. However, Risperidone has been associated with an increased incidence of EPS (when compared to placebo) and therefore may confer a higher risk for TD than other atypical antipsychotics.

14th September: Adds negative information to the Olanzapine article.

Olanzapine (Zyprexa) is another competitor to Seroquel.

14th September: Adds negative infromation to the Ziprasidone article.

Ziprasidone (Geodon) is yet another competitor of Seroquel.

26th October: Adds some marketing to the Quetiapine article.

Seroquel owes it’s #1 Prescribed Status due to it’s powerful tolerability (lack of Metabolic effects as seen with other atypical drugs, placebo-level occurence of EPS (including askithisia)**, decent weight profile, and no changes in serum prolactin or blood glucose.

** = Seroquel is the only agent which can make this claim.

28th October: A further three edits to the Quetiapine article.

And then chrisgaffneymd disappeared…

All this is rather concerning. Not only do we have AstraZeneca (or someone doing a good job of pretending to be them) editing articles on their own drugs, we also have them editing the articles for competitors to these drugs. Had this user not been banned at one point, forcing him to edit anonymously and hence fall prey to wikiscanner, it’s entirely possible his connections to the pharmaceutical industry would have gone unnoticed. How many other users like this are there, editing in their corporation’s interest?

The edits to the articles on bipolar disorder and bipolar spectrum are also concerning; they don’t promote specific drugs, but do promote a specific interpretation of the evidence. There are obvious reasons why it’s a bad idea for pharmaceutical companies to edit publicly-owned information about the disorders and diseases for which they produce drugs.

AstraZeneca have already stated that they’ll be investigating the original Seroquel edits that have been found. Unfortunately for them, it seems the problem is much larger than they originally thought.

[Note for journalists and other media types: If you happen to pick up on this story, a link would be appreciated. Thanks.]

A Sense of Humour: Classifying Mental Illnesses

Depression was, up until the 19th Century, seen as an excess of the melancholic humour. Mania, too much of the sanguine humour. Psychosis Choleric. Catatonia: Phlegmatic. And let’s be clear, these humours of the body weren’t metaphorical, we’re talking about black bile, blood, yellow bile and phlegm.

It’s one system of categorisation. Not a particularly useful one, but a system nevertheless. You know the rest of the story in its vague outlines: Madness, asylums, medicalisation, etc. etc. Leading to the development of the modern categories of madness, as outlined in the DSM and other similar manuals.

Categories are not real. They’re ways of organising information by specific properties. I’m going to take a quick detour via skin disease, we’ll get back to madness in a minute. Let’s take an example: Melanomas are a type of skin cancer. Melanomas are real things; in simple terms they’re a collection of skin cells (melanocytes, to be exact) that grow and divide uncontrollably. The category they’re put into is a way of understanding them. The international classification of diseases (ICD) categorises them as:

Neoplasms – Malignant Neoplasms – Malignant neoplasms, stated or presumed to be primary, of specified sites, except of lymphoid, haematopoietic and related tissue – Melanoma and other malignant neoplasms of skin.

Each subcategory adds information as it becomes more specific. The most important feature is that they’re neoplasms, the next that they’re malignant, and so on. This is useful, because it tells us that malignant melanomas can be treated in similar ways to other malignant neoplasms. Other skin diseases – warts for example – are in another category entirely (viral infections characterised by skin and mucous membrane lesions) despite looking superficially similar. What the ICD cares about isn’t looks, but aetiology – the causes behind the disease.

By comparison, a textbook from 1887 (Treatise on Diseases of the Skin, with Special Reference to their Diagnosis and Treatment by Thomas McCall Anderson) would have classified melanomas like so:

Diseases of the Skin – Organic Affections – New Formations – Epithelioma

For Anderson, the important thing is that it’s a disease of the skin, organic rather than function and involves a new formation rather than an inflammation or haemmorrhage. Warts are in the same category, because they present in the same way.

