Prevalence, Progression, Symptoms: what's good for one may not be good for the others.

For instance, there's good epidemiological evidence that smoking reduces the chance of getting PD. But that does not, of itself, mean that smoking slows progression or reduces symptoms for someone diagnosed with PD.

Or, for another example, taking levodopa lessons my symptoms, but its impact on my progression is unclear.

How does this affect us?

Well, probably most of us on this forum are more interested in progression and symptoms, rather than etiology, per se. But, it seems to me, that most of the research is to do with etiology.

I'm not, here at least, interested in the ethics of this distribution. I am interested in how we use etiological data as evidence for the impact on progression and symptoms.

Does anyone have any examples of risk factors or therapies that are good/bad for prevalence while having the opposite effect on progression or symptoms?

John

No one here has questioned your ethic of using surveys to obtain information. They are concerned with the quality of the information gathered from your survey. Your motivation for asking people to complete surveys is , without a doubt, absoluty pure. You would like to be able to offer hope and invite this community a chance to offer a symptom overlooked. You are most welcome here and at many other sites as well.

You are excited about your idea, but some people do not , for whatever reason, want to fall in line and cooperatewith idea. Please do not take it as an assualt on your ethical values. "I'm not, here at least, interested in the ethics of this distribution" If I misunderstood your post, I humbly apologize

Dianna.

Dianna,

Thank you for your reply. Unfortunately, you've misunderstood my post. But, it's for me to apologize for not being clearer.

The ethical question I refer to is how should society divide a finite research effort between working in areas that benefit future generations and efforts that benefit the present generation of PwP. But, as I said I don't want to discuss that in this thread.

You mention surveys. Yes, I am excited by their power and it saddens me that more people don't take part. But, it wasn't my intent to discuss them here either.

What I would like us to discuss is our use of evidence, mainly academic papers, in our discussions. It is common for us, and that includes me, to try to translate a piece of research that relates to pre-diagnosis behaviour into potential therapies to reduce post diagnosis symptoms and progression.

A good example of this is smoking.

The academic evidence suggests that people who smoke have about half the chance of getting PD as those who don't [1].

Now, what evidence does that give to the question: would starting to smoke reduce the progression rate of a PwP who has never smoked? And, if it did, would this be worth the dangers that smoking would bring?

The answer depends, at least in part, of your view of the disease's etiology. If you take a view that once triggered the disease progresses remorselessly then it might be too late to start smoking once you've been diagnosed. If, however, you take the view that the disease progresses because of a continuous environmental assualt, then it may make sense.

References

[1] "Parkinson's Disease Risks Associated with Cigarette Smoking, Alcohol Consumption, and Caffeine Intake"
Harvey Checkoway, Karen Powers, Terri Smith-Weller, Gary M. Franklin1, W. T. Longstreth Jr.,
Phillip D. Swanson
Am. J. Epidemiol. (2002) 155 (8): 732-738.
http://aje.oxfordjournals.org/content/155/8/732.long

John

https://www.michaeljfox.org/foundati...kinson-disease

soccertese, thanks for bringing to my attention the MJFF article. It highlights in a specific way what I would like us to discuss in general. The debate is more topical than I expected.

Unfortunately the article having set expectations high by being titled "Nicotine Patches to Stop... Parkinson's Disease?" contains the following assertion:
"Of course, smoking a pack a day to maybe prevent the onset of PD hardly makes sense — the adverse effects of puffing on nicotine cigarettes certainly outweigh any potential benefits."
This, it seems to me, underestimates the seriousness of PD.

The article also, IMHO, confuses possible pre-diagnostic outcomes - "prevent the onset of PD" - with a post diagnostic trial cohort - "will enroll 160 PD patients". This is exactly the kind of reasoning that I think is found in many posts. At least, we are in good company.

It goes on to say:
"The good news for people with Parkinson's, says Boyd, is that pre-clinical studies have shown that nicotine could protect dopamine-producing neurons in the brain from dying."
Whether this is good news to all PwP depends on your view of the etiology of PD. If you take the view that 80% of the doperminergic neurons in the SN are dead before symptoms occur and that this process continues during the course of the disease, it is probably too late to benefit advanced PwP. If, however, you have a different view of the disease's etiology, this protection property could be very useful.

The issue of timing is also important. The article says that it is hoped that "high level results" are available by 2015. That sounds great, but wait...
"A best case scenario: The results both show that disease progression is slowed, and are convincing enough to encourage a larger follow-up study which could prove to be more definitive." When is the earliest it could be approved? Probably too late for me.

I think that many of us on this forum are here because we believe that new, more effective therapies will arrive too late to benefit us; and, more positively, that we can short-cut the regulation process by intercepting promising therapies to improve our personal condition before our disease has progressed too far to get a benefit. In short, we have to weigh the cost of acting too soon, on insufficient, possibly incorrect data, against the cost of acting too late, while knowing that the disease is relentlessly progressing. Either way, there is no risk-free option open to us.

What makes this case particularly interesting is that, here in the UK at least, nicotine patches are readily available: even in supermarkets.

On the evidence of the data that we have, should we try them?

I am not going to use them until there is more evidence. Why? Because, and this is the point of the thread, most of the data refers to possibly preventing PD, not curing it. What may be good for one may not be good for the other.

As a final point, I note that the epidemiological evidence is about smoking, while the trial is about nicotine. It is possible to think of other routes by which smoking could affect PD. See Conductor71's thread.

http://neurotalk.psychcentral.com/thread182519-2.html

John

There is much interest at the moment in the role of alpha-synuclein in the pathogenesis PD. I thought it would be interesting to go through my posts, most of which were based on epidemiological evidence, and see if there were any implications of an involvement of alpha-synuclein.

Hong et al. write [1]:
"We show that nicotine and hydroquinone inhibit α-synuclein fibril formation in a concentration-dependent manner, with nicotine being more effective."

This suggests that smoking reduces both the incidence of PD and its rate of progression.

tag johnt:alpha-synuclein

References:

[1] "Smoking and Parkinson’s disease: Does nicotine affect α-synuclein fibrillation?"
Dong-Pyo Hong, Anthony L. Fink, and Vladimir N. Uversky
Biochim Biophys Acta. 2009 February; 1794(2): 282–290.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2647853/

John

Michael J. Fox used to be a smoke sucker. I wonder if he still is?