Yesterday was the Manager’s Hearing I had been asking for on many occasions as Nearest Relative. You will not be surprised to learn that I was completely ignored as I have been for months on end by the Mental Health Office. It could be that the MHA office are told my only point of contact is as Carers Champion but what right do a MHA office have to ignore you as Nearest Relative who has called for a Manager’s Hearing. A full investigation needs to be undertaken.
I have had another patronising ticking off by the person who is said to be a “carers champion” in that I am supposed to go through her for everything. However this is just like a messenger service where you get no answers and the RC above has been one of 3 who have avoided S17 leave and a junior Dr is then put in charge of a meeting because the RC does not have the time of day for you. Therefore you do not get treated fairly. It is just delaying tactics.
I have found out that a capacity assessment was carried out on Elizabeth without her knowledge by a nurse called G only recently.
Clearly noone wanted me to attend yesterday’s manager’s hearing so what they did was they worked together putting up barriers and perverting the course of justice legally as I as Nearest Relative would be entitled to have a manager’s hearing but instead this was done behind my back and the only reason I knew about it was because Elizabeth told me even down to the time it was taking place and I had been invited by her.
There is such ignorance or blatent disregard to the MHA under Ash Villa it makes this facility not fit for purpose.
The other thing is that Elizabeth has shared with her family her care plan.
From reading this disturbing care plan is revealed the hopelessness of her situation in this dreadful institution – the worst we have ever come across and NHS run. There is no respect for carers and there is no respect for the patient and her life is at risk and I want everyone to know about it as Elizabeth has actually said she is going to die in there.
Time and time again we have asked for CQC intervention at this facility and nothing is ever done. They are due an inspection. I fear that this facility is unsafe. I have now turned to my MP, Victoria Atkins and Healthwatch Lincs. The matter is being passed on to the DoH.
The whole situation has led to me becoming very ill, to the point I cannot visit right now. Thought I had covid but yesterday’s test was negative so it must be flu but this is the effect on you as a carer when you read the care plan that highlights ambulance and fire brigade notified due to her being bariatric and high risk of mortality. They are also missing the point about takeaways – deprived of exercise and meaningful contact with family Elizabeth could be held prisoner under the MHA on the say so of completely unaccountable professionals for years and years on end – a prisoner deprived of all human rights under LINCOLNSHIRE PARTNERSHIP TRUST and what on earth is happening about our complaint? If someone is in bed all day trying to keep out of the way that person is missing meals anyway and if that vulnerable person happens to get up in the night and dares to ask for a drink then they get callously told to get back into bed. I have been subject to severe bullying to the point where a member of staff tried to say I had assaulted a member of staff and in a letter by ward manager accused of threatening behaviour and now I want everything on me under GDPR rules. I have now had to apply for all CCTV footage to clear my name – what could have justified 3 x police cars coming out? I was standing beneath CCTV cameras alone at the time. Not for the first time, this facility whose professionals completely lack communication skills resort in bullying tactics using the police as if they are not busy enough. Anything to blacken your character that is how bad it is and I would welcome a full enquiry.
It was a big mistake coming to this area thinking that MH care would be good and for a long time I kept quiet, not wanting to rock the boat. Right now I couldn’t care less any more as I want something done about the situation before it is all too late now that I have seen the extent of risk to my daughter’s life. There are too many cases of people dying in these institutions who deprive patients of basic human rights and exercise leaving them to go downhill.
What was decided at the Manager’s Hearing was to raise medication to 400 mg near maximum with complete disregard to the fact that Elizabeth is of high risk of mortality and adverse reaction as proven by genetic tests P450 liver enzyme. Even Cygnet respected this certificate but there is no respect at Ash Villa – a hospital that destroys lives.
I am now going to share with you some disturbing but educational information. Elizabeth now said to have no capacity in a capacity assessment conducted by nurse G.
sent: Tuesday, May 24, 2022 1:28 pm
To: susanb ; Subject: Re: Managers hearing
You might be interested in the contents of this lecture, especially from slide 38 which explains the duties of Health Informatics Professionals.
As NR and with Elizabeth’s written consent you are entitled view the capacity report which must give full reasons for the decision on capacity.
Capacity is a legal construct and not a medical one. As Elizabeth’s NR you can challenge the capacity report. See the Bournewood case (also attached).
Subject: Dosing and P450 metabolism
Very important paper on poor metabolisers
“If a patient on psychotropic medication develops symptoms of delirium or of akathisia, every psychiatry textbook I have been able to identify advises dose reduction or change of medication to one more suited to the patient. The problem occurs on change of dose up or down and has been associated along with other extra pyramidal side effects, as well as sensitivity”
“The half-life of the zuclopenthixol depot preparation is 19 days, so if it is given fortnightly, toxicity will eventually develop”.
it is clear that Ash Villa staff have no idea about dosage and blood serum levels. they appear to be working on dosing regimes 20 years out of date
Clinical Case Studies and Reports
Clin Case Studie Rep, 2018 doi: 10.15761/CCSR.1000112 Volume 1(2): 1-8
The effect of CYP450 2D6*4 mutation on medication
response: Two cases with different outcomes
Forensic and medico-legal psychiatry, Pharmacogenomics and Personalized Medicine, Level 5, 203-233 New South Head Road, NSW 2027, Australia
This paper describes different outcomes for genetically similar persons bearing the mutation CYP450 2D6*4. They were treated with the same drugs; their condition
was called “schizophrenia” and in both cases the exclusion criterion essential for that diagnosis was ignored
*Correspondence to: Yolande Lucire, Forensic and medico-legal psychiatry,
Pharmacogenomics and Personalized Medicine, Level 5, 203-233 New South Head
Road, NSW 2027, Australia, Tel: 0411158246, E-mail: firstname.lastname@example.org
Received: August 07, 2018; Accepted: October 25, 2018; Published: October
Substance/general medical condition exclusion: The disturbance is
not due to the direct physiological effects of a substance (e.g., a drug of
abuse, a medication) or a general medical condition .
These cases support the notion that treatment of cannabis-induced
disorders with drugs that have been tested for schizophrenia and
bipolar illness may be counterproductive .
The paper highlights a need for doctors to diagnose to the criteria,
and to be aware of (a) the DSM decision tree for the differential
diagnosis of hallucinations, (b) the principles of pharmacogenetics, (c)
the high prevalence of diminished metabolic capability for cytochrome
P450 metabolised drugs, and (d) symptoms of neuroleptic toxicity,
including akathisia [3,4]. It points to the need to seek advice from
pharmacologists and pharmacogeneticists and not from peer clinicians
who may also lack relevant expertise.
C, 33, a university graduate, intermittently employed, had mild
brain injury at birth and chicken pox encephalitis at 20. (Brain
injury can cause akathisia and remains a risk factor for akathisia .