Both categorisations are designed for a particular use. Anderson’s classification works for a 19th century doctor, trying to diagnose skin diseases; the ICD works for modern medicine. And they are both based on assumptions about what knowledge is pertinent for a given use. All categorical systems do this: That’s what they’re for. The quality of a categorical system depends on the quality of the knowledge that informs it and the appropriateness of the use it’s put to.

I’m done with skin diseases: Back to madness. The ICD classification for bipolar disorder goes:

Mental and behavioural disorders – Mood [affective] disorders – Bipolar affective disorder

Which of the two classifications does this most look like? It’s nothing like the etiological classification for melanoma. The knowledge that informs it is, like Thomas McCall Anderson’s classification, based on what it looks like, not how it’s caused. Which is fair enough, because mental illnesses are famed for having unknown causes. We don’t know how they work, so it would be unreasonable to expect them to be classified that way.

Consider how the categorisation of melanoma allows us to generalise about them: All kinds of abnormal growths (neoplasms) have similar causes: Specific kinds of cells proliferating in an abnormal way. Malignant neoplasms have similar causes: Genes going wrong, which causes the abnormal proliferation of cells. All melanomas have similar causes: Genes going wrong in melanocytes, causing an abnormal proliferation of cells.

The categorisation of mental illnesses does not allow us to do the same thing: Do bipolar disorder and unipolar depression have similar causes? Who knows? For that matter is every case of bipolar disorder caused by the same thing? No clue.

Problems occur when people try to use a 19th century classification as if it were 21st century. Classifications are only as useful as the use they’re put to. Strict diagnostic criteria for malignant melanomas are a good thing. They can look like warts, but a quick application of salicylic acid isn’t going to help. Nor would you want chemotherapy for a verucca. Strict diagnostic criteria for mental disorders are nonsensical: They aren’t informed by the kind of knowledge that can distinguish between conditions that look the same, but present differently. Putting elaborate structures in place to hide this fact isn’t helpful: It informs neither diagnosis nor treatment.

To put it simply: All depressed people are probably not depressed in the same way. We cannot generalise about how depressed people should be treated because when we say “depression” we’re probably referring to a class of diseases that look the same, but have different causes. The same applies to every other mental illness. Most treatments for depression are only slightly effective when measured across a random sample of depressed people; one type of treatment may work for one depressed person, but not another. That’s hardly suprising if they’re different diseases that look the same. No drug is going to be very effective if it’s only targetted at a subset of the people that you think it’s targetted at.

This is why psychiatric treatment is so hit and miss. There’s plenty of psychiatrists who are fully aware of the limitations of their particular branch of medicine, but there’s plenty who aren’t. Diagnosis is fairly subjective, and focusing on sorting people into their correct categories so that you can follow a treatment protocol is useless. The process should be exploratory, like putting a jigsaw together in the dark. You can only feel the edges of the disease based on how it presents: You have to try to fit the edge pieces together to build up a picture of what you’re dealing with and intuit how to treat it.

The categories in the DSM and ICD are better than the four humours, but they’re far more limited and blurry than anyone usually wants to admit. They’re useful, but only when used appropriately and too often they’re not.

Last Night

Last night I was writing about how mental illness is categorised when I heard a noise. My flat is filled with noise at night. The flat upstairs has a leaky overflow pipe. Drops of water fall down and, depending on the breeze, hit my boiler’s overflow pipe. This results in the entire pipe, most of it inside my flat, making a loud clicking noise. There’s plenty of people in the building who get in late at night. Suffice to say that a single noise does not mean that anything’s invade my flat.

So my response of frantically tidying so I could more easily see if there was a creature of some sort here was perhaps not the most rational one. I’d been feeling vaguely agitated all day. My mum had called earler and I ended up ranting about my doctor (while avoiding any mention of my codeine mis-use). And with the sudden burst of activity, my anxiety exploded.

The visual symptoms are the worst bit of it. They got bad enough, possibly for the first time, that it was difficult to read from my monitor. I ended up sitting, curled up, on my sofa as everything devolved into chaos. Every surface was a mess of static. Shimmering lines moved across my field of vision, around a central circle of darkness. My peripheral vision was filled with moving patterns of light. There was a certain amount of dizziness to this. Making sense of anything became harder and harder – too much information to process, too much random craziness to filter out.

