Antidepressiva (SSRI)

Studie viser at mange feildiagnostiseres som depressive (chron.com 15.4.2007)

- Antidepressiva virker ikke (...) skadelige eller virkningsløse (pharmatimes.com 7.1.2010) (nrk.no 26.2.2008) (about.com 26.10.2009)

Negative legemiddelstudier publiseres ikke, ifølge rapport (reuters.com 17.1.2008) (mintankesmie.no)

SSRI-utløst aggresjon? (mintankesmie.no)

SSRI-er og såkalt serotonerg ubalanse (PLoS Medicine 2005;2:0101-0106 (December 2005))

Selektive serotoninreopptakshemmere i svangerskap og medfødte misdannelser: befolkningsbasert kohortstudie (BMJ 2009;339:b3569 (23.9.2009))

Links to FDA labels for approved antidepressants (themarketfinancial.com 12.12.2010)

Studie: Gentester ubrukelig for depresjon (upi.com capturewiz 4.1.2007)

Kan Cipralex gi spasmer og dystoni? (Bivirkningsartikkel fra RELIS 3.6.2005)

Antidepressiva ødelegger ansiktsmuskulatur (...) (medpagetoday.com 4.2.2009)

Serotonin syndrom (SS), kramper, parkinsonisme osv. (forhøyet kroppstemperatur) (mintankesmie.no)

- Hvorfor antidepressiva ikke alltid virker

Greater Risk Of Relapse In Patients Who Use Anti-Depressants (Større risiko for tilbakefall hos pasienter som bruker antidepressiva)
medicalnewstoday.com 20.7.2011
Pasienter som bruker antidepressiva er mye mer sannsynlig å lide av tilbakefall av kraftig depresjon enn de som ikke bruker legemidler i det hele tatt, konkluderer McMaster-forsker. (Patients who use anti-depressants are much more likely to relapses of major depression than those who use no medication at all, concludes a McMaster researcher.)

In a paper that is likely to ignite new controversy in the hotly debated field of depression and medication, evolutionary psychologist Paul Andrews concludes that patients who have used anti-depressant medications can be nearly twice as susceptible to future episodes of major depression.

Andrews, an assistant professor in the Department of Psychology, Neuroscience & Behaviour, is the lead author of a new paper in the journal Frontiers of Psychology. (...)

(Anm: Blue again: perturbational effects of antidepressants suggest monoaminergic homeostasis in major depression. Front. Psychology 2011;2:159 (Published online: 07 July 2011).)

Why Antidepressants Don't Always Work (Hvorfor antidepressiva ikke alltid virker)
depression.about.com 26.10.2009
Ifølge forskere ved Northwestern University har halvparten av de som får antidepressiva ingen nytte av midlene. Forskningen synes å indikere at det kan skyldes at hva vi tror trigger depresjon er fullstendig feil. (...) (According to background information provided in a new paper by Northwestern University researchers, over half of antidepressants fail to provide relief to depression sufferers. Their research seems to indicate it may be because what we believe about what triggers depression is entirely wrong.)

Konsekvensen av disse resultater? Redei og hennes gruppe konkluderte at stress ikke spiller noen rolle i trigging av genetiske endringer knyttet til depresjon; og, dersom stress ikke spiller noen rolle ved depresjon innebærer dette at antidepressiva, som stort sett er testet på dyr ved å stresse dyrene og så observere hvordan antidepressiva modifisere deres atferd, i virkeligheten behandler stress, ikke depresjon. (The implication of these results? Redei and her team concluded that stress does not play a role in triggering the genetic changes associated with depression; and, if stress does not play a role in depression then this means that antidepressants, which are generally tested on animals by stressing the animals and then observing how the antidepressant modifies their behavior, are actually treating stress, not depression.)

Redei sier at legemiddelutviklere har fokusert på effekten (stress) snarere enn årsaken til depresjon. "Det er derfor det tar så lang tid for midlene å virke og hvorfor de ikke er effektive for mange mennesker," forklarte Redei. De behandler faktisk ikke depresjon i det hele tatt. (...) (Redei says that drug developers have been focusing on the effect (stress) rather than the cause of depression. "That's why it takes so long for them to work and why they aren't effective for so many people," explained Redei. They are not actually treating depression at all.)

(Anm: Antidepressiva (nytteverdi) (mintankesmie.no).)

Public 'misled' by drug trial claims (Publikum "villedet" av påstander i legemiddelforsøk)
By Michelle Roberts Health reporter, BBC News
bbc.co.uk 13.10.2 010
Drugs need to undergo extensive testing in trials before approval

Doctors and patients are being misled about the effectiveness of some drugs because negative trial results are not published, experts have warned.

Writing in the British Medical Journal, they say that pharmaceutical companies should be forced to publish all data, not just positive findings. (...)

(Anm: Reboxetine for acute treatment of major depression: systematic review and meta-analysis of published and unpublished placebo and selective serotonin reuptake inhibitor controlled trials. BMJ 2010; 341:c4737 (12 October).)

(Anm: reboxetine (Edronax) (felleskatalogen.no).)

Reboxetine for acute treatment of major depression: systematic review and meta-analysis of published and unpublished placebo and selective serotonin reuptake inhibitor controlled trials.
BMJ 2010; 341:c4737 (12 October)
Objectives To assess the benefits and harms of reboxetine versus placebo or selective serotonin reuptake inhibitors (SSRIs) in the acute treatment of depression, and to measure the impact of potential publication bias in trials of reboxetine.

Design Systematic review and meta-analysis including unpublished data. (...)

Conclusions Reboxetine is, overall, an ineffective and potentially harmful antidepressant. Published evidence is affected by publication bias, underlining the urgent need for mandatory publication of trial data. (...)

Table 4 Examples of publication bias and industry sponsorship bias in trials of antidepressants

In addition to publication bias, outcome reporting bias has been identified as a major problem in the reporting of clinical trials, resulting in a distorted public record of an intervention.³⁵ ³⁶ ³⁷ ³⁸ Our review also identified this type of bias—for three reboxetine trials, only results on subpopulations or selected outcomes were available in the published literature (trials 047, 050, 052; table 1).

The more positive benefit-risk ratio in published data compared with unpublished data also affects the content of clinical guidelines. For example, the National Institute for Health and Clinical Excellence (NICE) guideline on the treatment and management of depression in adults is based on published studies of reboxetine, and concludes that “Reboxetine is superior to placebo and as effective as other antidepressants in the treatment of depression.”¹⁰ In our opinion, this conclusion can no longer be upheld.

The ongoing problem of publication bias shows that unbiased decision making in health care requires mandatory public disclosure of all clinical trial data. The US FDA Amendments Act of 2007³⁹ solves the problem in part by requiring protocol information and study results for clinical trials to be made public on the clinicaltrials.gov website (www.clinicaltrials.gov; please see accompanying comment (doi:10.1136/bmj.c4942) for further details). Similar legislation is also being introduced in Europe, with the mandatory public disclosure of data from the clinical trials database EudraCT (eudract.ema.europa.eu),^{40 41} but the date of implementation is not yet clear.

As the full assessment reports on reboxetine prepared by regulatory authorities are not publicly available, it is not clear as to how the comprehensive body of evidence (including that on efficacy outcomes) generated after reboxetine was approved in Europe in the late 1990s has been analysed by these authorities. The reason for the difference in approval status of reboxetine between Europe and the US thus remains unclear.(...)

Tvivl om antidepressiv medicin
videnskab.dk 21.9.2009
En kritisk artikel i det højt ansete, videnskabelige tidsskrift The New England Journal of Medicine har sat spørgsmålstegn ved effekten af 'lykkepiller'. (...)

Kun positive resultater publiceret
Faktisk var der nøjagtig lige mange undersøgelser med positive resultater (36), som med direkte negative resultater (24) samt tvivlsomme resultater (12), der hverken var klart positive eller negative med hensyn til en tydelig virkning af den antidepressive medicin. (...)

Firmaer skjuler negative medicinforsøg
ekstrabladet.dk 13.10.2010
Medicinalfirmaerne vildleder forbrugerne ved kun at offentliggøre de testresultater, som kommer positivt ud, advarer forskere (...)

Læger og patienter bliver ført bag lyset af medicinalfirmaerne, som skjuler negative resultater fra kliniske forsøg, så deres medicin fremstår mere effektiv end den er, advarer eksperter. (...)

Et tysk forskerhold har i det anerkendte tidsskrift British Medical Journal offentliggjort en gennemgang af ikke tidligere offentliggjorte forsøg med antidepressivet reboxetine (Edronax). De konkluderer, at medicinen ikke er blevet fremstillet i et sandfærdigt lys, skriver BBC.co.uk. (...)

'Vores fund understreger det tvingende behov for tvungen offelitggørelse af førsøgsdata' konkluderer undersøgelsens bagmænd ifølge BBC.co.uk. (...)

Undersøgelsen kommer i kølvandet på flere kritiske historier om medicinalindustrien: Medicinalgiganten Glaxo Smith Kline er ligesom Pfizer blevet anklaget for at tilbageholde kritiske resultater i forhold til diabetesmedicinen Avandia og antidepressivet Seroxat.

Tidligere på måneden blev medicinalfirmaerne i bogen 'Sex, lies and Pharmaceuticals' anklaget for at opfinde nye sygdomme og sygeliggøre raske, så de kunne sælge mere medicin. (...)

(Anm: Forskning og ressurser (mintankesmie.no).)

Studier skönmålade antidepressivt läkemedel
dagensmedicin.se 13.10.2010
Läkemedlet Edronax är inte effektivt mot depression och kan möjligen vara skadligt, enligt en ny metaanalys av publicerade och opublicerade studier. (...)

Forskarnas slutsats är att Edronax på hela taget är ett ineffektivt och potentiellt skadligt läkemedel. De anser att resultaten är ett ”slående” exempel på så kallad publikationsbias, där en annars negativ risk-nytta profil för Edronax blir positiv om man tar hänsyn enbart till publicerade data. (...)

Pfizer depression drug ineffective, may be harmful: study (Pfizers legemiddel mot depresjon ineffektivt, kan være skadelig, ifølge studie)
reuters.com 13.10.2010
(Reuters) - Pfizer's antidepressant reboxetine is an "ineffective and potentially harmful" drug and published data on it overestimates the benefits and underplays the risks, a study by German researchers said on Wednesday.

In a review published in the British Medical Journal, researchers from the German Institute for Quality and Efficiency in Health Care (IQWiG) found that nearly three quarters of the data on patients who took part in trials of reboxetine was not published until now -- a factor they said underlined the urgent need for mandatory publication of all clinical trial results.

Reboxetine, sold under the brand name Edronax, has been approved for the treatment of major depressive disorder in many European countries since 1997 but doubts have been raised about its effectiveness on the basis of recent studies and rejection of the application for approval in the United States in 2001.

"It is not a major drug in depression but every patient that is treated with an ineffective drug is one too many," said Beate Wieseler of IQWiG's department of drug assessment, who led the study. "Depression is a severe disease and there are effective drugs available, so if a patient is given an ineffective drug, that is unacceptable."