He smoked cannabis rarely. He was unable to say why he had been
prescribed fluvoxamine by his general practitioner (GP). He soon
developed a variant of erotomania (a side effect of all serotonergic
antidepressants, reported thus in the Physicians’ Desk Reference) in that
he became preoccupied with a former girlfriend, ruminating on what
might have been had he married her. He also harassed a friend of the
former girlfriend, driving in his street and breaking windows .
Charged with a stalking offence, he presented for an s32 report
under the NSW Mental Health (Criminal Procedure) Act 1990 that
encourages diversion from the criminal justice system of persons
suffering from a mental illness or condition. He was diagnosed with
“paranoid schizophrenia,” by his account in a 20-minute interview.
Olanzapine was added to fluvoxamine and when he became increasingly
depressed, restless and violently suicidal it was increased to 30 mg
daily while fluvoxamine was increased to 200 mg, and he continued to
deteriorate. Zuclopenthixol depot was added to 200 mg fortnightly and
cigarette smoking increased to 40 a day. There was no improvement
in his behaviour, so he was imprisoned on a certificate that called his
illness schizophrenia but held him responsible for his actions .
On release, he continued to drive obsessively in his quarry’s street
(indicative of both organic obsessional disorder and erotomania) and
was about to be imprisoned again on his treating psychiatrist’s certificate
attesting to his intentionality, when he made a suicide attempt and was
hospitalised with deep vein thrombosis . He had 35 mg diazepam
daily added but it gave no relief. Warfarin was added to the above for
the deep vein thrombosis. Zuclopenthixol was suspended in hospital.
The author diagnosed akathisia and erotomania and wrote a Section
32 report, and this avoided his receiving a second prison sentence. Four
years later, fully recovered, on no medication and showing no sign of
schizophrenia and working in three jobs, C described his mental state
at that earlier time:
I figured I had nothing to live for. I was feeling like I had no future
and I did not want 40 more years of this. I thought of hanging myself or
slashing my wrists. I do not know how often. I also thought of crashing
into a truck or jumping in front of a train. I was never suicidal before I
had fluvoxamine. I smoked heaps.
I had the injection because I thought it would keep me out of jail.
I could not sit and read, I could not focus on anything, I was restless,
and I could not sit down. The last five days in jail were hard. I could not
sleep at all, that carried on after I went out of jail. I could not do anything,
could not sit down and watch TV. I had to get up and pace around, a
hundred times a night. After I got out of jail, the world completely
changed. Home to me has always been a haven. For those eight months,
I had hell inside.
On legal advice, the author advised C’s mother that three
psychiatrists, one of whom was a personal friend of C, shared her view
that he had did not have schizophrenia or anything like it. His mother
researched akathisia on the Internet and requested a change of doctor
in view of a total breakdown of the doctor/patient relationship.
Lucire Y (2018) The effect of CYP450 2D6*4 mutation on medication response: Two cases with different outcomes
Clin Case Studie Rep, 2018 doi: 10.15761/CCSR.1000112 Volume 1(2): 2-8
Frustrated by administrative inaction, the mother made a
complaint to the Medical Board of NSW (MBNSW), which declined to
investigate it. However, the Board chose instead to pursue the author for
holding this allegedly minority view through a Professional Standards
The PSC found the author to have “inappropriately” destroyed
the mother’s confidence in the treating doctor, notwithstanding that
the mother gave evidence that she and her son had none. The author
was criticised for having insufficient respect for the diagnoses of her
colleagues and this was based on peer reviews, of peers who did not
acknowledge product information (PI).
The PSC unilaterally, without giving notice, decided to publish its
report where no such PSC matters had ever before been publicised. The
author was publicly humiliated as having “insufficient knowledge” and
as lacking respect for her colleagues’ diagnoses. This decision was based
on the author’s holding what the PSC considered to be a “minority
view” concerning antidepressant side effects and interactions, even
though four files of evidence that antidepressants induced psychosis
and suicide in some people were provided, together with PI and
relevant public health advisories. The MBNSW recommended that the
author seek the counsel of a colleague. The decision was misreported
in The Sun Herald to the effect that the author had been “ordered into
treatment by the Medical Board”.
C was allowed to reduce all his medications slowly. Four years
later, C works in three jobs and shows no signs of schizophrenia. He is
stigmatised by his criminal record and traumatised by the experience of
the painful mental state of some duration, but relieved to know that he
had suffered from a medication side effect rather than a mental illness.
While a 16-year-old schoolboy in 2004, smoked cannabis, used
other illicit drugs and experienced hallucinations. He was prescribed
risperidone and deteriorated . Olanzapine was added at both
variable and increasing doses. This produced worsening depression
and continuing hallucinosis. Fluvoxamine was added, and he became
Soon added in series and parallel were benztropine, haloperidol,
chlorpromazine, lithium, risperidone and its depot, consta, quetiapine;
previously ineffective treatments were recirculated in escalating doses.
Patient A remained violently akathisic, intensely suicidal,
aggressive and intermittently homicidal. He was seen tramping along
the motorway at night in the rain before he made a homicidal attack on
his stepfather in 2005. He spent four months in an interstate clinic. He
assaulted his psychiatrist in January 2006 and was imprisoned.
He made many suicide attempts and repeatedly complained that
his medication made him feel suicidal. His unremitting death wish was
recorded as “I cannot function on this medication. It makes me want to
kill myself ”. He continued to smoke cannabis, insisting it helped him,
and his tobacco use increased .
Zuclopenthixol depot was reinstated in prison at 400mg fortnightly
in the face of his protests and history. After his release it was increased
to 600 mg on one occasion and enforced by a Community Treatment
His penultimate suicide attempt from a cliff a day after his release
from hospital on a CTO caused police to return him to hospital where
the diagnosis of schizophrenia was amended to “antisocial personality”.
Two days later and after 4 years of treatment, he was found dead at the
bottom of the same cliff, in December 2006. No root cause analysis was
provided for the relatives.
The coroner gave the author very limited access to clinical records
and treatment sheets and refused permission to make copies. He
determined, on a report from police, that A had not committed suicide
at all but had been “skylarking”. On that basis, he declined to hear expert
evidence prepared for an inquest and did not respond to a suggestion
that genetic testing for CYP450 activity was needed. The issue of the
coroner perhaps having a conflict of interest was raised with both the
Chief Coroner and the Judicial Commission because, as a magistrate,
the coroner had previously been involved with A and because he was
involved with that health service on a daily basis. Both found that no
CYP450 testing revealed that both patients had a “null” metaboliser
gene 2D6*4 (in the case of A, after exclusion of his parents’ genotypes).
