Cpnhelp.org

Eveningdream,I'm afraid not. Huntington's is a genetic disease caused by a dominant gene, passed on by one of the parents.  This means that each child has a 50% chance of developing the disease:

http://www.essortment.com/all/whatishuntingt_rctd.htm

It must be truly awful for a parent to be told he or she has the disease, knowing then that all of the children have a 50% chance of developing the same thing...............Sarah

An Itinerary in Light and Shadow

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Yes, but, but, but...

Huntington's is genetic but the cause of death is infection that the body can't control. It seems to me that a protocol that controls cpni might keep the brain of a Huntington's patient functioning longer. It's been awhile since I read on Huntington's but I recall thinking the same thing about using some sort of antibiotic protocol to prolong the mind and the life in Huntingtons.

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Paula Carnes

"We administrated minocycline to 14 patients with genetically confirmed HD. The patients were psychiatrically, neurologically and neuropsychologically evaluated at baseline, and after 6 and 24 months of treatment, using the Unified HD Rating Scale and a neuropsychological test battery. After 12 months, three patients were lost to follow-up so that 11 patients were analysed at the endpoint. Minocycline was well tolerated. Unlike the expected natural course of HD, patients exhibited stabilization in general motor and neuropsychological function at endpoint, after improving in the first 6 months. Moreover, we found a significant amelioration of psychiatric symptoms that was not apparent after the first 6 months."

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rosaceaii : to

Its awful to say, but yes, Huntington's disease is definitely an autosomal dominant genetic disease.  The thing that causes death is often an infection, but it wouldn't be life threatening without the Huntington's.  Life in some form can maybe be prolonged for a short time, maybe in a slightly better form, but would your friend want that?

I knew someone with the disease, who eventually died of heart failure, not infection, the father of two people I knew who were both brilliant musicians.  I lost touch with them about fifteen years ago, but both could now be suffering the same thing, or neither of them hopefully.  The father's father didn't have the disease but his mother died when only in her twenties, so she might well have been the carrier but died before she knew it.

MSi has been thought to be caused by many things over the years, one of the first things, in the late nineteenth century was that it had an ineffective cause, disregarded in the interim because until recently no-one could find the infection.  It has a genetic component, but is neither autosomal dominant or regressive.  Nobody in my family has MS apart from me and this applies to most other sufferers................Sarah

An Itinerary in Light and Shadow

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Like Sarah says, no one in our family has MSi except Ella, so although there is a genetic predisposition for MS which has probably been passed down by Hamish's scottish ancestry there is every possibility that Cpni passed to Ella in the womb from me and my family.   There is strong evidence that my father, brothers and sisters have also suffered from the effects of Cpn but not MS.   But if there was a dominant faulty gene for MS as there is in Huntington's there would be others in the family suffering from MS.

That is not to say that infection does not play a part in the progression of Huntington's as it probably does in MS if you believe as we do here that Cpn has a role to play.

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Michèle (UK) GFAi: Wheldon CAPi 1st May 2006. Daily Doxyi, Azi MWF, metroi pulse. Zoo keeper for Ella, RRMSi, At worse EDSSi 9, 3 months later 7 now 6.5 Wheldon CAP 16th March 2006

Just like with Kennedy Disease, I would never doubt the genetic backround which is already known and discussing this matter from this angle is just pointless.

But... until we will not have the person with Kennedy's or Huntington's on CAPi, we will not know the potential bacterial aspect of this disease and how would it possibly relate to the geneticsi.

Trials with minocycline already put some light on it, so until the HD, KD person is not going through CAP and mainly Flagyli trial, we will propably not know whether there is a connection.

Nevertheless, reports of the lifethreatening Pneumoniae that may cause the fatal consequence among HD and KD sufferers looks to me much more then suspecious to say the least.

If you will go through the Kennedy disease data, you will find almost identical text to the one I pasted below.

The age of onset decreases, and the rate of progression of symptoms increase, with the number of CAG repeats. Individuals with greater than approximately 60 CAG repeats often develop juvenile Huntington's disease.^[74][75] There is a variation in age of onset for any given CAG repeat length, particularly within the intermediate range (40–50 CAGs). For example, a repeat length of 40 CAGs leads to an onset ranging from 40 to 70 years of age in one study. This variation means that, although algorithms have been proposed for predicting the age of onset, in practice, it can not be predicted confidently.^[76][77]

The life expectancy is around 15 to 20 years following the onset of characteristic manifestations of the disorder.^[78] Mortality is not caused by Huntington’s disease directly, but by associated complications; these include pneumonia (which causes one third of fatalities), heart failure (although heart disease, cerebrovascular disease and atherosclerosis show no increase), choking, malnutrition and physical injury.^[79] Suicide is an associated risk, with increased suicide rates of up to 7.3 percent, and attempted suicides of up to 27 percent.^[80][81][2]

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CFSi, Severe Peripheral neuropathy, Insomnia, Azitromycine/Clarithromycine, Doxycycline 2x100mg, Calcium Pyruvate 6000mg 5 days before pulse, Metronidazol 3x250mg, ACC 2 x 600 mg -  treatment duration: 7 months, Charcoal 1000 mg/day, Chlorella, Cholestyram

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CFSi, Severe Peripheral neuropathy, Insomnia, Azitromycine/Clarithromycine, Doxycycline 2x100mg, Calcium Pyruvate 6000mg 5 days before pulse, Metronidazol 3x250mg, ACC 2 x 600 mg -  treatment duration: 7 months, Charcoal 1000 mg/day, Chlorella, Cholestyram