Arrrrgh - Singh MMR autism findings were dismissed by NHS

[Guest guest]

Based on the comments from experts, such as

Professor Lachmann: http://www.lobbywatch.org/profile1.asp?PrId=74

I was too nauseous then to research into other expert quoted here http://news.bbc.co.uk/1/low/health/2182690.stm

[Guest guest]

Natasa,

This is mad how i only asked the Question on MBP just before you

found this on Mylein Shreath.

I was honestly going to post last night and say I had a crazy thought

that some autisms are caused my MMR being a autoimmune disorder that

causes metobolic disturbance (mito dys) and with a sensistive

immunue/neuroimmune (needed MMR as trigger). I only told my son's

tutors my mad theory on it yesturday....now I don't feel so mad!

I look to NIDS also and I believe in a neuro and bio route is what my

son needs. My next on the list to look at Yasko. He does need the

total dairy as both say but to be safe I will do total gluten too.

The NIDS is more approp for me as I have CFS and mutiple allergies. I

know that if I had had the MMR I would have regressed at that

age.....wish was me and not my baby :0(

I think my son's Dr is open to other areas and wants to help me as a

mum finding answers...all I know if my son has LQT (I have it) he

wont be able to have SSRI. But as soon as I read about buying the

cheapest white bread from Goldberg I did. Do you go to US Natasa for

NIDS? You answered my Q on NIDS when I asked was their one in UK ages

ago ;0)

As Lachmann contridicted himself, saying MMR was not a cause.... but

their is a big gap in autism research....thats why the pros will have

to disregard and forget what he said! he shot himself in the foot

their!

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> Based on the comments from experts, such as

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> Professor Lachmann: http://www.lobbywatch.org/profile1.asp?

PrId=74

>

>

> I was too nauseous then to research into other expert quoted here

> http://news.bbc.co.uk/1/low/health/2182690.stm

>

[Guest guest]

Hi, interesting you mention LQT – is it genetic or acquired?

if genetic (which type?) it could possibly be causing or contributing to autism

if it is acquired it is possibly downstream of whatever is causing your autoimmune problems as well as autism !!!

“... Acquired causes of the long QT syndrome include drugs, electrolyte imbalance, toxins, marked bradycardia, subarachnoid hemorrhage, stroke, myocardial ischemia, protein-sparing fasting, autonomic neuropathy, and human immunodeficiency virus disease...”

esp interesting the one describing worsening of LQT in simultaneuos HIV and hpC coinfection.... So obviously viral proteins able to affect cellular excitability/ionic exchanges in the heart

Also shame about first letter here on QT interval prolongation and antiretroviral treatment, not available for free

we are not on NIDS would love to try but £$£$

Clin Infect Dis. 2007 May 15;44(10):1388-9; author reply 1389-91.

QT interval prolongation and antiretroviral treatment: another point of interest.

Chinello P, Petrosillo N. Publication Types: * Comment * Letter PMID: 17443482 [PubMed - indexed for MEDLINE]

Arch Intern Med. 2006 Nov 13;166(20):2288-9; author reply 2289-90.

* Arch Intern Med. 2006 Jun 26;166(12):1280-7.

QTc prolongation in human immunodeficiency virus-infected persons.

Petrosillo N, Lisena FP, Chinello P. Publication Types: * Comment * Letter

PMID: 17101952 [PubMed - indexed for MEDLINE]

3: J Electrocardiol. 2006 Apr;39(2):199-205. Epub 2005 Nov 28.

Importance of hepatitis C coinfection in the development of QT prolongation in HIV-infected patients.

Nordin C, Kohli A, Beca S, Zaharia V, Grant T, Leider J, Marantz P.

Department of Medicine, i Medical Center, Bronx, NY 10461, USA. nordin@...