Both had received multiple interacting drugs that compete for
CYP450 2D6, a metabolising resource that is finite and may be limited
by genotype or P450 inhibitors or other health problems. When
a metabolic pathway is already in limited supply, lower doses are
recommended because the drug is likely to reach blood levels above the
“therapeutic window of opportunity’ for each drug” .
Both polypharmacy (endemic in Australian psychiatry) and the use
of higher than recommended doses are counterproductive. Akathisia
and other organic neurotoxic states supervene, and patient does not
recover. Standard doses of a single substrate accumulate in diminished
metabolizers and lead to blood levels higher than the therapeutic
window. The concurrent use of Cytochrome P450 inhibitors hastens
that process. More frequent dosing than permitted by the half-life of
each drug results sooner or later in neurotoxic state and hallucinatory
Both C and A were taking, simultaneously, several drugs requiring
the 2D6 pathway, in larger than recommended doses: olanzapine at 30
mg daily is 15 times the normal starting dose, fluvoxamine 200 mg is
4 times, zuclopenthixol injections at 600 mg fortnightly is 8 times the
standard dose. Eli Lilly does not guarantee the safety of olanzapine over
The notion that patients who have not responded to antidepressants
are ultra-rapid metabolizers (UMs) underpins the practice of increasing
a medication or adding another. However, it is many times more
likely that such patients are poor (PMs) or diminished metabolizers
(DMs), and as such need to have the dose decreased. From 5% to 14%
of Caucasians are PMs of 2D6 and a further 20% have diminished
metabolism. PMs may experience potentially lethal side effects within
days, whereas the slower metabolism of intermediate metabolizers
(IMs) causes a slow build-up of blood level while the chemistry of the
brain tries to follow. Rapid changes of psychoactive substances cause
violent mood and behavioural shifts, confusion and delirium in IMs.
UMs comprise only 1-10% of Caucasians .
If a patient on psychotropic medication develops symptoms of
delirium or of akathisia, every psychiatry textbook I have been able to
identify advises dose reduction or change of medication to one more
suited to the patient. The problem occurs on change of dose up or down
and has been associated along with other extra pyramidal side effects,
as well as sensitivity.
Lucire Y (2018) The effect of CYP450 2D6*4 mutation on medication response: Two cases with different outcomes
Clin Case Studie Rep, 2018 doi: 10.15761/CCSR.1000112 Volume 1(2): 3-8
Akathisia is a subjective desire to be in constant motion. A
manifestation of drug sensitivity, it may be confused with psychotic
agitation and incorrectly treated by increasing the dose of the offending
medication. The symptom subsides promptly when the offending
medication is discontinued and replaced by another one better tolerated
by the patient .
The subjective distress resulting from akathisia is significant and
can lead to non-compliance with neuroleptic treatment. Akathisia may
be associated with dysphoria, irritability, aggression or suicide attempts.
Worsening of psychotic symptoms or behavioral dyscontrol may lead to
an increase in neuroleptic medication dose, which may exacerbate the
problem. Akathisia can develop very rapidly after initiating or increasing
neuroleptic medication .
Substrates of 2D6 also include tricyclics, tetracyclics, amphetamines,
chlorpromazine (which has other pathways as well), fluvoxamine,
haloperidol, risperidone, quetiapine and, in part, olanzapine.
Cannabis, involved in both these cases, is metabolised by
cytochromes 3A4, 2B6 and 2C9. It is an inhibitor of 3A4 and induces
1A2. It remains in the body for up to 2 months, depending on the
amount used. Like tobacco, which induces IA2 and caffeine induces the
metabolism of psychiatric drugs as well as producing is own euphoric
neurotoxic state [15,16].
Pharmacogenetic theory and data provide an arena in which
adverse drug reactions can be explored, understood, theorised and
ultimately predicted . The development of pharmacogenetics has
ushered in a paradigm shift of massive proportions in medicine and,
particularly, psychiatry. It is predictable that this shift is resisted .
Pharmacogenetics has featured in American textbooks of psychiatry
since 1999, but it has not been taught in Australia until very recently
. Australia is the last of the U.K., Canada and the U.S. to inquire
into the potential of pharmacogenomics, by means of a report that,
unaccountably, expects a lead period of 10 years to full implementation
. “One size does not fit all” appears to be its theme.
Delay in implementing this education will result in more hospital
admissions for adverse drug events, already a major source of costs
in the U.S., as well as prolonged stays, misdiagnoses and unnecessary
deaths and medication-induced suicides and homicides [21-24]. No
psychiatrist can practise safely without this knowledge.
It may be that lack of this knowledge accounts for psychiatry’s
insatiable demand for resources, and for the increasing suicides, suicide
attempts, homicides and violence committed by patients under mental
health care [25,26]. Providing more resources for psychiatry without
questioning the source of this epidemic of seemingly intractable mental
ill health is unlikely to resolve the problem [27,28].
Nearly 90% of drugs are metabolised by the cytochrome CYP450
family of enzymes, 1000 enzymes determined by 40 genes . They
transform “exotoxins” into products that can be metabolised further
(stage II metabolism) and prepared for excretion by the kidney or
liver. Diminished capacity to metabolise drugs results in blood and
brain levels above the sometimes-narrow therapeutic window. These
concentration-dependent adverse effects manifest as neurotoxic
Drug Therapeutic window  Metabolism/transport site Enzymes/process inhibited Enzymes Induced/
chlorpromazine 30-300 ng/ml 2D6, 1A2, 3A4, UGT1A4, UGT1A3 2D6a
clomipramine 175-450 ng/ml 1A2, 2C19, 2D6, 3A4 2D6, 1A2, 2C19
cannabis 3A4, 2B6 and 2C9. 3A4 1A2 and 2E1
carbamazepine 6-12 μg/ml 3A4, 2B6, 2C8, 2E1, 2C9, 1A2, UGT2B7,
ABCB1 ?2C19 3A4, 1A2, 2B6, 2C8, 2C9,
clonazepam 20-40 ng/ml 3A4, acetylation
clozapine 350-600 ng/ml 1A2, 3A4, 2D6, 2C9, 2C19, FMO3 2D6c
diazepam 300-400 ng/ml (incl. metabolites) 3C19, 3A4, 2B6, 2C9, glucuronidation
doxepin 50-150 ng/ml 1A2, 2D6, 2C19, 3A4, UGT1A4, UGT1A3 1A2, 2C19, 2D6
fluphenazine 0.5 – 2 ng/ml 2D6a, 1A2 2D6a, 1A2
clopixol >2 ng/ml 2D6
fluvoxamine # 150-300 ngms/ml 2D6, 1A2 1A2a, 2C19a, 2B6b 3A4b, 2D6b, ABCB1
haloperidol 5-17 ng/ml 2D6
lithium 0.5–1.2 mmol/l
lorazepam 10-15 ng/ml UGT2B7, ?other UGTs
half-life 21-54 mean 30 hrs. 9-25
1A2, 1A4 partly by 2D6 and UGT3A4,
UGTs, ABCB1 None known
paliperidone # ? 2D6, 3A4 None known
perphenazine 0.6 – 2.4 ng/ml 2D6, 3A4, 1A2, 2C19 2D6, 1A2
quetiapine # 70-170 ng/ml 3A4, sulfation, ABCB1
risperidone 20-60 ng/ml (including 9-hydroxy) 2D6, 3A4, ABCB1 2D6b
risperidone consta ditto ditto ditto
temazepam UGT2B7,? other UGTs, 2C19, 3A4
valproate 50-100 μg/ml Complex: 2C9, 2C19, 2A6, UGT1A6, 1A9,
2B7 2D6, 2C9, UGTs, 1A4, 1A9, 2B7, 2B15, epoxide
zuclopenthixol 4-50 ngms/ml 2D6 ? 2D6 (European drugs are less well researched than
those used in the U.S.)
