F-Dopa scan result

[JayPwP]

My f-dopa scan result as per attached picture.

No idea what it means.

Have sent the report to the neurologist.

[WinnieThePoo]

Pretty sure it means you've got Parkinsons disease. right side affected more than the left. If you look at the "commas" on the scan your left comma has hardly any tail and a dim dot, and your right comma is dimming but not as bad as your left. I think

[JayPwP in reply to WinnieThePoo]

Thanks but I have no improvement with c/l

[CaseyInsights in reply to JayPwP]

Interesting! Do let us know the neurologist recommendations 🌺

[JayPwP in reply to CaseyInsights]

Sure. I have a hunch c/l did not work because it is not dopamine deficiency but rather the uptake of dopamine which is the issue.

Putamen requires Acetylcholine as one of the components, to function correctly.

I am thinking ahead. Let's see what the neurologist says. Trying to get an online video appointment by this weekend

[Hikoi in reply to JayPwP]

Now Im confused! Do you think you have lost some Dopamine neurons? Or are you saying you have not lost neurons its just that the neurons dont work properly in you and dont uptake dopamine correctly and this has to do with acetycholine or is it something completely different?

[JayPwP in reply to Hikoi]

I think I have not lost neurons its just that the neurons dont work properly in me

[Hikoi in reply to JayPwP]

Thanks for clarifying.

[JayPwP]

Picture updated

[MBAnderson in reply to JayPwP]

I don't see a picture??

[JayPwP in reply to MBAnderson]

Scan result at the start of the post

[MBAnderson in reply to JayPwP]

I'm only seeing text.

[JayPwP in reply to MBAnderson]

Strange. Anyone else have this problem?

I can see it right below my name under the title of the post. I don't know how to show that to you.

It says:

Findings:-

moderate to severely reduced tracer uptake is seen involving the left putamen. moderate to severely reduced tracer uptake is seen involving the left caudate.

moderate to severely reduced tracer uptake is seen involving the right putamen. Preserved tracer uptake is seen involving the right caudate.

Impression:-

Present F-DOPA PET reveals

* Dopaminergic defect involving the left corpus striatum (putamen>caudate)

* Dopaminergic defect involving the right corpus striatum (involvement of putamen with sparing of caudate)

[sharoncrayn in reply to JayPwP]

Your left and right putamen is impaired (i.e. decreased volume and altered connectivity with your brain's cerebellum) resulting in their decreased activity. Impacts your body's motor functions in a negative manner.

Your scan results are not a rare finding with PD.

Not everyone who has PD responds to sinemet (c/l).

Sharon

[JayPwP in reply to sharoncrayn]

Thanks Sharon. Appreciate it. Any thoughts on mitigation, maybe a Daniel Amen diet, keto, etc.

I believe this will need a mix of diet and exercise and oxygenation. Pharmaceuticals may not have a reparative effect on this.

[sharoncrayn in reply to JayPwP]

I think you have a problem, which is also related to ALZ.

" In addition to finding the expected association between hippocampal atrophy and cognitive decline in Alzheimer's disease, volumes of putamen and thalamus were significantly reduced in patients diagnosed with probable Alzheimer's disease." (Think of it as a "circuit" problem where the voltage is no longer what it once was so your house lights aren't as bright as they once were.)

The critical issue here in your scan (which doesn't address it directly) is that your putamen and caudate are connected to your substanttia nigra, which is the part of the brain that degenerates on the road to PD.

I am NOT saying you are a candidate for ALZ. I am saying your condition is not unique and unusual in PD as well.

I would focus on 1) reducing your levels of oxidative stress, 2) reducing your generation of free radicals, and 3) reducing your generation of ROS in your brain's neurons and glial cells.

How you do that is up to you and your medical professional. No easy task.

Sharon

[JayPwP in reply to sharoncrayn]

Thanks Sharon

[sharoncrayn in reply to JayPwP]

Jay,

Lay out a matrix table with your physician of your drug and supplement alternatives. You may have to work with an MD and a ND to develop it.

For example, in your drug matrix you have: 1) sinemet IR, 2) sinemet CR, 3) Rytary ER,and perhaps 4)stalevo; 5) possibly a dopamine agonist, and 6) a MAO-inhibitor.

Think of it as a chess board where you trying to find the "best" checkmate move. You will have to work through several moves to find it. Don't despair. At the same time, you are doing the same thing for your supplement protocol.