After a while, though I’m not sure exactly how long, I managed to get up and turn the light out. This made it worse for a while, the patterns continuing in the darkness, eyes awash with moving lights (mostly red, for some reason). Until my night vision started working, I was horribly disoriented – the sensation of movement in strange directions without any actual movement taking place. Eyes open/eyes shut, it didn’t make much difference. Music running through my head: “Justified candy / brandy for the nerves / eloquence belongs / to the conquerer”.

Lying down, still looking for the invading creature with my shimmering, grainy night-scope eyes. Dawn approaching behind my shut curtains. Disorganised thoughts giving way to sleep for a few hours. Eight AM. Wake up. Fall back to sleep. Nine AM. Wake up. A fly or wasp buzzes around the room. Sudden fear (I’ve been intensely phobic of wasps since I was a child). Just a fly. Hold open window, fly gets confused, smashes into mirror once or twice (the hazards of a visual system based on polarised light), then manages to find the exit. Too jangled to sleep again. Sit up. Drink Pepsi. Smoke cigarette. Vision still mildly screwed up more than normal. An edge of fear. Too many thoughts.

Splitting the Hyper from the Mania

So, I was thinking about some things and it occurred to me that describing my moods as depressed/hypomanic doesn’t really capture how I’m feeling at any particular time. There’s more to it that just “feeling awful” and “feeling great”. I could be wrong, but I think that applies to a lot of people.

I was also thinking about how “mixed state” is a really stupid term. If depression and mania are two distinct states at the opposite end of a spectrum, then mixing the two shouldn’t be possible, but lots of people seem to experience them. And this also implies that the classic single axis description of depression/mania isn’t capturing the whole story.

Frankly I’d be amazed if nobody’s suggested this before, but I can’t remember seeing it.

The classic axis goes:

depressed ---- normal ---- hypomanic ---- manic

But I can feel awful and be rather hyper at the same time. I can feel good and not want to do much. So maybe by splitting out depression/happiness from calmness/hyperness, things would make more sense:

psychotic|
         |
         |
agitated |
         |
         |
calm     |
         |
         |
apathetic|
         |_________________________________________
          dysphoric -- unhappy -- happy -- euphoric

In which case, we can fill in some labels:

psychotic|
         |  mixed state                       mania
         |
agitated |       anxiety/akathesia  hypomania
         |         
         |
calm     |           dysthymia   euthymia
         |
         |  depression
apathetic|
         |_________________________________________
          dysphoric -- unhappy -- happy -- euphoric

I’m still without a working computer mouse, which is why these graphs have been presented in mangled text graphics rather than the customary classy graphics. Please imagine each label as a hazily defined area, rather than a point.

Obviously this is completely free of any actual evidence, but this kind of graph makes more sense to me than picking a point on a line. I’d write ‘blissed out’ in the right hand corner, but that would make it look so much less scientific and I’m all about the pseudoscience.

If I’ve missed the stunningly obvious scientific work that I’ve been doomed to recreate badly, please let me know; other thoughts and comments are welcome.

Anti-psychopharmacology

I always find my blood pressure rising when I read anti-psychopharmaceutical websites and blogs. The two I’m most familiar with are Seroxat Weblog and Seroxat Secrets. I’m not entirely unsympathetic to some of their premises: I think pharmaceutical companies have often distorted and with-held important evidence about side-effects and often engage in questionable marketing techniques. But I find their conclusions to be deeply bizarre and their methodology to be relentlessly hypocritical.

The rational response to the problems with pharmaceutical companies would be to campaign for better regulation of pharmaceutical companies, the imposition of limitations on the way they market their products, and the introduction of legislation that requires pharmaceutical companies to disclose the results of all studies that they fund.

The irrational response seems to be to spread any negative story and opinion about pharmaceutical companies and their products, regardless of how accurate or reliable it may be. This is the hypocricy: When you’re claiming that others have distorted evidence and engaged in duplicitous marketing you should not then turn around and do the same thing from the opposite point of view.