Reboxetine is one of the first in a class of anti-depressant drugs called selective serotonin re-uptake inhibitors, or SSRIs. (...)

The German team analyzed the results of 13 trials of reboxetine, including eight previously unpublished trials from Pfizer, and concluded that overall the drug was ineffective as a treatment for depression and may have harmful side effects. (...)

(Anm: reboxetine (Edronax) (felleskatalogen.no).)

Northwestern Research Finds Antidepressant Drugs Aim At Wrong Target (Northwestern-forskning viser at antidepressiva bommer på målet)
medicalnewstoday.com 25.10.2009
More than half the people who take antidepressants for depression never get relief.

Why? Because the cause of depression has been oversimplified and drugs designed to treat it aim at the wrong target, according to new research from the Northwestern University Feinberg School of Medicine. The medications are like arrows shot at the outer rings of a bull's eye instead of the center. (...)

Both findings are significant because these beliefs were the basis for developing drugs currently used to treat depression.

Redei, the David Lawrence Stein Professor of Psychiatry at Northwestern's Feinberg School, found powerful molecular evidence that quashes the long-held dogma that stress is generally a major cause of depression. Her new research reveals that there is almost no overlap between stress-related genes and depression-related genes.

"Dette er en stor og statistisk sterk studie," uttalte Redei. "Denne forskningen åpner opp for nye veier for utvikling av antidepressiva som kan være mer effektive. Der har ikke vært et antidepressiva basert på et nytt konsept på 20 år." (...) ("This is a huge study and statistically powerful," Redei said. "This research opens up new routes to develop new antidepressants that may be more effective. There hasn't been an antidepressant based on a novel concept in 20 years.")

Why Antidepressants Don't Work For So Many
northwestern.edu 23.10.2009
CHICAGO --- For more than half the people who take antidepressants, relief from their symptoms never comes.

Advarsler

January 2009 Safety Labeling Changes (Januar 2009 sikkerhetsendringer pakningsvedlegg (Seroxat (Paxil), Celexa, Cipramil, Zoloft, Cybalta, Efexor, Prozac, Venlafaxine, Pristiq etc.)
fda.gov 6.3.2009
- Summary of safety-related revisions to the BOXED WARNING, CONTRAINDICATIONS, WARNINGS, PRECAUTIONS, and ADVERSE REACTIONS sections of drug Prescribing Information, plus Patient Package Inserts and Medication Guides. (Posted 03/06/2009) (…)

WARNINGS
Serotonin Syndrome or Neuroleptic Malignant Syndrome (NMS)-like Reactions

WARNINGS
The development of a potentially life-threatening serotonin syndrome or Neuroleptic Malignant Syndrome (NMS)-like reactions have been reported with SNRIs and SSRIs alone, including Celexa treatment, but particularly with concomitant use of serotonergic drugs (including triptans) with drugs which impair metabolism of serotonin (including MAOIs), or with antipsychotics or other dopamine antagonists (...)

(Anm: Serotonin syndrom (SS), kramper, parkinsonisme osv. (forhøyet kroppstemperatur) (mintankesmie.no).)

- Antidepressiva og risiko for bryst- og eggstokkreft: En gjennomgang av litteratur og forskernes tilknytning til industrien

Possible Link Between SSRIs and Breast, Ovarian Cancer (Mulig link mellom SSRI-er og bryst- og eggstokkreft)
medscape.com 14.4.2011
But Expert Says Results Should Be Interpreted With Caution

April 14, 2011 — A meta-analysis of 61 studies that looked at the relationship between cancer and antidepressant use shows a "small but statistically significant" increase in the risk for breast and ovarian cancer in women who use selective serotonin reuptake inhibitors (SSRIs).

A meta-analysis has its limitations, but still I feel that these results tell us that we really need to study further the use of SSRIs in women and the link to cancer. It's a fascinating question that really begs an answer. (...)

The study also found that researchers with industry affiliations were significantly less likely than researchers without industry ties to conclude that antidepressants increase the risk for breast or ovarian cancer, Dr. Cosgrove noted.

"There was a statistically significant relationship between researchers' industry ties and conclusions regarding antidepressants and cancer, with a P value as per 2-sided Fisher's exact test equal to .0012," she said. (...)

Antidepressants and Breast and Ovarian Cancer Risk: A Review of the Literature and Researchers' Financial Associations with Industry (Antidepressiva og risiko for bryst- og eggstokkreft: En gjennomgang av litteratur og forskernes tilknytning til industrien)
PLoS ONE 6(4): e18210 (April 6)
Antidepressant (AD) use has been purported to increase the risk of breast and ovarian cancer, although both epidemiological and pre-clinical studies have reported mixed results [1]–[6]. Previous studies in a variety of biomedical fields have found that financial ties to drug companies are associated with favorable study conclusions [7].

We searched English-language articles in MEDLINE, PsychINFO, the Science Citations Index and the Cochrane Central Register of Controlled Clinical Trials (through November 2010). A total of 61 articles that assessed the relationship between breast and ovarian cancer and AD use and articles that examined the effect of ADs on cell growth were included. Multi-modal screening techniques were used to investigate researchers' financial ties with industry. A random effects meta-analysis was used to pool the findings from the epidemiological literature. Thirty-three percent (20/61) of the studies reported a positive association between ADs and cancer. Sixty-seven percent (41/61) of the studies reported no association or antiproliferative effect. The pooled odds ratio for the association between AD use and breast/ovarian cancer in the epidemiologic studies was 1.11 (95% CI, 1.03–1.20). Researchers with industry affiliations were significantly less likely than researchers without those ties to conclude that ADs increase the risk of breast or ovarian cancer. (0/15 [0%] vs 20/46 [43.5%] (Fisher's Exact test P = 0.0012).

Both the pre-clinical and clinical data are mixed in terms of showing an association between AD use and breast and ovarian cancer. The possibility that ADs may exhibit a bi-phasic effect, whereby short-term use and/or low dose antidepressants may increase the risk of breast and ovarian cancer, warrants further investigation. Industry affiliations were significantly associated with negative conclusions regarding cancer risk. The findings have implications in light of the 2009 USPSTF guidelines for breast cancer screening and for the informed consent process. (...)

Questions raised about industry influence on anti-depressant studies (Stiller spørsmål ved industripåvirknining og antidepressiva)
southasiamail.com 30.4.2011
For more than two decades, researchers have been unable to settle an important question: Can anti-depressant medications stimulate the growth of breast and ovarian cancers?

Some studies pointed to a link, but others did not.

Now a re-examination of the available evidence has cast a new – and disturbing – light on the previous research. Many studies that seemed to absolve the drugs of blame were carried out by researchers with close ties to the pharmaceutical industry, according to a report published this week in the online journal PLoS (Public Library of Science) One.

“I think that’s an important piece of information,” said the lead author of the paper, Lisa Cosgrove of the Edmond J. Safra Center for Ethics at Harvard University in Boston.

For the review, Dr. Cosgrove and colleagues amassed a total of 61 studies, which included both laboratory and epidemiological research.

They then conducted separate searches on the principal investigators for each of the studies, looking for drug-company connections. “It was a lot of legwork,” said Dr. Cosgrove, noting that, in the past, such ties were not always publicly reported.

A clear pattern emerged. “None of the researchers with industry affiliation reported a positive association” between antidepressants and the risk of cancer, she said.

There were more mixed findings among researchers free of corporate ties. “Approximately 43 per cent of researchers without industry affiliation reported a positive association.”

A closer examination of these studies – using meta-analysis, which pools the data – suggests the risk is real, but not very large. Women with a history of antidepressant use faced an 11-per-cent increased chance of developing breast and ovarian cancer, compared with those who had not taken these medications. In the case of breast cancer, that means taking antidepressants would raise an average woman's lifetime risk to 13.8 per cent from 12.5 per cent, Dr. Cosgrove said. (...)

- Antidepressiva linket til hjertedød

'Lykkepiller' kan give hjertestop
videnskab.dk 24.11.2011
Det populære antidepressive middel Cipramil kan ifølge et nyt studie få hjertet til at slå ude af takt, så det i sjældne tilfælde går i stå. Lægemiddelstyrelsen ændrer nu sine anbefalinger til brugen af 'lykkepillerne'.

(Redaktionel note, 24. november 2011: Nyheden om det amerikanske studie har hurtigt fået mange patienter til at blive bekymrede for, om de skal holde op med at tage deres medicin. Lægemiddelstyrelsen beder i den forbindelse om, at man ikke ringer til styrelsen, men taler med sin egen læge, hvis man er usikker på sin medicin. Lægemiddelstyrelsen understreger samtidig, at det er sundhedsfarligt at holde op med at tage sin medicin uden lægens anbefaling.)

Et nyt amerikansk studie har for nylig afsløret en hidtil ukendt potentiel farlig bivirkning ved Cipramil, som mange depressive danskere for øjeblikket bliver behandlet med. Omkring 178.000 danskere er i behandling med Cipramil og kopiudgaverne af dette lægemiddel, der alle rummer det virksomme stof Citalopram. (...)

Det kan undre, hvorfor man ikke fra begyndelsen undersøgte, om lægemidlet havde denne effekt, men Lundbecks pressechef Mads Kronborg fortæller, at man ikke tidligere har været opmærksom på mekanismen, da indrapporteringerne fra læger og patienter i årenes løb ikke viser nogen tegn på, at der skulle være en forhøjet risiko. (...)

Dansk Psykiatrisk Selskab og Dansk Kardiologisk Selskab har netop behandlet dette spørgsmål og andre problemer med medicinen i en fælles rapport. (...)

Antidepressants linked to cardiac death (Antidepressiva linket til hjertedød)
hospitalpharmacyeurope.com 16.11.2011
People taking anti-psychotic drugs and anti-depressant drugs have a much higher risk of dying during an acute coronary event of a fatal arrhythmia than the rest of the population, according to research published in the European Heart Journal.

The study showed that the combined use of both antipsychotic and antidepressant drugs was associated with an even greater risk of sudden cardiac death (SCD) during a coronary event. (...)

(Anm: Antidepressant medication use and future risk of cardiovascular disease: the Scottish Health Survey. Eur Heart J (2011) 32 (4): 437-442 (November 30).)

Høye doser citalopram kan gi hjertebivirkninger
legemiddelverket.no 8.11.2011
Det er påvist sammenheng mellom høye doser citalopram og hjertebivirkninger. Ny maksimaldose for citalopram er 40 mg.

Citalopram brukes for å behandle depresjoner, panikkangst og tvangslidelse. En gjennomgang av studier og spontanrapporter viser er en sammenheng mellom bruk av høye doser citalopram og forlenget QT-intervall ved EKG. (...)