Table 1. Drugs metabolic pathways, inducers and inhibitors (of drugs used in these cases) from several sources 
a Potent inhibition of enzymatic pathway. b Moderate inhibition c Mild inhibition. Inhibition is also dose-related; mild inhibitors in high doses act as strong inhibitors. # Not licensed for use
in children or adolescents by the United States Food and Drug Administration (FDA) or its Australian equivalent, the Therapeutic Goods Administration, (TGA.
Lucire Y (2018) The effect of CYP450 2D6*4 mutation on medication response: Two cases with different outcomes
Clin Case Studie Rep, 2018 doi: 10.15761/CCSR.1000112 Volume 1(2): 4-8
brain syndromes. Many psychiatric patients are prescribed more than
one drug, with each drug increasing the risk of a pharmacokinetic
interaction. Table 1 shows metabolic pathways inducers and inhibitors,
and it has been brought up to date from primary sources.
There is an argument that patients would benefit from CYP-based
genotyping prior to the prescription of these drugs. Up to 79% of
islanders from around Vanuatu have PM status at 2C19 and around
25% of Caucasians have “diminished metabolism,” at 2D6, and for
them a drug metabolised by that pathway is likely to be or becomes
problematic and might be lethal . East Asians have a 50% prevalence
of the IM gene P2D6*10, as well as up to 35% prevalence of the PM
gene 2C19*2, putting that population at a huge risk from antidepressant
therapy. Testing for CYP450 2D6, 2C19 and 2C9 costs less than $150.
Basic knowledge of the ethnicity-based prevalence of mutations
is essential to counter a common belief among psychiatrists that
worsening depression and suicidality in a patient indicate a lack of
response, and that the patient is therefore a UM. Such reasoning leads
to more and more medication being given. In fact UMs are rare, often
cited in Caucasian populations as 3%.
Most adverse drug reactions occur as a result of simple over-dosing
of genetically normal persons whose cytochrome metabolism has been
inhibited or induced, leading to undesirable bloods levels. There are six
patterns of drug–drug interactions and some are described below .
The first effect of making testing available might be to make prescribers
aware that adverse drug events are both explicable and avoidable.
Conditions affecting metabolism include co-prescribed medications
that induce or inhibit the enzymatic pathways, age, nutrition, stress,
liver disease, hormones (natural and extraneous), the sequence in
which medications have been prescribed or taken away, the route of
administration, the range of half-life in any population, the potential for
multiple metabolic pathways, the size of the therapeutic window within
which the drug may be effective and outside of which it is ineffective or
toxic or both, the duration of therapy and duration of inhibition which
may persist after discontinuation . This paper does not deal with the
genetics of transporter and receptor systems.
3A4 is the “workhorse” of the P450 system, which means that
many drugs are substrates of it, and there are many inhibitors and
inducers. There are no PMs but there is 10–30-fold variability in the
efficacy of its functioning. 1A2 metabolises psychiatric drugs and is
induced by tobacco smoking, which also hastens the metabolism of
other psychiatric medicines not known to be metabolised by these
cytochromes. This seems to explain why patients on psychiatric
medications increase their tobacco use: to more quickly metabolise
medicines that have unpleasant or intolerable adverse effects.
Information grows and changes daily. All three are involved in the
metabolism of common antidepressants and antipsychotics .
Table 2 is compiled from research done by health insurers Blue
Cross Blue Shield who have found such testing to be cost effective. The
table lists the effects of genetic polymorphisms of CYP450 enzyme genes
on drug metabolism and describes relationships between genotype and
phenotype, as relevant for psychiatric drugs, many of which inhibit the
enzymes required for their metabolism [37-39].
A more useful concept adopted by the Diversity Health Institute
(DHI) at Cumberland Hospital is to describe both PMs and IMs as
having “diminished CYP 450 metabolism”. This is because the inhibition
or absence of one cytochrome may divert into metabolism by others,
which may or may not be available in any given individual. There can
be 1,000% variance in the metabolism of 2D6 drugs between PMs and
UMs and a 30-fold variance in metabolism by the enzyme cytochrome
Metaboliser status Metaboliser
status Genotype Phenotype Expected drug effects Prodrug concerns
2D6 2C9 2C19 2D6
(poor) *3, *4,
*5, *6, *7, *8,
*11, *15, *19,
*2 and *3
PM Homozygous or
for deficiency alleles.
“Standard” doses may lead
to toxic drug concentrations
and serious adverse reactions,
including suicide and
homicidal behaviours .
May not reach therapeutic levels of
active drug, i.e. does not convert
prodrugs into the analgesic morphine, so
they are ineffective. Conversely removal
of a 2D6 inhibitor may lead to rapid
conversion and toxicity and death (the
Heath Ledger phenomenon)
*9, *29, *36,
*1 and *2
two reduced activity
enzyme genes alleles
or heterozygous for an
inactive allele and a
reduced activity allele.
These may become PMs or
diminished metabolisers in the
presence of specific inhibitors.
A reduced dose of a single drug
is recommended, and IMs are
unable to metabolise multiple
drugs requiring that pathway.
Higher doses may lead to toxic
May experience some consequences
*1, *2, *35
Two copies of active
enzyme gene alleles.
Up to 80% of EMs at 2D6
become PMs in the course
of treatment with strong
inhibitors such as paroxetine
, fluoxetine and sertraline
and with mild inhibitors in
Standard doses lead to
expected drug concentrations
Expected response to standard dose.
Only 2D6 has
More than two active
copies of active enzyme
May not reach therapeutic
levels of active drug due to
May reach higher than expected
concentrations of active metabolite,
which may cause adverse reactions,
including death from morphine.
Notes: Genotype refers to the genetic makeup of the subject; phenotype refers to the way that the genotype manifests under a variety of conditions .