The lesson to be learned from the controversies surrounding the pharmaceuticals industry is that all data should be examined critically. What the anti-psychopharmaceutical campaigners fail to realise is that this also applies to the data that supports their position. The ideal situation is not one where drugs are outlawed because they have potentially serious side-effects and controversial levels of effectiveness, but one where the information about side-effects and effectiveness is reliable enough for doctors and patients to make informed decisions.

All this doesn’t annoy me quite as much as the fact that by taking these extreme positions, these people actively undermine their own arguments. Frankly, reading this kind of thing makes me want to side with Big Pharma. At least Big Pharma has a financial motivation for doing the less patient-centred things it does, whereas the people who claim to be fighting against it seem to be motivated mainly by the fact that their own experiences have been negative and therefore these drugs are evil.

Hospital Worker Hates Borderlines

I tend to look through the Tag Surfer here at WordPress when I’m bored (for those of you without WordPress blogs, it’s a nifty little gizmo that finds blogs with specific tags). Since I started writing about sleep I’ve been seeing a lot of posts from extremely tired parents with young children. I also see lots of posts about depression from well-meaning people who really don’t have a clue. (“Go for a walk and enjoy the sunshine! You’ll feel happier!” etc.) A lot of these seem to be from Christians, but then certain parts of Christianity get really confused about mental health issues.

I decided a week or two ago that when I see particularly annoying posts, I’m not going to let them drift by as I have before. So here we have the first of these. Surprisingly, it’s not from a Christian and it’s not about depression. I present to you: Are Borderline Personalities nuts? from Antagony of Words by S.. Antagony is a twenty-something American woman who works on a psychiatric ward. I’ll quote highlights of her post here.

Everyone involved in my personal life knows that I find Borderlines to be the bane of my existence. I simply loathe them.

My, what a professional attitude.

Most of my enjoyment comes from completely ignoring Borderlines. Sick and twisted? Perhaps. But, I like to call it a little dose of reality. For those of you that don’t know, when you first meet a Borderline, they typically come off as normal, almost likable. Generally, the traits don’t start to come out until a moment of chaos. And then they just sort of seem to stick.

Again, how professional. Let me get this right. There’s a group of patients who you work with who often seek attention. When they don’t get this attention they have a tendency to turn to riskier ways of seeking it out (see below), which can be potentially fatal. And you derive enjoyment from denying them attention and pushing them towards those riskier strategies? Am I missing something here or does that make you really sick?

At this point is where you factor in the widely known classic Borderline behavior of self-mutilation. A sad, sad cry for attention. Admittedly, part of my view on the self injurious behavior (SIB in the hospital world) when it comes to the Borderline is clouded by personal bias.

SIB, for those that don’t know, are completely different and separate than suicide attempts. Also to be noted is that people who engage in SIB are not always Borderlines, just as Borderlines don’t always engage in SIB.

Typically the Borderline who engages in SIB for attention, will cut, stab, insert foreign object beneath their skin. Almost always worse looking than it actually is, the injuries are typically surface wounds. Though, sometimes there could be a slip and the “attention wound” does become fatal.

No dice. Anyone who’s self-injured much is well aware of how to do it safely. It takes effort and determination to sever anything important. If someone’s cutting purely for attention then there’s no chance at all that they’ll injure themselves severely. You don’t like these people, therefore it’s for attention. Because if they really were cutting out of emotional distress that’d make you a horrible person, wouldn’t it?

One of the most irritating Borderlines I’ve ever met was a woman who spent months on my floor. We all hated her. […] When none of her other behaviors worked, she would just come out and say, “Would you just look at me? Just once?” […] I’m not quite sure if I would’ve preferred her to just do SIB and get it over with. Though, the fact that she didn’t definitely saved us a lot of trouble.

Borderlines of America: The staff would rather you cut yourself than they actually had to look at you.

To get back to the original question at hand, some people would call Borderline Personalities nuts. I call them annoying. There is no denying that there is a serious mental problem involved, but you can’t treat a personality. And so, Borderlines… just are.

Marsha M. Linehan must feel like she’s wasted her career.