- Antidepressiva øker risiko for åreforkalkning, erektil dysfunksjon, hjertesykdom og hjerneslag

Erectile Dysfunction May Be Linked With Cardiovascular Trouble (Erektil dysfunksjon kan være linket til kardiovaskulære problemer)
health.yahoo.com 14.9.2011
WEDNESDAY, Sept. 14 (HealthDay News) -- Men who suffer from erectile dysfunction are at increased risk for cardiovascular disease, stroke and death, Chinese researchers suggest.
Although it is well accepted that cardiovascular disease is a risk factor for erectile dysfunction, it has not been clear whether erectile dysfunction is an independent risk factor for cardiovascular disease, the researchers noted.

"Erectile dysfunction significantly increased the risk of cardiovascular disease, and the increase was probably independent of conventional risk factors," said lead researcher Dr. Li-Qiang Qin, from the department of nutrition and food hygiene in the School of Public Health at Soochow University in Suzhou.

As such, "erectile dysfunction may not only contribute to cardiovascular risk prediction, but also serve as a potential target for cardiovascular disease prevention," Qin said.

The report was published in the Sept. 13 online edition of the Journal of the American College of Cardiology. (...)

(Anm: CLINICAL RESEARCH: CARDIOVASCULAR RISK. Erectile Dysfunction and Risk of Cardiovascular Disease. J Am Coll Cardiol, 2011; 58:1378-1385
(September 20).)

FDA Warns Against High-Dose Citalopram (FDA advarer mot høye doser av citalopram (Cipramil; Celexa))
medpagetoday.com 24.8.2011
Citing increased risk of cardiac arrhythmias and a lack of therapeutic benefit associated with high doses of the selective serotonin reuptake inhibitor (SSRI) citalopram hydrobromide (Celexa), the FDA has reduced the recommended maximum to 40 mg/day.

Previously, the agency had approved a 60-mg/day dose of the antidepressant for certain patients.

The new dosing instruction was prompted by postmarketing surveillance reports and a prospective trial linking the 60-mg dose to unacceptable QT interval prolongations and Torsade de Pointes.

The trial -- a randomized, placebo-controlled, crossover study in 119 adults -- examined citalopram's effects on QT intervals at doses of 20 mg and 60 mg, the FDA said. (...)

Kobler antidepressiva til åreforkalkning
dagensmedisin.no 4.4.2011
Brukere av antidepressiva har mer åreforkalkning og dermed økt risiko for hjertesykdom og hjerneslag sammenlignet med ikke-brukere.

Det fremkommer av en tvillingstudie blant 500 mannlige tvillinger med en gjennomsnittsalder på 55 år. Funnene ble lagt frem på den årlige kongressen til American College of Cardiology (ACC) denne uken.

Uavhengig av depresjon
Bruk av antidepressiva førte til 5 prosent økning i tykkelsen på carotis – den store halspulsåren. Selv om tidligere forskning har vist en sammenheng mellom depresjon og økt risiko for hjertesykdom, hadde depresjon i seg selv ingen effekt på åreforkalkning (aterosklerose), skriver Reuters Health.

– Dette styrker argumentet om at det trolig er antidepressiva og ikke depresjon i seg selv som kan forklare sammenhengen med hjertesykdom, uttaler kardiolog Amit Shah, som presenterte resultatene i New Orleans.

Lavere biologisk alder
Økningen i tykkelsen på halspulsåren på grunn av antidepressiva-bruk ble beregnet å utgjøre en forskjell i biologisk alder på fire år. Med andre ord hadde tvillingen som brukte antidepressiva arterier som var fire år eldre enn brorens årer. (...)

(Anm: åreforkalkning (aterosklerose); Arteriene er de blodårene som frakter blod fra hjertet til resten av kroppen. Når du er frisk, har arteriene en glatt innside og de er elastiske nok til å tilpasse seg store blodtrykksvariasjoner, slik at blodet passerer fritt gjennom blodåren. (...) Noen ganger oppstår fettavleiringer på innsiden av arteriene. Disse avleiringene starter ofte på steder der arterien deler seg, eller der karveggen er noe skadet. En slik fettavleiring kalles for aterom. Et plakk er en stor aterom-masse. (...) Utviklingen av et plakk starter med at kolesterol "graver" seg inn i veggen på blodåren. Kroppen forsøker å reparere denne skaden, det dannes arrvev som gjør karveggen tykkere og stivere og blodåren smalere. Ettersom mer kolesterol avleires, blir karveggene tykkere og blodstrømmen inne i karet går saktere. Dette betegnes i medisinsk terminologi for aterosklerose (åreforkalkning) og er blant annet årsaken til trange arterier i hjertemuskelen, det vil si koronar hjertesykdom og hjerteinfarkt. (...) (nhi.no 16.9.2009)

(Anm: Forkalkning i halskar (carotisstenose); Hva er forkalkning i halskar? Forkalkning i halskar (carotisstenose) er en forholdsvis vanlig tilstand hos eldre mennesker. Sykdommen oppstår når kalkavleiringer fester seg i veggen på halskarene og gjør dem trangere. Carotisstenose oppstår først og fremst hos eldre mennesker. Ca 10% av alle 80-åringer har tilstanden. De fleste har ingen plager eller symptomer, og vi kaller dette asymptomatisk carotisstenose. En sjelden gang kan små biter fra forkalkningen løsne og følge blodstrømmen til hjernen. Dette vil kunne forårsake små drypp eller hjerneslag. Dette kalles symptomgivende carotisstenose. Tilstanden forekommer vanligst hos personer som også har forkalkninger i blodkar andre steder i kroppen. Det er beregnet at ca. 20% av alle hjerneinfarkter - den vanligste typen hjerneslag - er forårsaket av blodpropp fra a. carotis. (nhi.no 12.11.2010).)

Antidepressants linked to heart risk: twins study (Antidepressiva linket til hjerterisiko: tvillingstudie)
reuters.com 2.4.2011
(Reuters) - Middle-age men who use antidepressants are more likely to have a narrowing of blood vessels, increasing the risk of heart attacks and strokes, than those who do not use the medications, according to a study presented on Saturday.

A study of twins found evidence of atherosclerosis, as measured by the interior thickness of the carotid artery, regardless of the type of antidepressant taken.

Antidepressant use was found to cause a 37 micron increase in carotid artery thickness, or roughly 5 percent, according to the study of more than 500 male twins with a mean age of 55 which was presented at the American Cardiology scientific meeting in New Orleans.

In 59 sets of twins in which one brother was taking an antidepressant and the other was not, the brother taking the medication had on average a 41 micron thicker inner lining of the artery, the research found.

As each year of life has been associated with a 10 micron increase in carotid artery thickening, the brother taking the antidepressant had arteries that were essentially four years older than those of his non-medicated twin. (...)

Association of Cerebrovascular Events With Antidepressant Use: A Case-Crossover Study (Forbindelser mellom cerebrovaskulære hendelser (f.eks. hjerneslagslag, TIA "drypp") og bruk av antidepressiva, en kasus kontrollstudie (case-control study))
Am J Psychiatry 2011 (Published March 15) (American Psychiatric Association)
OBJECTIVE: The authors sought to assess the risk of cerebrovascular events associated with use of antidepressant medications.

RESULTS: The adjusted odds ratio of stroke risk with antidepressant exposure was 1.48 (95% confidence interval=1.37–1.59) using 14-day time windows. Stroke risk was negatively associated with the number of antidepressant prescriptions reported. Use of antidepressants with high inhibition of the serotonin transporter was associated with a greater risk of stroke than use of other types of antidepressants.

KONKLUSJONER: Disse resultater tyder på at antidepressiva kan være assosiert med en øket risiko for hjerneslag. Imidlertid er de underliggende mekanismer uklare. (...) (CONCLUSIONS: These findings suggest that antidepressant use may be associated with an increased risk of stroke. However, the underlying mechanisms remain unclear.)

(Anm: TIA - "drypp" (...) Plutselig mister du noe av følelsen i høyre arm og ben. Du må støtte deg mot et tre for ikke å falle. (nhi.no).)

(Anm: Hjerneslag (apopleksi) er plutselig innsettende tap av kroppsfunksjoner på grunn av forstyrrelser i hjernens blodsirkulasjon. Hjerneblødning er årsak i 10-15% av tilfellene, mens blodpropp i blodårer i hjernen (trombose) er årsaken i 80-85% av tilfellene. Går symptomene tilbake i løpet av 24 timer, kaller vi det transitorisk iskemisk atakk, TIA - på norsk brukes betegnelsen "drypp". De fleste TIA varer i under en time. (nhi.no).)

(Anm: apopleksi, apoplexia cerebri, hjerneslag, akutte fokale nevrologiske symptomer og utfall som varer i mer enn 24 timer og som skyldes skade av hjernevev enten på grunn av regionalt redusert blodsirkulasjon (hjerneinfarkt) eller på grunn av hjerneblødning. Kilde: Store norske leksikon.)

Antidepressants May Raise Risk for Cardiovascular Disease (Antidepressiva kan øke risiko for kardiovaskulær sykdom ( hjerte- og karsykdomsykdom))
depression.about.com 5.4.2011
New research suggests that antidepressants may raise the risk for cardiovascular disease.

In a study involving more than 500 middle-aged male twins, researchers found that those twins who took antidepressants of any type were more likely to have a thickening of the inner linings of the arteries in the neck than their twin brothers who didn't. This type of thickening has been previously found to be associated with heart attack and stroke.

"There is a clear association between increased intima-media [inner arterial lining] thickness and taking an antidepressant, and this trend is even stronger when we look at people who are on these medications and are more depressed," said lead investigator Dr. Amit Shah, a cardiology fellow at Emory University in Atlanta, in a written statement issued by the American College of Cardiology. "Because we didn't see an association between depression itself and a thickening of the carotid artery, it strengthens the argument that it is more likely the antidepressants than the actual depression that could be behind the association."

Dr. Shah noted that the link between heart health and antidepressants is not well-understood, but it could be that the chemical messengers that are affected by antidepressant use, such as serotonin and norepinephrine, might cause constriction of blood vessels, leading to increased blood pressure, a known risk factor for hardening of the arteries. (...)

Pfizer, Lilly Antidepressants Linked to Narrowed Arteries in Older Men (Pfizer-, Lilly-antidepressiva linket til innsnevring av arteriene (aterosklerose; åreforkalkning) hos eldre menn)
Bloomberg.com 2.4.2011
Antidepressants may narrow the arteries of middle-aged men, potentially putting them at risk for heart attacks and stroke, researchers said.

A study involving 513 male twins, with an average age of 55, found those who took medications like Forest Laboratories Inc. (FRX)’s Lexapro, Eli Lilly & Co. (LLY)’s Cymbalta or Pfizer Inc. (PFE)’s Zoloft had thicker blood vessel walls. The increase, a measure of fatty-plaque buildup linked to atherosclerosis, was seen regardless of what type of antidepressant the men were taking.

Arteries naturally thicken with age, and each 10-micron increase is linked to a 1.8 percent higher risk of heart attack and stroke. Men taking antidepressants had a 41-micron thicker lining than their twin brothers who weren’t on medication, making their arteries appear about four years older. The difference was greatest in men who were depressed while taking the drugs, according to the study presented today at the American College of Cardiology meeting in New Orleans.