PM = poor metabolizer; IM = intermediate metabolizer; EM = extensive metabolizer; UM = ultrarapid metabolizer. Prodrugs such as tramadol, oxycodone, codeine need to be activated,
i.e. catabolised to morphine by 2D6.
Table 2. Genotypes phenotypes and predictions
Clin Case Studie Rep, 2018 doi: 10.15761/CCSR.1000112 Volume 1(2): 5-8
Mutation P450 2D6*4 was found in more than one third of 30
persons tested at the author’s request because they had experienced
severe violent akathisia, suicidal behaviours, homicidal aggression,
behavioural dyscontrol, delirium with hallucinosis, and cognitive
impairment on standard doses of antidepressants (to be reported
elsewhere). The most publicised of these is Melbourne mother and
student Rebekah Beddoe, who published her harrowing account of
three years on antidepressants and antipsychotics, prescribed and coprescribed
by psychiatrists who failed to recognise her problems as side
Drugs relevant to these two cases
Side effects are listed in each drug’s PI, easily accessible through the
website of the U.S. FDA . PI published in the U.S. is substantially
larger and more detailed than that available in Australia. It categorises
“frequent” adverse events as occurring in at least 1/100 patients,
“infrequent” events as occurring in 1/100 to 1/1000 patients and “rare”
events as occurring in less than 1/1000.
By that standard, in clinical trials that were presented to the U.S.
FDA to get olanzapine licensed, death and suicide on olanzapine
occurred at a rate of 1 in 208, which is “rare.” No deaths occurred on
placebo. Khan et al. counted the suicides in antipsychotic trials 2001
but this paper failed to alert the psychiatric community .
A rate of 27% akathisia in a trial of olanzapine 10 mg was balanced
by an equally high incidence of akathisia on placebo . This
indicated that Eli Lilly either did not know what they were talking
about (as akathisia is always a medication-induced phenomenon), or
the participants had not fully recovered from whatever they had been
taking before entry to the trial. This been the subject of successful
litigation for fraudulent promotion of olanzapine, such as USA vs. Eli
Lilly which rewarded the whistleblowers with US$800 million .
The half-life of olanzapine ranges from 21 to 54 hours (5th to 95th
percentile; mean of 30 hr), and apparent plasma clearance ranges from
12 to 47 L/hr (5th to 95th percentile; mean of 25 L/hr). This means
that sooner or later more than 50% of users will become toxic on it if
the dose is not reduced. The half-life and clearance of olanzapine varies
among individuals on the basis of smoking, status, gender and age.
According to Eli Lilly Australia the therapeutic window of
olanzapine is 9-25 ngm/ml, but other figures are mentioned elsewhere
In drug company terms, “frequent” refers to adverse events affecting
more than 10% of users. The following effects are listed in the 2007
Olanzapine PI. (Olanzapine is licensed for bipolar disorder.)
Nervous System — Frequent: abnormal dreams, amnesia,
delusions, emotional lability, euphoria, manic reaction, paresthesia and
Infrequent: akinesia, alcohol misuse, antisocial reaction, ataxia, CNS
stimulation, cogwheel rigidity, delirium, dementia, depersonalization,
dysarthria, facial paralysis, hypesthesia, hypokinesia, hypotonia,
incoordination, libido decreased, libido increased, obsessive compulsive
symptoms, phobias, somatization, stimulant misuse, stupor, stuttering,
tardive dyskinesia, vertigo, and withdrawal syndrome;
Rare: circumoral paresthesia, coma, encephalopathy, neuralgia,
neuropathy, nystagmus, paralysis, subarachnoid hemorrhage, and
Australian PI is incomplete, but it does inform that hallucinations
are “very common” (≥ 10%). That is, they occur in more than 1 in 10
Eli Lilly was fined $US 1.42 billion in the United States for criminal
and fraudulent promotion of the drug, with the judge raising the issue
of racketeering . There are many lawsuits, settled and ongoing,
against Eli Lilly by State Attorneys General, as well as class actions for
suicides. With Eli Lilly reaping US $6 billion annually from olanzapine,
these fines and settlements are apparently insufficient to encourage the
company to change its promotional practices and have made no impact
on the behaviour of the company in Australia.
Four major studies (HGAD, E00, HGAJ and E003) were reviewed by
the U.S. FDA for the purpose of establishing the efficacy of olanzapine in
the treatment of chronic schizophrenia (acute exacerbation). According
to the U.S. FDA reviewers, the studies failed to establish any significant
effectiveness for olanzapine. Two thirds of clinical trial subjects dropped
out without completing 6 weeks. Even after they dropped out, 20 died,
12 by suicide. Concomitant drugs were permitted in these trials.
American PI also discloses that 67 of 3,100 subjects (including
a trial rejected by the U.S. FDA) took overdoses of olanzapine, but it
is silent on whether these patients were considered to be suicidal or
confused. As “only one” died (of the overdose) these numbers are put
forward as evidence of olanzapine safety in overdose. However, a courtordered
investigation of Eli Lilly archives disclosed the deaths and
suicides in the five clinical trials that were presented to the US FDA to
get it licensed . The figures are shown in Tables 3 and 4.
One in every 145 clinical trial subjects for risperidone, olanzapine,
quetiapine, and sertindole died, a total of 36 deaths, most by suicide
. Yet these deaths are not mentioned in the scientific literature nor
in PI. These deaths occurred even though two thirds of the olanzapine
subjects, nearly half of the risperidone subjects and 80% of the
quetiapine subjects did not complete the trials because the drugs were
poorly tolerated . A rate of 27% akathisia in a trial of olanzapine 10
mg was reported, balanced by an equally high incidence of akathisia
on placebo . This indicated that Eli Lilly either did not know what
they were talking about (as akathisia is by definition a medicationinduced
phenomenon), or the participants had not fully recovered
from whatever they had been taking before entry to the trial. Serious
adverse events affected 84 subjects who took risperidone.
None of this information appears in promotional material. Indeed,
47 serious adverse events in 87,000 users of olanzapine injectable in
Drug Number of Trial
Subjects Suicides Suicidal Acts
2500 (5000 started
and did not complete
12 Not disclosed#
Comparator 810 1 (2) Not disclosed
Placebo 236 0 (1) Not disclosed
# However, U.S. PI (2003) states that 67 subjects out of 3100 overdosed on olanzapine but
does not disclose if these overdoses were due to suicide attempts or delirium, and “only 1
Table 3. Incidence of suicides and suicide attempts in antipsychotic clinical trials drawn
from U.S. FDA license applications 
Drug Patient No. Suicides Suicidal Acts
Risperidone 2607 9 43
Comparator 601 1 5
Placebo 195 0 1
Table 4. Antipsychotic Drugs, FDA Trials: Source FDA, David Healy 
Clin Case Studie Rep, 2018 doi: 10.15761/CCSR.1000112 Volume 1(2): 6-8
clinical trials included eight deaths. We are assured that the deaths
were not related to the olanzapine but, given the number of suicides
and deaths associated with the oral preparation, this seems to be
improbable. The U.S. FDA issued a “black box” warning about sudden
death from the new antipsychotic medications (including quetiapine
and aripiprazole) but only for the elderly, in spite of evidence that all age
groups are adversely affected [56,57].