BACKGROUND: Case reports and unblinded studies suggest that human immunodeficiency virus (HIV) disease is associated with QT prolongation and torsade de pointes ventricular tachycardia. Hepatitis C coinfection is common in patients with HIV disease, and cirrhosis is also associated with QT prolongation. We therefore undertook a systematic analysis of the role of liver injury, nutritional state, and coinfection with hepatitis C in the etiology of QT prolongation in HIV disease. METHODS: We performed a blinded, controlled retrospective cohort study of 1648 patients over a 3-year period at a university-affiliated municipal hospital. All electrocardiograms were included if patients with HIV disease had measurements of CD4 count and viral load within 3 months and serum electrolytes within 30 days (n = 816). Control subjects were chosen randomly from the general medicine service (n = 832). QT interval was measured in lead II and corrected for heart rate by Bazett's formula (QTc). RESULTS: QTc was slightly but significantly longer in patients with HIV disease than in controls (443 +/- 37 vs 436 +/- 36 milliseconds, P < .001). Patients with hepatitis C had more pronounced QTc prolongation (452 +/- 41 vs 437 +/- 35 milliseconds, P < .001). CD4 count, HIV viral load, and HIV medications had no effect on QTc. When patients with hepatitis C were excluded from the analysis, there was no statistical difference between patients with HIV disease and controls (438 +/- 34 vs 436 +/- 36 milliseconds, P = .336). Multiple linear regression revealed that both HIV and hepatitis C infection predicted QTc prolongation, as did age, female sex, history of hypertension, use of opiates, low serum K+ and albumin, and high AST. Hepatitis C coinfection nearly doubled the risk of QTc of 470 milliseconds or greater in patients with HIV disease (29.6% vs 15.8%, P < .001). CONCLUSIONS: Human immunodeficiency virus and hepatitis C infections both independently prolong QTc. Coinfection with hepatitis C greatly increases the likelihood of clinically significant QTc prolongation in patients with HIV disease.

PMID: 16580420 [PubMed - indexed for MEDLINE]

4: Am J Med. 2002 Jan;112(1):58-66.

Clinical and therapeutic aspects of congenital and acquired long QT syndrome.

Khan IA. Division of Cardiology, Department of Medicine, Creighton University School of Medicine, Omaha, Nebraska, USA.

The long QT syndrome is characterized by prolongation of the corrected QT (QTc) interval on the surface electrocardiogram. It is associated with precipitation of a polymorphic ventricular tachycardia, torsade de pointes, which may cause sudden death. The syndrome is a disorder of cardiac repolarization caused by the alterations in the transmembrane potassium and sodium currents. Six genetic loci for the congenital forms of the syndrome have been identified; sporadic cases occur because of spontaneous mutations. Acquired causes of the long QT syndrome include drugs, electrolyte imbalance, toxins, marked bradycardia, subarachnoid hemorrhage, stroke, myocardial ischemia, protein-sparing fasting, autonomic neuropathy, and human immunodeficiency virus disease. Clinical symptoms are the result of the precipitation of torsade de pointes and range from such minor symptoms as dizziness to syncope and sudden death. Short-term treatment is aimed at preventing the recurrences of torsade de pointes and includes intravenous magnesium and potassium administration, temporary cardiac pacing, and correction of electrolyte imbalance; rarely, intravenous isoproterenol is indicated. Long-term management includes use of beta-blockers, permanent pacemaker placement, and cardioverter-defibrillator implantation. Asymptomatic patients are treated if under the age of 40 years at the time of diagnosis.

Publication Types: * Review

PMID: 11812408 [PubMed - indexed for MEDLINE]

5: Ann N Y Acad Sci. 1999 Apr 30;868:418-22.

Virus-mediated modification of cellular excitability.

s DC, Marban E, Nuss HB.

Section of Molecular and Cellular Cardiology, s Hopkins University School of Medicine, Baltimore, land 21205, USA.

Publication Types:

* Research Support, Non-U.S. Gov't

PMID: 10414312 [PubMed - indexed for MEDLINE]