“Because we didn’t see an association between depression itself and a thickening of the carotid artery, it strengthens the argument that it is more likely the antidepressants than the actual depression that could be behind the association,” said lead researcher Amit Shah, a cardiology fellow at Emory University in Atlanta, in a statement.

The U.S. National Institutes of Health funded the study.

Antidepressants increase levels of brain chemicals including serotonin and norepinephrine, which may cause blood vessels to constrict, Shah said. The narrower opening may limit blood flow and boost hypertension, triggering atherosclerosis and heart disease, he said. Additional studies are needed to confirm whether the medications, the condition or other factors are responsible for the changes, he said. (...)

TIA Doubles Risk for Later Heart Attack (TIA dobler risiko for hjerteinfarkt)
medpagetoday.com 24.3.2011
The occurrence of a transient ischemic attack (TIA) doubles a person's risk for a subsequent myocardial infarction, a population-based study found.

The relative risk for myocardial infarction (MI) among a cohort of patients who had experienced a prior TIA was 2.09 (95% CI 1.52 to 2.81), according to Robert D. Brown Jr., MD, and colleagues from the Mayo Clinic in Rochester, Minn.

The risk was highest for patients whose TIA occurred before age 60 (RR 15.1, 95% CI 4.11 to 38.6), the researchers reported online in Stroke: Journal of the American Heart Association. (...)

Tricyclics Increase CVD Risk (Trisykliske øker risiko for hjerte-kar-sykdom (CVD; Cardiovascular Disease))
medpagetoday.com 30.11.2010
(...) In a prospective cohort study that included 14,784 adults, those using tricyclics had a 35% increased cardiovascular risk after adjustment for potential confounders including symptoms of depression and anxiety, which are known risk factors for cardiovascular disease (HR 1.35, 95% CI 1.03 to 1.77). (...)

Some previous studies have suggested that any association between the use of antidepressants and risk of cardiovascular disease can be attributed to depression, not the drugs.

Hamer and colleagues disagreed. (...)

Further analysis showed that both tricyclic and SSRI users had a higher risk of stroke in age- and sex-adjusted models:

Tricyclics, HR 2.23 (95% CI 0.85 to 6.39)
SSRIs, HR 3.32 (95% CI 1.20 to 9.18)

But the researchers cautioned that the findings on risk of stroke should be interpreted with caution.

They pointed out that there were only 78 events and the association with SSRIs was weakened after multivariate adjustment (HR 2.46, 95% CI 0.87 to 6.96). (...)

(Anm: Antidepressant medication use and future risk of cardiovascular disease: the Scottish Health Survey. Eur Heart J 2010 (First published online: November 30, 2010.)

Antidepressants May Raise Women's Stroke Risk (Antidepressiva kan øke kvinners risiko for hjerneslag)
minorityhealth.hhs.gov 14.12.2009
(…) It found that women on selective serotonin uptake inhibitors (SSRIs, which include Celexa, Paxil, Prozac and Zoloft) had a 45 percent increase in risk for stroke and a 32 percent increase in risk for death from any cause, compared to non-users. Similar results were found for women on tricyclic antidepressants. (…)

- Pfizers Zyvoxid (Zyvox) og antidepressiva kan være en dødelig kombinasjon

Zyvox (linezolid): Drug Safety Communication - Serious CNS Reactions Possible When Given to Patients Taking Certain Psychiatric Medications
fda.gov 21.10.2011
(...) ISSUE: FDA has received reports of serious central nervous system (CNS) reactions when the antibacterial drug linezolid (Zyvox) is given to patients taking psychiatric medications that work through the serotonin system of the brain (serotonergic psychiatric medications. A list of the serotonergic psychiatric medications that can interact with linezolid can be found in the Drug Safety Communication. Safety information about this potential drug interaction and important drug usage recommendations for emergency and non-emergency situations are being added to the drug labels for serotonergic psychiatric medications and linezolid.

BACKGROUND: Linezolid is used to treat infections, including pneumonia, infections of the skin, and infections caused by a resistant bacterium (Enterococcus faecium). It is a reversible monoamine oxidase inhibitor (MAOI). Although the exact mechanism of this drug interaction is unknown, linezolid inhibits the action of monoamine oxidase A — an enzyme responsible for breaking down serotonin in the brain. It is believed that when linezolid is given to patients taking serotonergic psychiatric medications, high levels of serotonin can build up in the brain, causing toxicity. This is referred to as Serotonin Syndrome — signs and symptoms include mental changes (confusion, hyperactivity, memory problems), muscle twitching, excessive sweating, shivering or shaking, diarrhea, trouble with coordination and/or fever.

A separate Drug Safety Communication (DSC) is being released today for methylene blue due to similar potential drug interactions with serotonergic psychiatric medications and includes drug usage recommendations. (...)

FDA Warns About Nervous System Reactions from Zyvox, Methylene Blue (FDA advarer om reaksjoner i nervesystemet fra Zyvoxid (Zyvox), Methylene Blue)
aboutlawsuits.com 27.7.2011
Federal drug regulators are warning that there is a risk of serious central nervous system reactions when the drugs Zyvox and methylene blue are used with some antidepressants, including Paxil, Zoloft, Prozac and Cymbalta, among many others.

The FDA issued a drug safety communications for methylene blue and Zyvox on Tuesday, indicating that the agency analyzed adverse event reports that included reports of central nervous system (CNS) toxicity and some deaths. The reactions were due to drug interactions between the two drugs and psychiatric medications that affect the serotonin system of the brain, according to the FDA warning.

Methylene blue and Zyvox are both reversible monoamine oxidase inhibitors (MAOI). Methylene blue is used to treat cyanide poisoning, methemoglobinemia, vasoplegic syndrome and ifosfamide-induced encephalopathy. It is also used as a dye in therapeutic and diagnostic applications. Zyvox (linezolid) is used to treat infections, including pneumonia, skin infections and methicillin-resistant Staphylococcus aureus (MRSA).

The FDA warning includes a full list of serotonergic psychiatric medications that could react with the drugs. The list includes selective serotonin reuptake inhibitors (SSRIs), which are the most common psychiatric drugs on the market, as well as tricyclic antidepressants, serotonin-norepinephrine reuptake inhibitors (SNRIs) and other MAOIs and psychiatric drugs. The list includes some of the most prescribed drugs in the world, such as Paxil, Prozac, Zoloft, Celexa, Lexapro, Effexor, Cymbalta, Wellbutrin and Zyban.

Why the interaction between the drugs causes CNS toxicity is unknown, but the FDA states that some experts believe that the Zyvox and methylene blue cause high levels of serotonin to build up in the brain when used with the serotonergic drugs, resulting in toxicity. This is known as serotonin syndrome and can cause confusion, hyperactivity, memory loss, muscle twitching, excessive sweating, shivering and shaking, diarrhea, fever and trouble with coordination.

The agency is recommending that patients prescribed methylene blue and Zyvox should be taken off of any of the listed antidepressants two weeks prior. However, in some cases the drugs are given as an emergency treatment. In those instances, doctors should attempt to find an alternative method of treatment, the FDA recommended.

The antidepressants can be resumed 24 hours after the last dose of methylene blue and Zyvox, the FDA stated.

(Anm: linezolid (antibiotika; Zyvox i USA); Zyvoxid (in Europe), and Zyvoxam (in Canada and Mexico). Generics are also available in India, such as Linospan (Cipla). (en.wikipedia.org).)

(Anm: Serotonin syndrom (SS), kramper, parkinsonisme osv. (forhøyet kroppstemperatur) (mintankesmie.no).)

(Anm: Seroxat (Paxil) (paroxetine; paroksetin) (SSRI) (mintankesmie.no).)

Pfizer's Zyvox and Antidepressants May Be Fatal Combination (Pfizers Zyvoxid (Zyvox) og antidepressiva kan være en dødelig kombinasjon)
sfgate.com 26.7.2011
July 26 (Bloomberg) -- Pfizer Inc.'s Zyvox antibiotic can cause potentially fatal central nervous system reactions in patients who also take antidepressants that increase levels of the brain chemical serotonin, U.S. regulators said.

Pfizer's Zoloft and Pristiq, Eli Lilly & Co.'s Cymbalta and GlaxoSmithKline Plc's Paxil and Wellbutrin are among 29 psychiatric drugs that patients may need to stop taking temporarily when they require treatment with Zyvox, the Food and Drug Administration said today in a drug safety communication.

Zyvox, used to treat some types of drug-resistant bacteria including MSRA or methicillin-related Staphylococcus aureus, skin infections and nosocomial pneumonia, can interact with the antidepressants to cause a toxic reaction known as serotonin syndrome in which excess amounts of the chemical build up in the brain, according to the FDA.

Some deaths among patients who suffered such a reaction were reported to the FDA's adverse-event database, the agency said. Pfizer, based in New York, reported $1.18 billion in revenue from Zyvox last year. (...)

(Anm: linezolid (antibiotika; Zyvox i USA); Zyvoxid (in Europe), and Zyvoxam (in Canada and Mexico). Generics are also available in India, such as Linospan (Cipla). (en.wikipedia.org).)

FDA Warns of Serious Drug Interactions in Patients Taking Psychiatric Drugs (FDA advarer mot alvorlige interaksjoner hos pasienter som tar psykiatriske legemidler)
JAMA 2011 (July 27)
Patients taking certain psychiatric drugs may experience serious neurological problems if they are given the antibacterial medication linezolid (sold under the brand name Zyvox) or methylene blue, a drug that is also used as a dye in some diagnostic procedures and for certain other uses, such as treating cyanide poisoning, according to a pair of warnings issued yesterday by the US Food and Drug Administration (FDA).

The warning applies to psychiatric drugs that affect the brain’s serotonin system and includes those used to treat depression such as selective serotonin reuptake inhibitors, serotonin-norepinephrine reuptake inhibitors, tricyclic antidepressants, monoamine oxidase inhibitors, and certain other psychiatric drugs. A full list of these drugs is available on the FDA’s Web site. (...)

(Anm: linezolid (antibiotika; Zyvox i USA); Zyvoxid (in Europe), and Zyvoxam (in Canada and Mexico). Generics are also available in India, such as Linospan (Cipla). (en.wikipedia.org).)

FDA: Avoid Methylene Blue or Linezolid With Serotonergics
medscape.com 26.7.2011
July 26, 2011 — Physicians generally should avoid prescribing either methylene blue or linezolid (Zyvox,Pfizer) in combination with serotonergic agents such as paroxetine or duloxetine to avoid a potential drug interaction causing a dangerous condition called serotonin syndrome, the US Food and Drug Administration (FDA) announced today.

Linezolid is an antibacterial agent, and methylene blue is a dye used in diagnostic procedures and in the treatment of conditions ranging from methemoglobinemia to cyanide poisoning.

