These 2 sentences were the lead sentences in the APDA citation provided in one of our recent threads.
Let's see how many our many "fuax" medical types can answer my question correctly. Perhaps the individual who provided the citation as a benefit to our newbies can provide the correct answer. Perhaps he can figure out the contradiction.
Does anyone actually read the citations they post?
"Carbidopa/Levodopa: Answers to Frequently Asked Questions"
"Loss of neurons in the brain that use dopamine to communicate is one of the hallmark features of Parkinson’s disease (PD), causing slowness, stiffness, tremor and balance problems. Replacing the brain’s dopamine is therefore one of the key treatment strategies to help improve the motor symptoms of PD."
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sharoncrayn
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You are absolutely correct. I looked at Lisa Sommers bio by mistake.
Doesn't change the contradiction. Current conventional pharmaceutical approaches to treating Parkinson's disease aim to replace the lost dopamine usually in cycles throughout the day, but these drugs don't address (nor can they) the ongoing destruction of dopaminergic cells. Over time, the ability of medications like Sinemet to replenish dopamine levels becomes overwhelmed by continued loss of dopaminergic cells.
Did the loss of your brain's neurons (for any number of reasons) cause PD, or did PD cause the loss? No one, but no one really knows.
In conclusion, replacing your bain's dopamine on a temporary basis with the drugs we now have isn't going to replace your lost or damaged (take your pick) dopaminergic cells. Replace dopamine to a certain extent yes, replace relevant cells no.
You are trying to fill a bucket that has more and more holes in its bottom without anything to plug the holes and keep them plugged.
I would rewrite her lead sentences in the following manner. Probably too complicated, too brutally honest for most, but it addresses the contradiction (the fallacy actually) that Sinemet, etc. by replacing dopamine in cycles will replace or rebuild your dopaminegeric brain cells. A huge fallacy that continues to be perpetuated by people who should know better.
"Parkinsons Disease is a progressive degenerative disease that is the result of your dopaminegeric brain cells (cells in your central nervous system that synthesize dopamine) losing their ability to utilize dopamine as they once did. It occurs for a variety of reasons. Medications such as Sinemet replace dopamine for a brief time to alleviate some PD symptoms but in no way do they repair or replace lost or damage dopaminegeric brain cells. Therefore, Parkinsons Disease and its symptoms is irreversible for the most part in the long term as the continued loss of brain cells at an ever rapid and increasing rate overwhelms the input of any dopamine medication."
Regarding the wording in the APDA citation, the only change I would make is to the first sentence. I would replace the phrase "that use dopamine to communicate" with the phrase "that produce dopamine". The second sentence requires no change.
Very well put and I do understand that for now my medication is helping me daily but I know reality that I’m progressing and let’s face will get worse not better .......With that being said , I will call upon you and your expertise to confirm my situation when I am trying to file papers with SS for a medical retirement to prove to them I will not get better. 😊. Karen. Just kidding .
you make it sound like there is no hope, why bother with the definition. There are many things that complicate the big picture and offer opportunity . Every one is not the same . Use your time more productively like take the dog for a walk . Get up get out get moving .Be happy . I bet you dont even have a dog.
in fact it is not logical to analyze the accuracy of an article outside the context in which it was written, that is, for the general public. I will always find inaccuracies when I analyze technical topics that are simplified to communicate them to the general public. All analysts know this thing, there is data analysis and analysis of the situation that produced the data and for the latter it takes FAMILIARITY with the real scene that I can't find on the web. I'm not saying that those who don't have chronic diseases he cannot easily fully understand all aspects of disease, but he should be a little cautious. Personally I have difficulty even with the relationship and understanding between caregiver and patient. I find it difficult simply because he does not live the same situation as me. In-depth understanding of other people is a skill that is acquired through education about it and practical experience, but it always starts with a bit of admiration and love for even the smallest person, who is never so small.
Sorry, Sharon, but I do have a bit of a problem with your re-write, specifically:
"Therefore, Parkinsons Disease and its symptoms is irreversible for the most part in the long term as the continued loss of brain cells at an ever rapid and increasing rate overwhelms the input of any dopamine medication." It is accurate due to the addition of the qualifier "for the most part". But it is overly general and succumbs to the logical fallacy put forward by most medical professionals of using statistical statements as statements of fact. So what does "for the most part" really mean? Does it mean that > 68% of PWP's will succumb to the progression? I personally am more interested in what those on the 5% side of the bell curve look like after a good amount of time applying what I call the "5 pillars" of neuro-protection: exercise, diet, nutrition, good quality sleep, and stress reduction. My problem is not with the accuracy of your post. It's just not where I choose to spend my time and energy.
"Loss of neurons in the brain that use dopamine to communicate is one of the hallmark features of Parkinson’s disease (PD), causing slowness, stiffness, tremor and balance problems. Replacing the brain’s dopamine is therefore one of the key treatment strategies to help improve the motor symptoms of PD."
There is no contradiction there. The loss of dopaminergic cells is part of the pathogenesis of PD. Dopamine, via levodopa, reduces the symptoms of PD. That's, by no means, a good state of affairs, but it isn't a contradiction.
