27 Apr 2018

Connection btwn Huntington's and CPN?


Hi,I am wondering if there is a connection between Huntington's Disease and CPN or other gram negative bacteria infections. A friend of the family has this desease and it has progressed to the point that she has just checked herself into a nursing home, she has 2 children and is only 36.


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:


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

Completed Stratton/Wheldon regime for aggressive secondary progressive MS in June 2007, after four years, three of which intermittent.   Still improving bit by bit and no relapses since finishing treatment.

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 cpn 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.


Paula Carnes

They've tried minocycline in Huntington's disease, and it appears to do a lot of good. To quote the abstract of this paper:

"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."

OK, so it is this defective gene that is allowing infection to take place? and the infections cause the degeneration? Do they know what the normal function of the gene is?...and how certain are they that it is genetic? didnt they once think that MS was genetic, but one of the purposes of this site is to educate pple that it is actually caused by a pathogen? I also have a friend who has MS, and she was told that it was genetic, and was told never to have children because there is a 50% chance they could have it. (not because CPN can pass through uterine wall, but because it was "genetic")

rosaceai : 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.

MS 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

Completed Stratton/Wheldon regime for aggressive secondary progressive MS in June 2007, after four years, three of which intermittent.   Still improving bit by bit and no relapses since finishing treatment.

Like Sarah says, no one in our family has MS 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 Cpn 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.

Michèle (UK) GFA: Wheldon CAP 1st May 2006. Daily Doxy, Azi MWF, metro pulse.

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 CAP, we will not know the potential bacterial aspect of this disease and how would it possibly relate to the genetics.

Trials with minocycline already put some light on it, so until the HD, KD person is not going through CAP and mainly Flagyl 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]

CFS, Severe Peripheral neuropathy, Insomnia, Azitromycine/Clarithromycine/Roxytromycine, Doxycycline 2x100mg, Caffeine every day, Tinidazol for pulsing, ACC 2 x 600 mg -  treatment duration: 24 months

Spinobulbar muscular atrophy (SBMA) is a late-onset disorder characterized by progressive muscle loss, degeneration of motoneurons in the spinal cord and brainstem, and partial androgen insensitivity. SBMA is directly correlated with the expansion of CAG repeats encoding a polyglutamine tract (polyQ) of extended length. The identification of polyQ expansion in SBMA led to the discovery of an entire class of neurodegenerative disorders. In fact, at least eight different diseases, including Huntington’s disease, share a common molecular mechanism involving an expansion of a polyQ tract within different proteins. The elongated polyQ tract causes a toxic gain of function in the mutant protein and is associated with the formation of intracellular aggregates, whose pathogenetic role has not been fully established yet. Our observations in a motoneuron cell line (NSC34), indicate that the expression of the androgen receptor (AR) carrying the elongated polyQ tract (AR-Q48) has a toxic effect in aggregate-independent manner. In fact, in basal condition, AR-Q48 shows a cytoplasmic diffuse distribution, yet it reduces the viability of transfected NSC34. In contrast, testosterone treatment, while inducing aggregation of the mutant AR, also increases cell viability. Aggregates in NSC34 are localized mainly in the perinuclear region and occasionally in the neuropil, whereas no nuclear aggregate has ever been found. Further observations of the minor subset of cells showing neuropil aggregates, reveal an alteration of the neurite morphology, suggesting a different role of the two types of cytoplasmic aggregates.http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WGC-4RHFVJJ-2&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=46017593c3b112395edc0c9b296ea40d

CFS, Severe Peripheral neuropathy, Insomnia, Azitromycine/Clarithromycine/Roxytromycine, Doxycycline 2x100mg, Caffeine every day, Tinidazol for pulsing, ACC 2 x 600 mg -  treatment duration: 24 months


Just saw this study tonight and it made me think of this thread.  Here's an interesting study out of CNRS and Stanford on the potential for participation of infection in the root cause of Huntington's Disease:



Treatment for Rosacea

  • CAP:  01/06-07/07
  • High-Dose Vit D3, NAC:  07/07-11/08
  • Intermtnt CAP, HDose Vit D3:  11/08-01/09
  • HDose Vit D3, Mg, Zn: 01/09-