Fluvoxamine is metabolised by 2D6 and 1A2. 1A2 is induced
by cannabis and tobacco, so smoking both gives relief from toxicity.
Fluvoxamine is best described as a pan inhibitor as it is a potent
inhibitor of 1A2 and 2C19 and a mild to moderate inhibitor of 2B6,
2C9 and 3A4. Fluvoxamine was used in both A and C with olanzapine,
in the face of advice against this combination in PI.
Fluvoxamine, a CYP1A2 inhibitor, decreases the clearance of
olanzapine. This results in a mean increase in olanzapine Cmax following
fluvoxamine of 54% in female nonsmokers and 77% in male smokers.
The mean increase in olanzapine Area Under the Curve (AUC) is 52%
and 108%, respectively. Lower doses of olanzapine should be considered in
patients receiving concomitant treatment with fluvoxamine.
Fluvoxamine was the drug prescribed to one of the children
who perpetrated the Columbine High School massacre. Most school
massacres have been perpetrated by children taking prescribed
antidepressants or medications for ADHD .
The “atypical” antipsychotics: Risperidone and Consta, its
Risperidone is metabolised by 2D6, has a shorter half-life than
olanzapine and may need twice daily administration. In trials presented
to the U.S. FDA, two thirds of subjects did not complete. Those subjects
have never been mentioned in PI or the scientific literature, but this
information is available at http://www.lillytrials.com and was summarised
by Grace Jackson for litigation against Eli Lilly in Alaska . None
of the dropout rates, suicides and attempts is disclosed to prescribers
and patients. As a result, treating doctors, not knowing or expecting
these drugs to be poorly tolerated because they were misinformed
about clinical trials, organise for Mental Health Review Tribunals to
enforce them, by injection, to persons who cannot tolerate them orally,
as happened with Patient C. Coroners, if not willing to examine the
activities of hospitals where they are deployed several times a week, can
create a situation where regulatory agencies cannot be made aware of
The FDA trials and 52 subsequent studies evaluated in 2000, by
John Geddes of Oxford University demonstrated no clear evidence
that atypical antipsychotics were more effective or better tolerated
than conventional antipsychotics . Thirty-six, that being one in
every 145 clinical trial subjects for Risperdal, Zyprexa, Seroquel,) and
Sertindole died; most by suicide, yet these deaths are never mentioned
in scientific literature or prescriber information. These deaths occurred
even though two thirds of Zyprexa, nearly half the Risperdal and 80%
of Seroquel subjects did not complete the trials because the drugs were
poorly tolerated . A rate of 27% akathisia in a trial of Zyprexa 10 mg
was balanced by an equally high incidence of akathisia on placebo .
This indicated that Eli Lilly either did not know what they were talking
about (as akathisia events including suicide and homicide are always a
medication-induced adverse drug event or, alternately, the participants
had not fully recovered from whatever they had been taking before
entry to the trial. Serious adverse events affected 84 subjects who took
Zuclopenthixol depot has been associated with mental health
homicides, but invariably in combination, with other drugs that are
substrates of 2D6, as in the two cases presented here. The author has
personal experience of admitting patients homicidal on zuclopenthixol,
often co-prescribed with antidepressants and atypical (new generation)
antipsychotics. Several reports of this combination causing violent
attacks and homicidal behaviours were dismissed by the MBNSW, and
her report about patient C was turned into a complaint about her. As
did patients C and A here, many were experiencing akathisia, with
homicidal as well as suicidal ideation and acts [63-65].
The half-life of the zuclopenthixol depot preparation is 19 days, so
if it is given fortnightly, toxicity will eventually develop.
Patients C and A are but two of 48 people from the author’s clinical
and medico legal practice for 2D6, 2C9 and 2C19. Of the people tested,
42 were found to be poor or intermediate metabolizers and the rest
were overmedicated by PI standards. They were tested because they
experienced violent, homicidal and suicidal akathisia on standard
doses of antidepressants; one of them committed suicide, most had
made many attempts and three committed homicide on single doses of
antidepressants after 3 days, 2 weeks and 6 weeks on drugs that genetic
studies showed they could not metabolise; none of these three had a
psychiatric illness before or since, nor any history of violence. Only six
had normal CYP450 cytochromes, but they had either been given large
doses or had inhibitors in play. They had experienced many years of
counterproductive psychiatric treatments.
In the decade a following the introduction of the first of these
drugs, fluoxetine, in 1990, the population under mental health care in
Australia doubled and it has continued to increase. This is reflected in
Australian psychiatry’s vastly increased demands for resources .
Many ‘second generation’ drugs have followed this. The treatment of
schizophrenia with new drugs has increased mortality so care needs
to be taken before that diagnosis is applied, along with its remedies
[67-69]. Patients C and A are typical of persons under mental health
care who were not schizophrenic before they used drugs or received
treatment that induced symptoms similar to those of schizophrenia. Yet
testing for CYP450 mutations is available, for $140.00. That is the start
of appropriate personalised medicine.
Cannabis, its metabolites and 2D6
Cannabinols are metabolised by P3A4 and also inhibit it while
inducing 1A2. Sohayla et al. investigated the role of genetic factors in
cannabis dependence (hashish smokers) by CYP 2D6*4 genotyping of
46 habituated volunteers. Their findings suggest that genetic factors may
determine a person’s attraction to the effects of cannabis and other illicit
substances, but the mechanism is not obvious from existing research.
Diminished metaboliser status may cause cannabis to be experienced as
pleasurable, and if so, a propensity to substance-induced mood disorder
is a possibility. Cannabis smokers are said to have a tendency to become
psychotic later in life, but the mechanism is also obscure. Drug clinics
generally yield higher proportions of diminished metabolizers, for
reasons that have not yet been researched.
The common mislabelling of cannabis effects and other toxic
states as schizophrenia mania, major depression or bipolar disorder
Clin Case Studie Rep, 2018 doi: 10.15761/CCSR.1000112 Volume 1(2): 7-8
is counterproductive. The diagnostic criteria for all those disorders
contain an exclusion criterion for substance or medication use.
Misdiagnosis of mental and behavioural disorders as being attributable
to psychoactive substance use appears to contribute to the furphy that
cannabis causes schizophrenia.
Clinical prescriptions are available at F10-F19 “Mental and
Behavioural Disorders due to psychoactive substance” of the ICD 10,
still Australia’s official diagnostic system.