You go on, in a reply to jeffreyn, to write:
"the contradiction (the fallacy actually) that Sinemet, etc. by replacing dopamine in cycles will replace or rebuild your dopaminegeric [sic] brain cells. A huge fallacy that continues to be perpetuated by people who should know better."
Who are these people? Where are they claiming that Sinemet, for instance, goes beyond reducing the symptoms of PD, and slows the progression?
Again, in a reply to jeffreyn, you write:
"the continued loss of brain cells at an ever rapid and increasing rate overwhelms the input of any dopamine medication."
Continued loss of cells, yes. But, I can't find any reference in the literature to an accelerating loss of cells. Perhaps you could point me to the source of your assertion.
Since you are a refugee from NueroTalk, and we have had at least 1 disagreement, I want to say I appreciate the time and effort you put into your reply. Now to your reply.
#1 You and the good Dr. are regurgitating one of many theories about what causes PD. Cell loss is not a "fact"; it is a theory. (some would argue that the loss occurs before PD; and others would argue just the opposite; some would say cell loss is universal because it is all about aging...neither you or the good Dr. or anyone else really knows). I realize you, and you alone are so gifted to have the ability to count the loss of dopaminegeric cells in PD patients while they are living. You cut open their brain and count the billions lost? Even on a cadaver we don't know. They can weigh the brain and make an estimate but that is hardly accurate in terms of what you and the good Dr. are talking about. Nor do the pathologists have the ability to discern and therefore accurately count dopaminegeric cells from other cells. It's fantasy to believe they do.
#2 To say Sinement (or your Stalevo which you are on), replaces your dopamine is another fallacy and a contradiction. It doesn't do it but on a very temporary basis. If it did it permanently, you wouldn't be on Stalevo. Even if you believe blood plasma levels of dopamine are relevant, the dopamine released by these drugs irrevocably EVAPORATES TO BASELINE...EXTREMELY QUICKLY. which is close to zero in many PD patients. Do you get where I am going? I hope you do. Which is why your are probably on multiple doses of Stalevo day in and day out, 365, ad infinitum.
#3 So many thousands and thousands of PD patients world wide are on Sinemet, Stalevo, or Rytary because they have been told by their doctor it will help them, help slow the progression of PD. You are telling me they never heard that? Doctors don' tell their PD patients those exact words or something similar? I can guarantee they do from spending 10 years coordinating two support groups. No doubt about it.
#4 Presumably, as we age, we lose an ever increasing (more rapidly) number of brain cells. By the time we die (say beyond 70), most of us are way, way down in comparison to our 20s. Granted, it is pure speculation that we lose brain cells because the measurement is done on cadavers who are "dissimilar" in age, race, gender, etc. where the measurement is basically "weighing". No "baseline, pre-post exists unless you want to go off the deep end and do a Jeff Dahmer with your chemistry set. NO baseline? NO pre-post? Come on John. You know where I am going, or should know.
#5 I don't waste my time doing citations. I have a full time job, and it isn't posting on this forum.
I believe I addressed that issue by saying it all depends on what "Theory" you want to espouse or promote (especially if you work for a pharma or foundation). If Dr. Bergman says he knows, he is living in La-La Land or Youboob land. What total nonsense.
Think about your question. Think. For all we know the development and increase in Lewy Bodies are more important than anything else. It isn't that simple, and it doesn't help to regurgitate something that hasn't been proven as some sort of fact. If Dr. Bergman had the answer, he would have been awarded the Nobel Prize in medicine. Last time I looked, I didn't see his name.
If it was all that simple, we would have cured Cancer, ALS, MS PD, blah, blah, blah a long time ago.
I don’t understand the anger that seems to seep into your writings. We all know what we’re dealing with and I’ve seen improvement with 2 people at a gym for Parkinson’s run by a former boxing coach. I’ve shared the story of one but the other man had what they referred to as Parkinson’s plus he was in his 30’s and could barely get around using a walker. They told me his story and I had the opportunity to meet him. He now walks literally 5 1/2 miles to the gym most days,11 miles round trip. The coach said “when I was coaching if everyone had as much heart and dedication as Tony I would have had many more champions” Tony wasn’t perfect his gait was slightly off, his speech was slightly slurred but compared to where he was he was doing amazing. Improving from something that was supposed to be deadly. There have been cases where people have improved. We all know the statistics but this is a group with heart and hope that lifts each other up! We look for ways to help each other! We need people to encourage us and be our cheerleader! I don’t know if it’s anger or frustration that comes across in your writings but I think a positive attitude would help those people in your support group a great deal!! We don’t need anyone telling us the ugly details we already know it. The writings you’ve done on sleep and good water, that’s helpful and appreciated! Anger, sarcasm, a superior attitude this is not the place. Why would you want to tell people who are dealing with a lot already “you’re doomed”. I don’t get it. Regardless of your education in my opinion it’s just unkind.
