A $25,000 grant was awarded to Maria Pennuto, Ph.D. from the National Institute of Health. Dr. Pennuto has spent the past few years investigating the molecular switches on the AR that are involved in the movement of the AR into the nucleus upon addition of hormone. She has discovered that certain chemical changes to the AR seem to reduce the ability of the AR to bind to hormone and thus not enter the nucleus (and cause KD!!). She has discovered that the exposure of cells to a substance known as IGF-1 can induce these chemical changes to occur to the mutant AR and thus prevent the movement of the AR to the nucleus. Thus, the addition of IGF-1 to a cell with mutant AR appears to prevent the formation of the toxic fragment and thus the cell stays alive. Dr. Pennuto will continue this work by determining if any other chemical changes to the AR may alter its movement to the nucleus and she will also determine if IGF-1 prevents the formation of KD symptoms in a KD mice model (up to this time, the effect of IGF-1 has only been shown to work in cell cultures. This work could lead to new therapies for KD.
i was getting to that. I have been looking up CAG repeats and stuff. basically this disease is something that doesnt rear its head until later in life. from what i have been reading it starts off/worsens when testosterone hits the androgen receptors. usually shows up mid 30s-40s. what if we have this disease and we kick started by suppressing the 5AR and building up too much testosterone. its a horrible possiblity but one none the less that would help explain our symptoms and it seems easy enough to test for to confirm or rule out.
further, there are researchers for this right now that are working on studying AR mutations and perhaps we could reach out to them regarding our situation!?
also if i am reading this right it looks like she was able to curb off the effects of the mutation with IGF-1
isnt that the point of the “theories” section?
I was worried I was getting Kennedys or some other androgen receptor disease at the beginning with my muscle loss and shrinkage, neuro seemed to rule it out. I thought you’d seen a neuro?
How did he rule this out? A nerve conduction test?
I don’t think so, he made me walk about and did that thing where they hit your knee for a reflex. He probably did a couple of other things I’ve forgotten about. He was cool and believed my story but said it would ‘flush out of my system’ then referred me on to an endo. No EMG testing or whatever it was that mew got.
I did see a Neuro but who knows what she is thinking
soemthing else of note. i remember that JN had gotten much better with HGH which increases IGF-1
Its your theory, so prove it right or wrong or youre wasting everyones time
haha ordering right now buddy its open in the other tab right now - by the way im hoping for the love of GOD that this ISNT what we have this would be aweful. a disease that makes your AR not work and the more testosterone you give it the worse it gets
thank you for doing that wontgiveup
no worries! whats another hundred bucks at this point
mda.org/publications/Quest/e … /sbma.html
Mice with an SBMA-like disease benefited from extra IGF1 genes in their muscle fibers
Note: “LIKE-disease” even if we dont have this disease… this wasnt the exact thing either but IGF1 helped
Nice one bud, 
Got tested for this this morning via an emg and nerve conduction test - which let me tell you is not pleasant (they stick needles in your muscles and move them around) and it was 100 percent normal.
Have you had any muscle loss/twitches?
Guys, do you know dutasteride is Kennedy Disease patients miracle drug?
Maybe we suffer something similar, in that andorgens/ dht are harmful for us ever since they returned when dropping finasteride
Post links to info regarding this to elaborate further please.
kennedysdisease.blogspot.com/2011/07/dutasteride-update-five-months.html
kennedysdisease.blogspot.com/2011/09/dutasteride-and-asc-j9-updates.html
ncbi.nlm.nih.gov/pubmed/21216197
Kennedy’s disease is completely different to PFS obviously, but i think it’s interesting because it is something to do with the androgen receptor and DHT is not good for these guys. Considering so many of us ‘crashed’ when DHT probably came flooding back, you never know, maybe it is harmful for us too? i am not trying to put forward a serious theory here, simply writing down some thoughts. I am most interested in there use of dutasteride.
I think Blase is onto something when he talks about DHT being pro inflammatory in some cases. The ‘crash’ event makes me think we had/ are having a bad reaction to DHT since we stopped suppressing it by 70% using finasteride.
“Spinal and bulbar muscular atrophy (SBMA) or Kennedy’s disease is a slowly progressive,
X-linked motor neuron disease for which there is currently no treatment. It is caused by a
mutation in the androgen receptor that results in a polyglutamine repeat expansion. Recent
animal studies have demonstrated that decreasing endogenous androgen levels leads to
functional improvement and increased survival. Studies have also shown that high levels of
5 alpha-reductase, the enzyme that converts testosterone to the more potent
dihydrotestosterone (DHT), are present in the ventral spinal cord, while low levels of this
enzyme are found within skeletal muscle. Thus, by selectively decreasing levels of DHT with
dutasteride, a 5 alpha-reductase inhibitor, it is hypothesized that there will be a
selective protection of motor neurons, without the adverse effects of reducing the anabolic
effects of androgen on muscle.”
I don’t know how long you guys want to ignore the fact that 5 AR inhibitors have in cases helped PFS. I certainly am not.
Efficacy and safety of dutasteride in patients with spinal and bulbar muscular atrophy: a randomised placebo-controlled trial
ncbi.nlm.nih.gov/pubmed/21216197
Phase 2 trial of leuprorelin in patients with spinal and bulbar muscular atrophy
ncbi.nlm.nih.gov/pubmed/19259967
Followed by…
Efficacy and safety of leuprorelin in patients with spinal and bulbar muscular atrophy (JASMITT study): a multicentre, randomised, double-blind, placebo-controlled trial (2010)
ncbi.nlm.nih.gov/pubmed/20691641
Spinal and bulbar muscular atrophy: ligand-dependent pathogenesis and therapeutic perspectives.
ncbi.nlm.nih.gov/pubmed/15133611
There are some interesting similarities; ‘ligand-dependent toxicity’. But anti-androgens arent used for this condition and its not a miracle drug for them - even for the person in the blog.
Can I ask bluecloud87 aka Joe-91/Uk20/sanfran55/BaldyLocks to stop lying and trying to encourage continued use of Finasteide.