Through its Adverse Event Reporting System (AERS) database, the FDA has learned of serious central nervous system reactions when either drug has been given to patients taking other drugs that work through the serotonin system of the brain. (...)

Zyvox (linezolid): Drug Safety Communication - Serious CNS Reactions Possible When Given to Patients Taking Certain Psychiatric Medications (Zyvox (linezolid): Sikkerhetskommunikasjon legemidler - Alvorlige CNS-reaksjoner mulig når det gis pasienter som inntar visse psykiatriske legemidler)
fda.gov 26.7.2011
ISSUE: FDA has received reports of serious central nervous system (CNS) reactions when the antibacterial drug linezolid (Zyvox) is given to patients taking psychiatric medications that work through the serotonin system of the brain (serotonergic psychiatric medications. A list of the serotonergic psychiatric medications that can interact with linezolid can be found in the Drug Safety Communication. Safety information about this potential drug interaction and important drug usage recommendations for emergency and non-emergency situations are being added to the drug labels for serotonergic psychiatric medications and linezolid. (...)

RECOMMENDATION: Linezolid should generally not be given to patients taking serotonergic drugs. However, there are some conditions that may be life-threatening or require urgent treatment with linezolid such as when:

Linezolid is used to treat vancomycin-resistant Enterococcus faecium (VRE) infections.
Linezolid is used to treat infections such as nosocomial pneumonia and complicated skin and skin structure infections, including cases caused by methicillin-resistant Staphylococcus aureus (MRSA).

Patients should not stop taking their serotonergic psychiatric medicine without first talking to a healthcare professional. Read the Drug Safety Communication for other specific recommendations for Healthcare Professionals and for Patients. (...)

(Anm: linezolid (antibiotika; Zyvox i USA); Zyvoxid (in Europe), and Zyvoxam (in Canada and Mexico). Generics are also available in India, such as Linospan (Cipla). (en.wikipedia.org).)

Methylene Blue: Drug Safety Communication - Serious CNS Reactions Possible When Given to Patients Taking Certain Psychiatric Medications
fda.gov 26.7.2011
ISSUE: FDA has received reports of serious central nervous system (CNS) reactions when the drug methylene blue is given to patients taking psychiatric medications that work through the serotonin system of the brain (serotonergic psychiatric medications). A list of the serotonergic psychiatric medications that can interact with methylene blue can be found in the Drug Safety Communication. Safety information about this potential drug interaction and important drug usage recommendations for emergency and non-emergency situations are being added to the drug labels for serotonergic psychiatric medications. (...)

RECOMMENDATION: Methylene blue should generally not be given to patients taking serotonergic drugs. However, there are some conditions that may be life-threatening or require urgent treatment with methylene blue such as when it is used in the emergency treatment of methemoglobinemia, ifosfamide-induced encephalopathy, or cyanide poisoning.

Patients should not stop taking their serotonergic psychiatric medicine without first talking to a healthcare professional. Read the Drug Safety Communication below for other specific recommendations for Healthcare Professionals and for Patients. (...)

- Bruk av antidepressiva under svangerskapet linket til høyere risiko for autisme

Antidepressants in Pregnancy and Autism: A Possible Link (Antidepressiva i svangerskapet og autisme: En mulig link)
boston.com 13.11.2011
Studies abound that aim to answer both the question "What causes autism?" and "What is the reason for the increase in incidence and prevalence of autism?" A study published in the November issue of the Archives of General Psychiatry, Antidepressant Use During Pregnancy and Childhood Autism Spectrum Disorders caught my attention. As both the prevalence of autism and the use of SSRI's (selective serotonin reuptake inhibitors) have increased dramatically in recent years, and SSRI's are powerful medications that act on the brain, the findings do seem plausible. (...)

In this population based study done at the Kaiser Permanente Medical Care Program in Northern California, the researchers found

a 2-fold increased risk of ASD (autism spectrum disorder) associated with treatment with selective serotonin reuptake inhibitors by the mother during the year before delivery, with the strongest effect associated with treatment during the first trimester.

They found that there was no increase in risk for ASD if a mother had been treated for mental health problems but did not receive SSRI's. This finding attempts to answer the question of whether it is the depression or the drug that is associated with ASD. Their findings suggest that it is the drug. (...)

Antidepressant Use During Pregnancy Linked to Higher Risk of Autism (Bruk av antidepressiva under svangerskapet linket til høyere risiko for autisme)
healthland.time.com 5.7.2011 (Time)
Children whose mothers use antidepressants during pregnancy may be more likely to develop autism than kids whose mothers do not, say researchers in California.

In a study involving data on more than 1,800 children — fewer than 300 of whom had an autism spectrum disorder (ASD) — and their mothers, the scientists found that women who were prescribed drugs to treat depression in the year before giving birth were twice as likely to have children with an ASD, compared with women who did not take antidepressants. The risk was even greater for women who were prescribed the drugs in the first trimester: their children were nearly four times more likely to develop autism or a related disorder.

The study focused on one type of antidepressant, selective serotonin reuptake inhibitors (SSRIs), a class of drug that includes fluoxetine (Prozac), paroxetine (Paxil) and sertraline (Zoloft). These antidepressants work by increasing available levels of the neurotransmitter serotonin surrounding nerve cells in the brain, which helps boost mood. (...)

Antidepressant Use During Pregnancy and Childhood Autism Spectrum Disorders (Bruk av antidepressiva under svangerskapet og autisme)
Arch Gen Psychiatry 2011 (Published online July 4)
(...) Results Prenatal exposure to antidepressant medications was reported for 20 case children (6.7%) and 50 control children (3.3%). In adjusted logistic regression models, we found a 2-fold increased risk of ASD associated with treatment with selective serotonin reuptake inhibitors by the mother during the year before delivery (adjusted odds ratio, 2.2 [95% confidence interval, 1.2-4.3]), with the strongest effect associated with treatment during the first trimester (adjusted odds ratio, 3.8 [95% confidence interval, 1.8-7.8]). No increase in risk was found for mothers with a history of mental health treatment in the absence of prenatal exposure to selective serotonin reuptake inhibitors.

Conclusion Although the number of children exposed prenatally to selective serotonin reuptake inhibitors in this population was low, results suggest that exposure, especially during the first trimester, may modestly increase the risk of ASD. The potential risk associated with exposure must be balanced with the risk to the mother or fetus of untreated mental health disorders. Further studies are needed to replicate and extend these findings. (...)

SSRI's And Environment Strong Autism Contributing Factors Over Genes
Editor's Choice
medicalnewstoday.com 5.7.2011
New research this week points to a link between the use of selective serotonin reuptake inhibitors (SSRIs), a type of antidepressant, and the occurrence of autism in unborn kids. Another study found that among twins, the environment plays a bigger role in the development of autism than genetics which is a game changer considering past investigation into autism cause factors.

Over the past 30 years, the number of children with autism has increased from about 4 in 10,000 to about 40 in 10,000.

First off, research led by Kaiser Permanente Northern California reviewed the medical records of more than 1,600 children, 298 of whom had autism spectrum disorders (ASDs). They found that the risk of having a child with autism spectrum disorder was about twice as high among women who took SSRIs in the year before delivery. That risk was even four times higher in women who took SSRIs during their first trimester. SSRIs include such well-known brands as Prozac, Zoloft, Paxil and Celexa. (...)

Data Confirm Trend of Sharp Rise in ASD Cases (Data bekrefter trend med sterk økning av autismetilfeller)
Psychiatr News 2011;46(14):20 (July 15) (American Psychiatric Association)
Among 388,644 children born in one state from 2001 to 2005, more than 3,000 were enrolled in an early-intervention program for autism spectrum disorders by age 3, and in that period, the numbers rose steeply.

In a reflection of national trends, a recent study of children in Massachusetts reports that diagnoses of autism spectrum disorders (ASDs) are increasing, particularly among boys. The study was published online May 16 in Pediatrics. (...)

They discovered that 1 of every 129 children born in Massachusetts in that five-year period was enrolled in an early intervention for an ASD by age 36 months. Early ASD diagnoses increased linearly from 1 in 178 for the 2001 birth cohort to 1 in 108 for the 2005 birth cohort, an increase of 66 percent. (...)

Serotonin and the Autisms (Serotonin og autisme)
Arch Gen Psychiatry 2011 (Published online July 5)
A Red Flag or a Red Herring?

The struggles to provide mechanistic insight regarding the causes of the autisms (autism spectrum disorder [ASD]) continue as the data mount from the newest population-based studies finding that ASD diagnoses affect 1% to 2% of the population.^1-2 Twin and sibling studies support the highly heritable nature of ASD risk, and at-risk younger siblings may have a recurrence risk of 15% to 20%. The newest estimates concur that rare mutations and copy number variants may account for up to 20% of cases.³ What about the other 80%? The genomecentric emphases have resulted in an opacity regarding the idea that through enhanced risk and/or endophenotype modulation, environmental factors are likely to interact with genetic components to participate at some important level in ASD etiology. Yet, the generation of convincing evidence of specific environmental factors remains a struggle, with the few exceptions of medication (eg, valproate sodium) or prenatal infection. Co-occurrence does not impart guilt, so the many candidates identified based on increases of exposures to a variety of agents that parallel an increase in ASD prevalence remain unsubstantiated. The problem is that even benign environmental elements can affect brain development in experimental systems because the building of well-functioning brain architecture is exquisitely sensitive to both genetic and environmental regulation. So, the field is left with basic findings that implicate a variety of genetic and epigenetic factors, together with associated small to modest increases in odds ratios for ASD due to a lengthening list of investigated environmental factors. (...)

Perhaps it is a coincidence that the odds ratio for ASD risk in the study by Croen and colleagues increases when first-trimester exposure to SSRIs is the sole factor. However, it is exactly that time of human brain development during which cortical and subcortical neuronal populations are being produced, migrating to their final destinations and beginning the long process of wiring. While much occurs later, the establishment of a strong foundation developmentally may be an essential component of healthy brain development. Croen and colleagues note more than once in their article that the study should not be taken as carte blanche for withholding SSRI treatment from pregnant mothers who are suffering the stress of depression and related disorders. Altered neurochemistry and stress response systems during pregnancy may affect the fetus as well. New basic neurobiology studies that focus on the importance of 5-HT in brain development and further advances in analyzing prospectively collected clinical data and outcomes will lead to a sound evidence-based approach to the clinical management of individuals who are suffering during a period that should be among the most joyous in their life. (...)

Is Autism, at Least in Part, a Disorder of Fetal Programming?
Arch Gen Psychiatry 2011 (Published online July 5)
The year 1977 marked an important milestone in the history of autism. In this year, the first twin study in autism was published by Folstein and Rutter¹; it demonstrated a striking difference in concordance rates between monozygous (MZ) and dyzgyous (DZ) twins. The studies that followed reported even higher MZ concordance rates, up to 90%, for a broader phenotype resembling what is currently labeled as autism spectrum disorder (ASD)^2-4 and DZ concordance rates at or close to 0%. This resulted in heritability estimates greater than 90%, suggesting that almost all of the variance in phenotypic expression could be attributed to inherited genetic factors.