Drug clinic and cannabis users
The role of diminished P450 metabolism, specifically 2D6*4,
in cannabis smokers and the prevalence of mutations in drug clinic
populations generally bear further examination. One possibility is
that in diminished metabolism, 2D6 capacity may increase both
the pleasurable effects of cannabis and maybe other drugs and the
tendency to medication-induced psychotic phenomena. It may be that
they are already taking medication and are using cannabis to moderate
it. Suspicion of a high prevalence of diminished metabolizers at 2D6
among cannabis smokers might caution against the use of medicines
demand that substrate.
Misdiagnosis of mental and behavioural disorders due to
psychoactive substance use appears to contribute to the furphy that
cannabis causes schizophrenia.
Although ecological studies report an increase in schizophrenia
and bipolar illness, detailed analysis of such cases suggests that the
population that becomes psychotic on cannabis also develops neurotoxic
syndromes on olanzapine and risperidone, as well as antidepressants,
particularly those metabolised by 2D6.
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DC: American Psychiatric Association 1994. And ICD International Statistical
Classification of Diseases and Related Health Problems ICD 10. Tenth Edn. Geneva:
World Health Organization.
2. DSM-IV-TR® Handbook of differential diagnosis (2007) Ch. 2. Differential diagnosis
by the trees american psychiatric publishing.
3. De Leon, J Scott, Armstrong Cozza, Kl Med-Psych (2006) Drug-drug interactions
update. Clinical guidelines for psychiatrists for the use of pharmacogenetic testing for
CYP450 2D6 and CYP450 2C19 Psychosomatics 47:1.
4. Sachdev P (1995) Akathisia and restless legs, Cambridge University Press. Cambridge.
5. Physicians Desk Reference Oradell New Jersey: Medical Economics Company 2003.
6. Hálfdánarson Ó, Zoëga H, Aagaard L, Bernardo M, Brandt L, et al. (2017)
International trends in antipsychotic use: A study in 16 countries, 2005-2014. Eur
Neuropsychopharmacol 27: 1064-1076. [Crossref]
7. Teicher MH, Glod CA, Cole JO (1993) Antidepressant drugs and the emergence of
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8. de Leon J, Susce MT, Pan RM, Fairchild M, Koch WH, et al. (2005) The CYP2D6 poor
metabolizer phenotype may be associated with risperidone adverse drug reactions and
discontinuation. J Clin Psychiatry 66: 15-27. [Crossref]
9. Zullino DF, Delessert D, Eap CB, Preisig M, Baumann P (2002) Tobacco and cannabis
smoking cessation can lead to intoxication with clozapine or olanzapine. Int Clin
Psychopharmacol 17: 141-143. [Crossref]
10. Bauman P, Hiemke C, Ulrich S, Eckermann G, Gaertner I (2004) The ANGP-TDM
expert group consensus guidelines: therapeutic drug monitoring in psychiatry.
Pharmacopsychiatry 37: 243-265. [Crossref]
11. Ingelman-Sundberg M (2005) Genetic polymorphisms of cytochrome P450 2D6
(CYP2D6): clinical consequences, evolutionary aspects and functional diversity.
Review. Pharmacogenomics 5: 6-13.
12. Kaplan HI, Saddock BJ, Freedman AM (1980) Comprehensive textbook of psychiatry.
Baltimore: Wilkins and Wilkins.
13. Diagnostic and statistical manual of mental disorders (DSM-IV) (1994) American
Psychiatric Association. Drug Induced Akathisia.
14. Cannabis is metabolised by 3A4, 2B6 and 2C9. It is an inhibitor of 3A4 and induces
1A2. It remains in the body for up to two years depending on how much was used.
15. Shirley KH, YY Penzak, SR Lam, YWF Spratlin, V Jann MW (2003) Correlation
of cytochrome P450 (CYP) 1A2 activity using caffeine phenotyping and olanzapine
disposition in healthy volunteers. Neuropsychopharmacology 28: 961-966.
16. Cozza KL, Armstrong SC, Oesterheld JR (2003) Drug interaction principles for
medical practice: cytochrome P450s, UGTs, P-Glycoproteins. Arlington, Va, American
17. Refinetti R (1997) Philosophy of science and physiology education. Am J Physiol 272:
18. Hales R, Yudofsky S, Talbot, JA (1999) Textbook of psychiatry. Third ed. Washington
DC: The American Psychiatric Press.
19. Improving the quality use of medicines in Australia: Australian centre for health
research realising the potential of pharmacogenomics (2008).
20. Lazarou J, Pomeranz BH, Corey PN (1998) Incidence of adverse drug reactions in
hospitalized patients: a meta-analysis of prospective studies. JAMA 279: 1200-1205.
21. Schulte JL (1985) Homicide and suicide associated with akathisia and haloperidol.
American Journal of Forensic Psychiatry 6: 3-7.
22. Healy D, Herxheimer A, Menkes DB (2006) Antidepressants and violence: problems at
the interface of medicine and law. PLoS Med 3: e372. [Crossref]
23. Breggin PR (2003) Suicidality, violence, and mania caused by selective serotonin
reuptake inhibitors: A review and analysis. Ethical Human Sciences & Services 5: 225-
24. Yolande Lucire (2005) New Drugs, New Problems. Australian Journal of Forensic
Sciences 37: 19-25.
25. NSW Mental Health Sentinel Events Committee. Tracking Tragedy: A systemic look at
suicides and homicides amongst mental health inpatients (2004).
26. Healy D, Whitaker C (2003) Antidepressants and suicide: risk-benefit conundrums. J
Psychiatry Neurosci 28: 331-337. [Crossref]
27. Whitaker R (2005) Anatomy of an epidemic: psychiatric drugs and the astonishing
rise of mental illness in America. Ethical human psychology and psychiatry. An
International Journal of Critical Inquiry 7: 23-35.
28. Tanaka E, Hisawa S (1999) Clinically significant pharmacokinetic drug interactions
with psychoactive drugs: antidepressants and antipsychotics and the cytochrome P450
system. Journal of Clinical Pharmacy & Therapeutics 24: 7-16.
29. Oesterheld, JR Cozza, K Armstrong SC, Neil B Sandson (2007) Drug-drug interactions:
a compendium of case vignettes for the practicing clinician. American Psychiatric
30. Letter from Eli Lilly Australia, cf Bauman, opp cit.
31. Communiqué: mayo reference services. Cytochrome P450 enzyme genotyping:
optimizing patient care through pharmacogentics. September 2005.
32. Armstrong SC, Cozza KL, Sandson NB (2003) Six patterns of drug-drug interactions.
Psychosomatics 44: 255-258. [Crossref]
34. Sandson NB (2007) Drug-drug interactions primer. A compendium of vignettes for the
practicing clinician. American Psychiatric Press.