Most importantly, You want to make sure your small intestine microbiome is in very good health because you convert your levodopa in your small intestine. If your SIM is screwed up, you are not going to be able to convert much levodopa. It will never get to the brain.

Therefore, any drug with levodopa isn't going to have any impact (or very little) on you and your PD.

Sharon

[JayPwP in reply to sharoncrayn]

Thanks

[JayPwP in reply to sharoncrayn]

I believe "You want to make sure your small intestine microbiome is in very good health because you convert your levodopa in your small intestine. If your SIM is screwed up, you are not going to be able to convert much levodopa. It will never get to the brain." is incorrect (no offense)

Ldopa converted to dopamine outside the brain does not cross the BBB, that is why cardibopa is added to ldopa to stop ldopa from converting to dopamine outside the brain.

[sharoncrayn in reply to JayPwP]

L-Dopa is an amino acid that undergoes digestion and assimilation in your SIM.

If your SIM is screwed up, it doesn't matter how much Carbidopa you take, or how much L-Dopa you take with it. It all has to go through your SIM before it can be assimilated. If it is only marginally assimilated, only so much of your dose has a chance of getting to the BBB regardless of carbidopa. L-Dopa isn't somehow transported to your BBB by helicopter!

If on top of your SIM being defective, your BBB is also defective, then all the drugs and supplements in the world won't help which is it what happens in end stage PD.

[JayPwP in reply to sharoncrayn]

Thanks

[MBAnderson in reply to JayPwP]

Sharon,

Thank you for ALL your substance.

Do you have a suggestion for getting the small intestine microbiome healthy?

[JayPwP in reply to MBAnderson]

* for getting

[MBAnderson in reply to JayPwP]

Voice recognition software often gets it wrong and I'm not very good at editing.

[JayPwP in reply to MBAnderson]

Same here with typing, and voice recognition doesn't understand my slurred speech

[JayPwP]

DM Neuro says all symptoms and reports point to a dopamine deficiency (& I disagree), but he has no idea why ldopa doesn't work.

Now he has prescribed Syncapone 100 tds.

[sharoncrayn in reply to JayPwP]

I already explained why L-Dopa with carbidopa doesn't work in some cases no matter how much someone takes. If you can't assimilate it, it doesn't work.

Syncapone (150,100,50) or Stalevo is entacapone+levodopa+cabidopa and inexpensive.

Whether ENT is synergistic with carbidopa in preventing L-Dopa from being broken down before crossing the BBB is debatable. Sometimes it is; sometimes it isn't. Side effects from this combination are not unusual.

Sharon

[sharoncrayn in reply to sharoncrayn]

Stalevo is rarely prescribed in the US.

[Kia17]

One of the main important factors for L-dopa to cross the BBB is a good insulin response. If your insulin respose doesn’t work efficiently then chance for Ldopa to get to the brain and making dopamine is slim.

Pre-diabetic people are in this category . How is your diet?

PS: Insulin action has also been shown to regulate neuronal signaling and plasticity.

[JayPwP in reply to Kia17]

Thanks

[sharoncrayn]

Look at your scan results. It is telling you something that is blatantly obvious. On both sides of your brain, especially the left, your dopaminergic neurons are moderately to severely defective.

Therefore, signalling isn't occurring as it should.

Stalevo isn't going to "repair" those damaged neurons, especially the severely damaged ones. It isn't like repairing a car with a new part.

Sharon

[JayPwP in reply to sharoncrayn]

Thanks Sharon.

[sharoncrayn in reply to JayPwP]

The insulin response post above is somewhat obtuse and potentially misleading. Much more specific is the following from Dr. Rice from her rat study (2015) where this THEORY originated from:

“We found that when there’s more insulin in the brain, there will be more dopamine released, not less”

" insulin helps trigger the reuptake of dopamine when insulin levels rise, but also are the first to show that the net effect is a rise in dopamine levels. The results may also be the first to demonstrate that insulin’s role in the dopamine pathway may affect and explain food choices."

" animals fed low-calorie diets had a 10-fold greater sensitivity to increasing insulin levels in the brain (meaning that it took only a tenth of a rise in insulin levels as seen in rats on a normal diet to spur dopamine release)."

"rats on high-calorie diets lost all striatal-brain insulin responsiveness."