There was an important need to revisit those early heritability estimates given that there have been significant improvements in the diagnosis of ASD and that the prevalence rates on which the original models were based are now much greater. In addition, the fact that the concordance for DZ twins was so close to 0% has always been a puzzling finding largely ascribed to the imprecision of the estimates. Family studies of nontwin siblings have suggested that the recurrence risk is closer to 5%, or even 10%, once stoppage rules are taken into account.⁵ Even so, based on these twin studies, ASD was often described as the most heritable of psychiatric disorders. It must be admitted, though, that the field has been frustrated by the difficulty in identifying the specific inherited genetic mechanisms for the etiology of ASD. Even the recent genome-wide association studies have not given us any smoking guns, and the top hits have been difficult to replicate. (...)

- Økt dødsrisiko dødsrisiko for psykotrope legemidler

Concern over elderly antidepresssant use (Bekymringer over eldres bruk av antidepressiva)
irishhealth.com 3.8.2011
The prescribing of antidepressants to older people needs to be carefully considered, as newer antidepressants may not be as safe for this population as previously thought, a new study suggests.

According to recent research, depression remains a significant public health problem across all parts of the world, affecting 121 million people, including up to 400,000 people in Ireland.

The condition is common among older people due to a number of specific risk factors, such as changes in roles and/or lifestyle, illness and hormonal changes triggered by the menopause.

UK researchers noted that there is very little known about the safety of new generation antidepressants in older people. These drugs are known as SSRIs (selective serotonin reuptake inhibitors) and include Seroxat and Prozac. (...)

The participants were monitored until the end of 2008. During that time, almost nine in 10 received at least one prescription for an antidepressant. Just over half of these prescriptions were for SSRIs, while one in three were for older antidepressants, known as tricyclic antidepressants (TCAs). The rest were prescribed other types of antidepressants.

The study then looked at the link between antidepressant use and a number of adverse outcomes, such as heart attack, stroke, attempted suicide, attempted self-harm, falls, fractures and epilepsy.

After taking into account other factors which may have influenced the results, the study found that SSRIs increased the risk of a number of adverse outcomes compared to TCAs.

This increased risk was also found among people who took other types of antidepressants.

Overall, SSRIs appeared to increase the risk of all-cause mortality, stroke, epilepsy or seizures, falls, fractures and hyponatraemia (high salt levels in the blood) when compared with TCAs.

Meanwhile the other antidepressants appeared to increase the risk of all-cause mortality, stroke, epilepsy or seizures, attempted suicide or self harm and fractures.

The researchers found that depressed people who were not taking any antidepressants had a 7% risk of dying during the next year. This risk rose to just over 8% for those taking TCAs. However, for those taking SSRIs, the risk increased to almost 11%, while those on other antidepressants had the greatest risk of dying during the following year, at just over 11%.

In terms of suffering an adverse outcome, the most risky time appeared to be during the first 28 days of antidepressant use, as well as the first 28 days after stopping the medication. (...)

Some Psychotropics Risky in Older Patients (Noen psykotrope legemidler utgjør en risiko for eldre pasienter)
medpagetoday.com 28.3.2011
Psychotropic drugs are often used to control behavioral symptoms in nursing-home residents, but data on almost 11,000 older patients found a significantly increased risk of death and other adverse outcomes in those treated with conventional antipsychotic drugs, antidepressants, and benzodiazepines, compared with atypical antipsychotic drugs.

Treatment with conventional antipsychotics increased the relative risk of death by 47% and femur fractures by 61%, reported Krista F. Huybrechts, PhD, of Brigham and Women's Hospital and Harvard Medical School in Boston, and colleagues.

Benzodiazepines were associated with a 54% increased risk of heart failure, while antidepressant users had a 20% to 30% increased risk of death and femur fracture, Huybrechts and co-authors wrote online in CMAJ. (...)

(Anm: Risk of death and hospital admission for major medical events after initiation of psychotropic medications in older adults admitted to nursing homes. CMAJ 2011 (Published online ahead of print March 28).)

Antidepressant Use and Risk of Incident Cardiovascular Morbidity and Mortality Among Postmenopausal Women in the Women's Health Initiative Study
Arch Intern Med. 2009;169(22):2128-2139 (Dec 14/28)
(...) Background Antidepressants are commonly prescribed medications, but their effect on cardiovascular morbidity and mortality remains unclear. (...)

Conclusions In postmenopausal women, there were no significant differences between SSRI and TCA use in risk of CHD, stroke, or mortality. Antidepressants were not associated with risk of CHD. Tricyclic antidepressants and SSRIs may be associated with increased risk of mortality, and SSRIs with increased risk of hemorrhagic and fatal stroke, although absolute event risks are low. These findings must be weighed against quality of life and established risks of cardiovascular disease and mortality associated with untreated depression. (...)

Fosterskader

SSRI-antidepressiva til gravide øker risikoen for høyt blodtrykk i lungene hos barnet
fhi.no 13.1.2012
Kvinner som behandles med antidepressive legemidler av typen SSRI under siste del av graviditeten har en økt risiko for å føde barn med vedvarende høyt blodtrykk i lungene. Det viser en ny studie utført av forskere fra de fem nordiske landene. Fra Norge har forskere ved Folkehelseinstituttet deltatt.
Studien er en såkalt kohortstudie og har vært koordinert av Karolinska Institutet i Stockholm med aktivt bidrag fra forskere ved Folkehelseinstituttet i Oslo. Artikkelen publiseres i det vitenskapelige tidsskriftet British Medical Journal (BMJ). (...)

(Anm: Selective serotonin reuptake inhibitors during pregnancy and risk of persistent pulmonary hypertension in the newborn: population based cohort study from the five Nordic countries. BMJ 2012;344:d8012 (12 January).)

Nordisk studie bekräftar tidigare känt samband mellan SSRI-behandling och ökad risk för högt blodtryck i lungorna hos det nyfödda barnet
lakemedelsverket.se 13.1.2012
En ny nordisk studie omfattande 11 000 barn bekräftar tidigare studieresultat att behandling av kvinnor med depression med SSRI-läkemedel i senare delen av graviditeten kan leda till ökad risk att föda barn som drabbas av högt blodtryck i lungornas blodkärl. (...)

SSRI till gravid ökar risken för högt blodtryck i lungorna hos barnet
ki.se 13.1.2012
[PRESSMEDDELANDE 2012-01-13] Nyfödda barn till kvinnor som behandlas med antidepressiva SSRI-läkemedel under senare delen av graviditeten har en ökad risk att drabbas av kvarstående högt blodtryck i lungornas blodkärl, så kallad persisterande pulmonell hypertension. Det visar en ny samnordisk studie som letts från Karolinska Institutet och som publiceras i den vetenskapliga tidskriften British Medical Journal (BMJ). (...)

Mødre kræver depressionspille-erstatning
politiken.dk 23.12.2011
ANTIDEPRESSIVT. Præparatet Cipramil har været i søgelyset flere gange på grund af uheldige bivirkninger.

Sager om mødres brug af antidepressions-piller under graviditeten strømmer ind.

Nye sager i forbindelse med mødres brug af piller mod depression under graviditeten er det seneste år strømmet ind hos Patientforsikringen.

Alene i 2011 har Patientforsikringen fået syv nye sager om aborter, misdannelser, problemer i udviklingen og andre alvorlige symptomer. Det skriver Ekstra Bladet.

Sagerne er kommet ind efter avisens afsløringer af, at myndighederne har reageret alt for langsomt i forhold til at advare gravide om depresisonspiller, hvilket har fået kvinderne og deres familier til at søge forsikringen om kompensation for skader på deres børn. (...)

Nye alvorlige lykkepiller-sager: Baby uden kranium
ekstrabladet.dk 23.11.2011
Nye choktal fra Lægemiddelstyrelsen: Dødfødt baby, stribevis af aborter og foster uden kranium (...)

Før Ekstra Bladet i foråret satte fokus på sagen havde Styrelsen modtaget 51 indberetninger over en periode på over 10 år. Nu her fem måneder efter Ekstra Bladets første artikler har Lægemiddelstyrelsen pr. 28. september modtaget 35 nye indberetninger om alvorlige bivirkninger, så man i alt er oppe på 86.

Læs også: Gravide proppet med livsfarlige lykkepiller

- De nye tal bestyrker mistanken om, at antidepressiv medicin under graviditeten kan give alvorlige bivirkninger, siger Lektor Lise Aagaard fra Institut for Farmakologi og Farmakoterapi på Københavns Universitet

Bivirkninger kan ramme børn senere i livet
Hos Lægemiddelstyrelsen har man særligt fokus på de bivirkninger, der rammer børn senere i livet:

- Det som vi lægger ekstra mærke til, er rapporterne om forsinket psykomotorisk udvikling. Altså det, at børn flere år efter de har været eksponeret for den her medicin under graviditeten, måske udvikler sig unormalt.

- Det emne vil vi se nærmere på og blandt andet undersøge om andre lande har set det samme og tage kontakt til danske læger, der arbejder med disse patienter, siger overlæge Doris Stenver. (...)

Paxil Plaintiff Settles Birth Defects Lawsuit (Seroxat-saksøker forliker fødselsdefekt-søksmålsøksmål)
lawyersandsettlements.com 20.10.2010
Watertown, SD: A woman who recently settled her Paxil birth defects lawsuit ended a legal ordeal that began with the 2004 death of her newborn son. The woman's Paxil lawsuit alleged her son suffered from Paxil birth defects, including persistent pulmonary hypertension of the newborn (PPHN). (...)

Soldater dør og ikke bare grunnet våpen

Soldiers are dying and not just from guns (Soldater dør og ikke bare grunnet våpen)
romeobserver.com 3.6.2010
(...) When soldiers return from Iraq or Afghanistan, and they have suffered either emotional or physical wounds, especially Traumatic Brain Injury (TBI), they are sent to Warrior Transition Units (WTU’s). Some shocking news has come to light concerning the large numbers of deaths in these WTU’s. For example, an article in the Chicago Tribune in February of 2008 has the Army Surgeon General stating that there has been a "series, a sequence of deaths" in the WTU’s. Many of these deaths were attributed to suicide, but an Army Times article which appeared in April of this year stated that "more than 70 soldiers died while assigned to the 36 WTU’s," but that "suicide is not the major cause of death." That honor belongs to something being referred to as "sudden cardiac arrest." Now, these soldiers may be as young as 20, so we would not expect to see this rate of cardiac arrest in those so young. What is going on? And, further, the wife of a veteran did some basic research and found that 128 veterans had died under similarly strange circumstances, such as "in barracks," "at work station," and none of them were found in a coma. They simply dropped dead.

For some insight into this horrible phenomenon, we can turn to the musings of another psychiatrist, Grace Jackson, who is distinguished in the field of psychopharmatoxicology, or, the ability of psychiatric drugs to poison those who take them. In studying these military deaths, Dr. Jackson has come up with several hypotheses as to the mechanisms of action. Her theories are quite complicated and technical, but I will try to sum them up.