35. Blue Cross Blue Shield Association (2004) Special report: genotyping for cytochrome
P450 polymorphisms to determine drug-metabolizer status. Technology Assessment
Program 19: 1-34.
39. Wynn GH, Oesterheld, JR Cozza, K, Armstrong SC (2009) Clinical Manual of Drug
Interaction Principles for Medical Practice. American Psychiatric Publishing Inc.
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2D6 phenotype and occurence of adverse effects. General Physiology & Biophysics
Clin Case Studie Rep, 2018 doi: 10.15761/CCSR.1000112 Volume 1(2): 8-8
Cc: PALS(LPT) (LINCOLNSHIRE PARTNERSHIP NHS FOUNDATION TRUST)
Subject: FW: Endocrinologist
Being deprived of meaningful contact with my daughter through her not having any section 17 leave which has been avoided for months on end – there is no greater punishment than that. It is in effect having a drastic effect on my physical health.
Knowing my daughter is getting no better and never will under Ash Villa and held a prisoner in bed most of the day is heartbreaking.
It is hard knowing the true reality that we should never ever have come to this area where I wanted so much to provide the right living accommodation and support in the community. That clearly is not happening and never will because it costs £4000 thereabouts to hold my daughter under Ash Villa a prisoner. She will never get off the section whilst staff write negatively and constantly do so and all the time my daughter is lying there in bed during the day and becoming weaker and weaker physically. Mentally she has capacity and is sharing information with me which I then share with the rest of the family in accordance with her wishes.
I do not expect a penny or any support from this area. Such restrictive punishment in deprival of Section 17 leave is not conducive to recovery and is having a knock-on effect to my physical health and is of great upset to all my family.
My daughter was not seen as a risk to others in the former area otherwise she would not have been released without a Section in place. She was also complying with treatment.
Please see meeting notes from todays meeting.
- S17 leave has not changed and remains at 2 x 30 minutes ground leave escorted by 2 members of staff.
- Risk was explained regarding why E …… is escorted by 2 x members of staff.
- Nursing advised that Elizabeth does see her advocate on a one to one basis however Elizabeth has refused from time to time.
- Dr S advised the a consultant would be available next week to be involved in the meetings.
- We discussed Takeaways and how these are becoming more frequent.
- That you would like some inclusion.
- You was offered invitations to Carers support groups and you refused these.
- You would like to continue with the weekly meeting with a consultant.
- You wish to visit on a Saturday @14.00
I will look at booking next weeks appointment and forwards to you in due course.
Working hours Monday to Friday 09.00-17.00 pm
Subject: Re: stress induced psychosis
They recognise that Elizabeth has stress induced psychosis but signally fail to recognise that they are the cause of much of the stress. Do they not realise that being deprived of liberty is about as stressful as it gets.
Oh, and nasty tastes are an effect of the anticholinergic effects of the drugs. Odd they don’t recognise that either.
Ask for a detailed explanation of why Elizabeth cannot be given s.17 leave. Including a full appraisal of her current state of mind.not some utterly inadequate reference to outdated diagnostic criteria. Section 17 leave is part of the rehabilitation programme and patients do not get better permanently locked up in a bizarre setting with hostile staff.
It is patently obvious that if Elizabeth does not want to engage with the staff in Ash Villa that they need to make better arrangements. She clearly needs one to one psychotherapy with someone she can trust and who can break through the barrier that these mental health professionals themselves create.
No amount of incarceration in a locked ‘rehabilitation’ ward will improve her quality of life and all it will do is make her more determined to reject their interventions. The idea that rehabilitation can be achieved in a lock-up is bloody ridiculous in any case.
As for schizophrenia I would suggest that the nurse needs to do some CME training. Virtually no-one considers this an organic condition anymore and even where it is recognised as a disorder it is syndromal and not a condition with either aetiology or prognosis. Thousands of those accused of being schizophrenics recover if properly treated. Millions of others are simply drugged and locked up for convenience.
I think that Elizabeth would show signs of recovery if she was given seven days leave and later attended as a voluntary patient. If they cannot see that her defiance will not subside after this length of time they need to reconsider their chosen professions.
From: : ZB 24 May 2022 10:12
To: susan bevis
Subject: RE: Managers hearing
Good morning Susan
I hope your well.
As advised on many occasions I am your single point of access, others will not reply but I will seek to gain the relevant answers and feed them back to you.
You will not be sent the link to the managers meeting today, Elizabeth has not given verbal consent to any member of staff although we have tried to gain this on many occasions.
Elizabeth has not been deemed to have Capacity to consent to your request on this occasion.
Email: ZB Friday 09.00-17.00 pm
Good afternoon susan
To be clear Elizabeth does not have unlimited ground leave ground leave is 2 x 30 minutes a week
However we have a locked garden which elizabeth can access this does not fall under leave.
Hope this clarifies for you.
Email: ZB Working hours Monday to Friday 09.00-17.00 pm
Sent: 09 May 2022 16:22
To: susan bevis
Thank you for your email.
To be clear on the garden, we have a private garden on the grounds and Elizabeth has full use of them when ever she wishes to have some fresh air.
This has been mentions on a couple of occasions.
As you are aware Elizabeth is held on a section 3, this went to tribunal and was upheld.
The professionals in the meeting have agreed this is the right things for Elizabeth at this point in her recovery.
All next possible steps will be considered for Elizabeth moving forwards.
Working hours Monday to Friday 09.00-17.00 pm
From: B Sent: Saturday, May 7, 2022 8:21:34 PM
Subject: Re: Negligence
There is no tangible reason why Elizabeth cannot be given s.17 leave and the refusal to allow her some respite form permenant confinement is positively detrimental to her mental health.
In a nutshell they are institutionalising her by stealth. This is a human rights issue and not one for half-assed tribunals. I am quite prepared to help you put together a case if Elizabeth agrees. The matter needs taking to the High Court on the grounds they are acting ultra vires.
This circumvents the institutional bias of the tribunals and involved decisions based on well establish law rather than the convenience of the staff at Ash Villa. It is utterly absurd that she has not had some home leave in eight months. Even a restricted patient would have been allowed some leave.
From: susan bevis <susanb
Sent: Sat, 7 May 2022 18:32
Subject: RE: Negligence
I will try and do that tomorrow but doubt this will be allowed. They are totally avoiding the issue of leave. One doctor after another. I am not racist but they seem to be and do not seem to care one bit. I have not spoken to elizabeth for several days. Cannot get through on the phone.
What they are trying to do is isolate and keep her away from her family as they have their own agenda clearly and none of us agree with that. Why should my daughter have to go to another locked prison instead of coming home in accordance with her wishes.
This area is an absolute disgrace when it comes to mental health and the facilities are not fit for purpose.
I thought Enfield was bad enough. Elizabeth has been held now a prisoner deprived of contact and leave now since September.