Perhaps this is why the ketogenic diet is sometimes successful when one's dopaminegergic neurons are still prevalent enough to function. But keto diets aren't by definition low calorie though some are in the 800-1200 calorie range which is low to very low depending on body weight...80-10-10

Or think strictly vegetarian green veggies with some apples, grapefruit, strawberries, clementines, lemons...very few calories.

So....Go low calorie vegetarian but when you take L-Dopa load your mannitol up which is a sugar polyol. Perhaps. Especially if you believe in rat studies.

But does dopamine increase insulin sensitivity/secretions? Probably not but probably does decrease insulin concentrations.

Sharon

[sharoncrayn]

Jay,

Even though I have a Ph.d in biochemistry and 10 years of experience in working with 2 PD support groups, I don't have the answers to what causes PD or why it progresses, or what can be done to stop the progression. Everyone has an idea, but when it comes down to it, it is all theory.

Some will argue otherwise citing this study or that study, but nothing much has really changed in the PD world since the 1970s on a treatment level for most PD people. We can cure rats, mice and fruit flies, but not people, at least not in the long term.

So your ideas or your doctor's ideas are as good as anyone's. The only thing that is important is finding what works for you. Just keep hunting and pecking.

Good luck.

Sharon

[JayPwP in reply to sharoncrayn]

Unfortunately that is very true. Even though C/L did not elicit a response, I am now prescribed C/L/E.

No one's even thinking of a MAO-B inhibitor like Rasagiline, even though it is neuroprotective and makes existing dopamine last longer.

[JayPwP in reply to JayPwP]

Plus everyone knows pwp have higher iron in the brain and it is also known that high iron and dopamine in the brain is highly toxic.

Alas the only answer the neuro has is to load more ldopa with more combinations, which can be actually detrimental.

[JayPwP in reply to JayPwP]

ncbi.nlm.nih.gov/pmc/articl...

[sharoncrayn in reply to JayPwP]

You are guessing once again and it is totally absurd to suggest "everyone" knows excessive iron is the real problem with PD.

IMO It is not known whether excessive in vivo iron directly contributes (causes) to tissue damage or is solely an epiphenomenon ( a secondary effect).

Furthermore, Crichton even admits as much:

"A vital question remaining is whether inflammation may influence chelation efficacy, with a recent study suggesting that high levels of inflammation may diminish the ability of the chelator to bind the excess iron."

He goes on to admit the low feasibility of his theory, "Interestingly, PD patients exhibiting high inflammatory markers in the blood, e.g., IL-6, did not respond well to iron chelation, leading to the suggestion that chelatable iron was not freely available for chelation. "

" Such a side effect (of chelating iron) required that all PD patients entering the clinical trial undertook a weekly white cell count. " We know why don't we. Scary.

And he then goes into the proverbial grave yard: " In addition, it remains unclear whether the long-term use of such chelators might alter(! sharon) oligodendrocyte function, since they have a large requirement for iron. Really? Geez. Say goodbye to your central nervous system!

Bottom line on iron --- if you have excessive inflammation like most PD types, chelating isn't probably going to work. Regardless if EXCESSIVE iron is neurotoxic, you aren't going to remove it without potentially turning yourself into a veggie.

Sharon

[JayPwP in reply to sharoncrayn]

That 'everyone' comment seems to be taken out of context. Its alright, I am not as qualified as you in these areas, I will go with your views as you are the PhD

[sharoncrayn in reply to JayPwP]

Assuming the neuro who read your scan did it correctly, and he/she mentions the tracers for a reason, at this point the chances of any drug or supplement or diet protocol repairing your damage neurons or creating new ones, or changing the damage to your putamens is pretty slim, really slim.

Sure, if you did all the right things BEFORE the serious damage, some protocols would definitely help. But the cow has left the barn. C/L/E by the bucketful isn't going to give you a new brain.

What is the lesson here for anyone who is in early PD and preferably even before?

Don't wait until your engine has blown a couple of rods and your electronic ignition isn't igniting your engine like it should. Make sure you are putting high quality gas in your tank, your oil and fuel filters are clean, and your oil and water isn't old, and your tires and brakes aren't worthless.

Otherwise, you are sitting on the side of the road with a little red flag on your antenna.

Sharon

[JayPwP in reply to sharoncrayn]

Wow Sharon, you are motivating!!

[aspergerian]

This thread: an example of HU PM at its best.