• The psychiatric drugs these soldiers were taking, many of them involving the neurotransmitter serotonin, could have caused a massive dysregulation of the autonomic nervous system, which, by the way, is a possible explanation for Sudden Infant Death Syndrome.

• Legemidler som Seroquel og Seroxat (Paxil) kan ha fremtvunget uoppdagede hjernestammeeffekter, slik som slag, anfall eller forstyrrelser i hjerneaktivitet. (The drugs Seroquel and Paxil may have precipitated undetected brainstem effects, such as stroke, seizure or other disruption of brain activity.)

• Those soldiers with TBI may have sustained endocrine anomalies associated with pituitary damage, and drugs such as Seroquel and Paxil exacerbate these pre-existing deficiencies. These drugs could contribute to sudden cardiac death in these cases, as well.

• Sleep apnea is also associated with TBI (I can attest to this from personal experience counseling returning veterans: They ALL had sleep apnea!) The drugs the soldiers are receiving disrupt lung function, and disrupt the electrochemical processes of which contribute to regular sleep, and produce heart arrhythmia, leading to sudden cardiac death. (...)

(Anm: Serotonin syndrom (SS), kramper, parkinsonisme osv. (forhøyet kroppstemperatur) (mintankesmie.no).)

Daily Mail: - Liv ødelagt av lykkepiller

Lives destroyed by happy pills: As our use of antidepressants DOUBLES in a decade, experts say thousands are being given dangerous drugs they don't need (Liv ødelagt av lykkepiller: Idet vårt forbruk av antidepressiva DOBLES på et tiår, sier eksperter at tusener er gitt legemidler de ikke trenger)
dailymail.co.uk 29.6.2010
(...) After about six weeks she went to see her doctor, who diagnosed depression and anxiety. 'I asked him if he was sure, because there were other symptoms such as diarrhoea, weight-loss and vomiting. But he confirmed his diagnosis and prescribed an antidepressant.' (...)

Unfortunately this only made her feel worse; she developed the shakes as well as suicidal thoughts. In an attempt to remedy this, her GP changed the medication three weeks later. But nothing changed.
And after mentioning her suicidal thoughts to her doctor, she was put under the supervision of a mental health team.

Six weeks later, Clare was put on yet another antidepressant, along with a tranquilliser and an anti-psychotic drug. She was now sleeping 14 hours a day; unable to work, she had to rely on her boyfriend for support.

'I was zombified, but still felt the anxiety and the terror, and that didn't seem right. However, my doctor simply increased my dose.' (...)

'The only good part was a brilliant nurse, who took me seriously when I said I'd always felt that something physical had caused my symptoms and put me in touch with a sympathetic private doctor,' she says.

A year-and-a-half after her symptoms began, Clare was diagnosed with an overactive thyroid and a problem with her adrenal glands. 'That was why I had been so bizarrely agitated, had diarrhoea and had lost weight.' (...)

Clare's story is extreme, but it is far from unique. Increasing numbers of Britons are taking antidepressant drugs, with prescriptions doubling over the past ten years, according to a report this month. In 2000, there were 20 million prescriptions - this rose to 39 million last year.

While this rise is partly being blamed on the recession, experts are concerned that misdiagnosis is a major factor. Indeed, a study published recently in The Lancet found that the average GP will wrongly diagnose 16 out of every 100 patients they see with depression and anxiety. (...)

Dyskinesi linket til serotonin

Some PD Dyskinesia Linked to Serotonin (Dyskinesi linket til serotonin hos enkelte med parkinsons sykdom (PD))
medpagetoday.com 30.6.2010
Fetal tissue transplants for Parkinson's disease initially seemed promising, but after a period of improvement, most patients began experiencing involuntary movements. Now British and Swedish researchers think they've worked out the paradoxical cause of that so-called "graft-induced dyskinesia" and in the process identified ways to prevent and treat it, according to Marios Politis, MD, of Imperial College London, and colleagues.

The key is an excess of serotonin-producing neurons in the grafted striatum, Politis and colleagues said in the June 30 issue of Science Translational Medicine.

Dyskinesias in Parkinson's disease are thought to be a result of dopamine, not serotonin, stimulation, but the graft-induced dyskinesias occur in the absence of dopaminergic medication. Politis and colleagues thought that the explanation might lie in the ability of the serotonin neurons to switch to a different neurotransmitter -- to use dopamine as a so-called "false transmitter."

To test the idea, they used brain imaging techniques on two patients who had been given fetal tissue transplants, 12 Parkinson's patients who had not been transplanted, and 12 healthy volunteers.

Positron emission tomography radioactive tracers that bind to dopaminergic neurons and to the dopamine receptor showed that, in the two patients, the grafts had restored the dopamine neurons that decay during Parkinson's disease.

In both patients, the neurons and the amount of dopamine they released returned to normal values after the transplant, Politis and colleagues found.

But in both, there were more serotonin neurons than usual. Specifically:

•In one patient, the ratio of serotonin to dopamine neurons in the grafted region increased by a factor of 2.3 compared with the ratio in normal controls -- at 356 versus 108.
•In the second patient, the ratio was also increased, by a factor of 1.46 -- at 266 versus 108.

The findings suggested that blocking the action of the serotonin neurons might improve the symptoms, Politis and colleagues said. To test the idea, they treated both patients with 15 milligrams of the 5-HT1A agonist buspirone (BuSpar), given in three doses of five milligrams at 30-minute intervals.(...)

(Anm: dyskinesi; dyskinesi. (av dys- og gr. 'sette i bevegelse'), forstyrrede kroppsbevegelser. (...) mer eller mindre permanent art, oftest ved langvarig bruk av nevroleptika. (...) Typisk er stereotype, rytmiske bevegelser i ansikt, tunge og kjevemuskulatur. En viss samtidig muskulær urofølelse kan forekomme (akathisi). Kilde: Store norske leksikon.)

(Anm: akatisi; manglende evne til å sitte stille, sterk rastløshet og trang til å vandre rundt. Akatisi skyldes oftest utilsiktede og uønskede forandringer i sentralnervesystemets funksjon. De er fremkalt av medisiner og er bivirkninger. Akatisi er oftest fremkalt av nevroleptika, spesielt såkalte lavdosenevroleptika, vanligvis ved behandling av alvorlige psykiske lidelser (se psykose). Kilde: Store norske leksikon.)

(Anm: dystonia; dystoni; endring i muskulaturens spenningstilstand, ofte i form av ufrivillige muskelsammentrekninger (f.eks. i nakkemuskulaturen og svelgmuskulaturen. Dystoni kan være symptom ved indremedisinske og nevrologiske sykdommer, men kan også opptre som bivirkning av legemidler som blokkerer signalsubstansen dopamin. Akutte dystonier sees hos yngre menn noen dager etter at vedkommende har begynt på relativt høye doser med nevroleptika. (...) Ved akutte dystonier på grunn av legemidler er behandlingen tilførsel av antiparkinsonmidler. Kilde: Store norske leksikon.)

- Antidepressiva linket til betydelig risiko for hjerneslag, fall og benbrudd

Do Antidepressants Raise the Risk of Stroke?
Am J Psychiatry 2011; 168:511-521 ( May 2011)
(...) Previous studies have had conflicting results, though some have suggested a link between antidepressant use and stroke. For example, in the large Women's Health Initiative study of postmenopausal women, those receiving treatment with selective serotonin reuptake inhibitors (SSRIs) had a 45% relative increased risk of stroke compared with women not receiving antidepressant treatment (4). In addition, SSRI use was associated with a doubling of the risk of hemorrhagic and fatal stroke (4). (...)

(Anm: TIA - "drypp" (...) Plutselig mister du noe av følelsen i høyre arm og ben. Du må støtte deg mot et tre for ikke å falle. (nhi.no).)

The risk was highest for patients whose TIA occurred before age 60 (RR 15.1, 95% CI 4.11 to 38.6), the researchers reported online in Stroke: Journal of the American Heart Association. (...)

Some previous studies have suggested that any association between the use of antidepressants and risk of cardiovascular disease can be attributed to depression, not the drugs.

Hamer and colleagues disagreed. (...)

Further analysis showed that both tricyclic and SSRI users had a higher risk of stroke in age- and sex-adjusted models:

Tricyclics, HR 2.23 (95% CI 0.85 to 6.39)
SSRIs, HR 3.32 (95% CI 1.20 to 9.18)

But the researchers cautioned that the findings on risk of stroke should be interpreted with caution.

They pointed out that there were only 78 events and the association with SSRIs was weakened after multivariate adjustment (HR 2.46, 95% CI 0.87 to 6.96). (...)

(Anm: Antidepressant medication use and future risk of cardiovascular disease: the Scottish Health Survey. Eur Heart J 2010 (First published online: November 30, 2010.)

Older antidepressants linked to heart risk
irishhealth.com 2.12.2010
People who use older generation antidepressant drugs may be at an increased risk of developing heart disease, the results of a new study indicate. (...)

Secondly, people taking the antidepressants are also more likely to smoke, be overweight, and do little or no physical activity. By giving up smoking, losing weight, and becoming more active, a person can reduce their risk of CVD by two to three-fold, which largely outweighs the risks of taking the medications in the first place. In addition, physical exercise and weight loss can improve symptoms of depression and anxiety," Dr Hamer said.

He pointed out that the majority of previous work in this area has focused on patients who already had heart problems, however this one looked at a healthy population. (...)

Antidepressants linked with significant risk of stroke and fracture (Antidepressiva linket til betydelig risiko for hjerneslag og benbrudd)
pulsetoday.co.uk 3.8.2010
Forskrivning av antidepressiva er assosiert med en betydelig økt risiko for slag, fall og benbrudd hos eldre pasienter ifølge analyser av data fra primærhelsetjenesten utført av britiske forskere. (Antidepressant prescribing is associated with a significantly increased risk of stroke, falls and fractures in older people, according to analyses of primary care data by UK researchers.)

Two analyses by the same team of researchers from the University of Nottingham of the QResearch database – a network of 602 practices in England – found antidepressants increased the stroke rate by up to half, the rate of falls by more than three quarters and the fracture rate by 87% compared with no antidepressant use.

Figures from the NHS information Centre show antidepressants are the 10th most commonly prescribed class of drugs in primary care, with 39 million prescriptions issued in England in 2009.

Although depression is common in older people, clinical trials for antidepressants often under-represent the elderly population so little is known about the risks of adverse events in older patients and the relative safety of individual drugs in this class. (...)

Serotonerg ubalanse? (Svindelen som aldri tar slutt)

Study Undermines Case For Antidepressants (Studie undergraver bevis for antidepressiva)
forbes.com 5.1.2010
(...) Såkalte selektive serotoninreopptakshemmere (SSRIer) slik som Seroxat, Prozac og Zoloft, er utstrakt brukt på bakgrunn av teorien om at deprimerte mennesker lider av mangel på hjernekjemikaliet serotonin. Men få harde data støtter det populære konseptet, ifølge Kirsch. "Hele idéen med serotoninmangel er en myte." (...) (So-called selective serotonin reuptake inhibitors such as Paxil, Prozac and Zoloft, gained widespread use on the theory that depressed people suffer from a deficit of the brain chemical serotonin. But little hard data supports the popular concept, Kirsch says. "This whole idea of serotonin deficiency is a myth.")

Det er ikke eksakt kjent hvor mange pasienter med mild depresjon som tar antidepressiva. Men en undersøkelse sitert av forskerne fant at 71 % av alle pasienter som søker behandling for depresjon faller i den mildere kategori, hvor det er sannsynlig at placebo virker like bra. (...) (It is unknown exactly how many patients taking antidepressants have milder cases of depression. But one survey cited by the researchers found that 71% of all patients seeking treatment for depression fall in the milder category, where placebos are likely to do as well.)

(Anm: paroksetin (paroxetine); markesføres i Norge under handelsnavn som bl.a. Seroxat; Paxil i USA.)

(Anm: Svindelen som aldri tar slutt (forskning.no 17.4.2004).)

(Anm: Antidepressant Drug Effects and Depression Severity A Patient-Level Meta-analysis. JAMA. 2010;303(1):47-53 (January 6).)

Ads for SSRI antidepressants are misleading, say researchers (Reklamer for SSRI-antidepressiva er villedende, ifølge forskere)
medicalnewstoday.com 12.11.2005
Reklamer for en klasse antidepressiva kalt SSRI-er påstår ofte at depresjon skyldes kjemisk ubalanse i hjerne, og at SSRI-er korrigerer denne ubalansen, men disse påstander er ikke støttet av vitenskapelig bevis, uttaler forskere i PLoS Medicine. (Consumer ads for a class of antidepressants called SSRIs often claim that depression is due to a chemical imbalance in the brain, and that SSRIs correct this imbalance, but these claims are not supported by scientific evidence, say researchers in PLoS Medicine.)

Selv om forskere på 1960-tallet antydet at depresjon kan være linket til lavt nivå av serotonin (den såkalte "serotonin-hypotese"), sier de at forskning hittil har mislykkes å bekrefte hypotesen. (Although scientists in the 1960s suggested that depression may be linked to low brain levels of the chemical serotonin (the so-called "serotonin hypothesis"), contemporary research has failed to confirm the hypothesis, they say.)

Forskerne--Jeffrey Lacasse, doktorgradkandidat Florida State University og dr. Jonathan Leo, professor i neuroanatomi ved Lake Erie College of Osteopathic Medicine--gransket amerikansk forbrukerreklame for SSRI-er publisert i trykte medier, fjernsyn, og internett. De fant mange påstander om at SSRI-er gjenoppretter serotoninbalansei hjernen. "Men likevel er der ikke etablert noe vitenskapelig som tilsier at "balanse" av serotonin korrigeres," ifølge forfatterne. (...) (The researchers--Jeffrey Lacasse, a doctoral candidate at Florida State University and Dr. Jonathan Leo, a neuroanatomy professor at Lake Erie College of Osteopathic Medicine--studied US consumer advertisements for SSRIs from print, television, and the Internet. They found widespread claims that SSRIs restore the serotonin balance of the brain. "Yet there is no such thing as a scientifically established correct 'balance' of serotonin," the authors say.)

(Anm: Serotonin and Depression: A Disconnect between the Advertisements and the Scientific. PLoS Medicine 2005;2:0101-0106 (December 2005). (PDF).)

Debate Simmers Over Popular Antidepressant Ad Claims (healingwell.com) (Debatten koker grunnet reklamepåstander om populær antidepressiva)
healthfinder.gov 28.2.2006
Der er ingen bevis for at depresjon stammer fra en kjemisk ubalanse i hjernen, hevder kritikere. (There's no evidence depression stems from a chemical imbalance in the brain, critics say.)

-- Mange amerikanere har sett TV-reklamer for Pfizers reseptbelagte antidepressiva Zoloft. (...) (-- Many Americans have seen the television ad for Pfizer Inc.'s prescription antidepressant Zoloft.)

Denne type utsagn er formidlet i reklamekampanjer så ofte overfor forbrukere av selektive serotoninreopptakshemmere (SSRI) at kritikere sier at disse påstander nå tilsynelatende oppfattes som en slags vitenskapelig sannhet. (Statements like these have been repeated so often in direct-to-consumer ad campaigns for selective serotonin reuptake inhibitor (SSRI) antidepressants that critics say they now have the ring of scientific truth.)

Derfor kan mange amerikanere "bli svært overrasket over at ikke en eneste artikkel kan fremvises som direkte påviser at depresjon er et resultat av mangel på serotonin," sa Jeffrey Lacasse, en doktorgradsstudent ved Florida State University's College of Social Work. (...) (That's why many Americans "might be particularly surprised that not a single article can be produced which directly demonstrates that depression is the result of a serotonin deficiency," said Jeffrey Lacasse, a doctoral student at Florida State University's College of Social Work.)

New Strategy For Developing Antidepressants
medicalnewstoday.com 10.12.2007
Researchers may be able to develop an antidepressant which takes effect almost immediately by directly targeting novel molecules in the brain instead of taking a less direct route, which can lead to longer times for medication to take effect, according to a new study presented at the American College of Neuropsychopharmacology (ACNP) annual meeting. The antidepressant is also thought to be effective in people for whom previous treatments have been ineffective. This human and rodent research is among the first to examine the effects of rapid antidepressant strategies. (...)

Onset of action of antidepressants
BMJ 2007;334:911-912 (5 May)
(...) A meta-analysis of 76 double blind placebo controlled trials of antidepressant treatment for depression in 2005 found that 60% of overall improvement occurred during the first two weeks and that half of all patients who respond to a six week trial respond in the same period.¹⁰ More recently, a meta-analysis of placebo controlled trials of selective serotonin reuptake inhibitors suggested that therapeutic response is greatest in the first week, with a gradual decline in the size of benefit over successive weeks of treatment.¹¹ One third of the total effect seen at six weeks was apparent in the first week.¹¹ As the studies were placebo controlled trials, this improvement was unlikely to be a placebo effect. (...)

Widow to testify at Senate committee hearing on drug safety
expertclick.com 14.3.2007
Kim's husband, Timothy (Woody) Witczak, was a 37-year-old dynamic and upbeat, happily married man who was prescribed Zoloft because he was having difficulty sleeping due to job-related stress. He was on Zoloft for about five weeks with an increased dose before he committed suicide (by hanging himself from the rafters in his garage). He had no history of mental illness or suicidality.

His symptoms after Zoloft and before his death included profuse sweating, worsened insomnia, horrible nightmares, headaches, agitation and an odd feeling in his head (he told his wife that he felt like his head was "detached from [his] body.") This phenomenon has been acknowledged by Pfizer in internal company documents to be a side effect of Zoloft.

Kim Witczak has become an influential victim advocate for drug safety. As a result of Woody’s death, Kim established www.woodymatters.com. The website serves as an information clearing house on antidepressant risks and a forum for other victims. FDA reform has become an increasingly important goal of woodymatters.com. Kim has traveled to Washington D.C. over 20 times to advocate for antidepressant warnings as well as FDA reform. Kim has, on numerous occasions, testified before the FDA, US Congress, and Minnesota legislature concerning these issues. Kim’s story has been featured in a number of news reports, including the November 2005 issue of Fortune Magazine and in an I-Team feature on WCCO TV in Minneapolis. She has also been on NPR regarding drug advertising.

See: WCCO TV I-Team Report: www.wcco.com/iteam/local_story_142142535.html
Star Tribune article “The Battle for Woody”: www.baumhedlundlaw.com/media/ssri/Zoloft/Witczak/Battle-for-Woody.pdf (...)

SSRIs start to relieve depression soon after the start of treatment
BMJ 2006;333 (9 December)
Abstract
Research question Do selective serotonin reuptake inhibitors take weeks to work?

Answer Probably not. Symptoms of depression improve during the first week of treatment (...)

UM study links genetic mutations to depression
sun-sentinel.com 26.9.2006
University of Miami researchers reported new evidence Monday that clinical depression appears to be caused by inborn genetic mutations. (...)

New Depression Findings Could Alter Treatments
nytimes.com 8.8.2006
The results of two new studies may signal a substantial shift in the way psychiatrists and researchers think about treatment for severely depressed patients. (...)

Clinical & Research News Brain Protein Could Be Treatment Breakthrough
Psychiatr News 2006;41:45 (April 21)
American Psychiatric Association
The finding that substance P is implicated in depression and posttraumatic stress disorder should boost efforts to see whether substance P antagonists can counter the disorders.

It looks as though a small protein discovered in horses' brains 75 years ago, and since dubbed substance P, may play a role in depression and posttraumatic stress disorder (PTSD). (...)

Hjerneskader årsag til depression
netdoktor.com 7.4.2006
Er man over 50 år og får sin første depression, kan det skyldes blodpropper i hjernen. Delresultater fra et forskningsprojekt under den nyoprettede neuropsykiatriske enhed i Risskov viser nemlig, at fire ud af ti patienter har læsioner i hjernen.

Hjerneskader og depressioner ser derfor ud til at være tæt forbundet, men det er svært at sige, hvad der opstår først. Overlæge Poul Videbech fra Center for Psykiatrisk Grundforskning håber, at den nye viden fra undersøgelsen kan være med til at fjerne det sociale stigma ved depression.

Formålet med undersøgelsen er at fastslå årsagen til hjerneskaderne og at forhindre, at de udvikler sig og forårsager demens. (...)

Depression kan måles i hjernen
netdoktor.com 20.10.2005
Depression kan måles i hjernen, da den ser anderledes ud hos personer, der lider af en svær depression end hos raske personer.

Depressive personer har nemlig en væsentligt forhøjet blodgennemstrømning i hippocampus området i hjernen. Det område har blandt andet betydning for følelser, drifter og hukommelse ligesom det regulerer kroppens respons på stress.

Det viser en ny stor undersøgelse af deprimerede patienters hjerner fra Center for Psykiatrisk Grundforskning i Århus. Man undersøgte 42 svært

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- Hvorfor antidepressiva ikke alltid virker

Advarsler

- Antidepressiva og risiko for bryst- og eggstokkreft: En gjennomgang av litteratur og forskernes tilknytning til industrien

- Antidepressiva linket til hjertedød

- Antidepressiva øker risiko for åreforkalkning, erektil dysfunksjon, hjertesykdom og hjerneslag

- Pfizers Zyvoxid (Zyvox) og antidepressiva kan være en dødelig kombinasjon

- Bruk av antidepressiva under svangerskapet linket til høyere risiko for autisme

- Økt dødsrisiko dødsrisiko for psykotrope legemidler

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Daily Mail: - Liv ødelagt av lykkepiller