Very well said Connie and I share your sentiments. I’m not quite sure it’s anger though and to be honest I don’t really care. It’s a shame when someone has something to offer but has such a negative spin that people tend to shy away from any gifts she may have. Be nice if she has the ability to take criticism. Sharon, a lot of nice people here and you should, as you very well know write a little more compassionately. Perhaps your audience will grow.
I think she has a lot to offer but personally I don’t like the tone, it seems to be putting people down. I have been part of this group for a long time and think of it as a supportive place. But I think we need to be respectful of one another.
Connie: you cannot just be and let be, live and let live? You have to go on a preaching mission to fix and correct people? You are so much better than they are, you and that Despe person who likes to tell people that she knows how they think and knows what is right and that of course they therefore are not, by definition and a given? Don't you have enough problems and a life to live sufficient to keep your attentions filled for the moment, let others decide for themselves who they are and what their worth is, and leave being being Holy for another day? Take away what you can, give what you can, that's so hard for you? If you have such extra time to determine people are broken and that you will fix them, you are really very blessed.
Pessimistic and stoic are well-settled features associated with the base depressive spectrum of emotion, which has been rather conclusively shown to produce sharper and more skillfully critical thinking than the other, positive side of the emotional spectrum. Can't do without it.
Be aware...arrogating to oneself what is "right" in someone else's attitude. Habitually discounting others is a personality trait that is in "the book."
You write in No3: “I can guarantee they (pwp) do (believe that levadopa meds will help slow progression) from spending 10 years coordinating two support groups. No doubt about it."
Is it arrogance or naiveté to believe that coordinating two support groups in the USA can be generalised to include all people!!! So you assume that what happens in the US happens everywhere. Well in general doctors and neuros dont say drugs will slow your disease or similar except, it appears, in the US
Right?? I agree with you. I don’t need someone else telling me I’m progressing and getting worse, all I have to do is look in the mirror. I just try to be happy for today and do my best to take care of myself . Bottom line , I wouldn’t wish this disease on anyone and the only people who truly understand where I’m coming from are others with PD. Take care everyone . ❤️ Karen
"Motor" dopamine is a EPS phenomenon, thus located outside of the brain. C/L components are not dopamine, they are dopamine "precursors," or nearby "building blocks" of dopamine, and they can traverse the blood-brain barrier, whereas actual dopamine cannot. The dopamine molecule itself cannot cross the blood-brain barrier and is manufactured in other parts of the body outside the brain for motor functions, and inside the brain for signalling functions. Also, dopamine can be ingested and absorbed and have effects outside of the brain, as will be experienced, for example, by eating fava beans with a nice chianti.
Also, we need to define "replacing," since absorbed through diet, dopamine cannot enter the brain. Becauae C/L components are dopamine precursors, not themselves dopamine...then and once inside the particular manufacturing cells (presuming they are still working to some extent) they are synthesized by those cells to the extent that they can do so into dopamine. So what do we mean by "replace?"
If the cells inside the brain (several locations, but the ones we are concerned with are in the "subtanta nigra," literally translated as "black stuff") can no longer manufacture dopamine from C/L, then there is no particular benefit to C/L except for supplying perhaps other places that manufacture dopamine, and perhaps some benefit, I'm not sure, from help in manufacturing the other two catecholamines (dopamine is the third), epinephrine and norepinephrine, which may provide some benefit, except for the side effects caused by l-dopa (one of the two "active" ingredients of C/L) or an excess of norepinephrine and epinephrine, such as increased heart rate, blood pressure, sweating.
Heres what I know about C/l. Carbidopa is added to L-Dopa to prevent it from being metabolized peripherally (outside of the brain) so more can be delivered to the brain where it is needed. L-Dopa aka Levodopa is not dopamine, it is an amino acid precursor to dopamine. It converts direrctly into dopamine, whereas without supplementing this, your body would have to go through many steps to process ingested protein into dopamine.
quotinig Dr Marty Hinz, L-3,4-dihydroxyphenylalanine (L-dopa) is a metabolite of L-tyrosine and the immediate precursor of dopamine. Dopamine does not cross the blood–brain barrier. L-dopa freely crosses the blood–brain barrier, then is synthesized into dopamine without biochemical feedback inhibition. Greater amounts of L-dopa need to be administered if increased synthesis of dopamine in the central nervous system is required. 12 L-tyrosine does not have this ability, due to norepinephrine biochemical feedback inhibition of tyrosine hydroxylase.
Humans taking no supplemental serotonin or dopamine amino acid precursors are in the endogenous state. The endogenous state also exists when L-dopa or 5-HTP is administered without adequate amounts of serotonin or dopamine precursors, respectively. The amino acid intermediates 5-HTP and L-dopa do not occur in the normal diet in amounts sufficient to produce a significant metabolic effect. The competitive inhibition state does not occur with normal or optimal food intake due to biochemical feedback inhibition of L-tyrosine and L-tryptophan. Their respective conversion to L-dopa and 5-HTP in a normal or optimal diet are inadequate to establish competitive inhibition. This limits the amount of dopamine and serotonin synthesized to levels less than are required to place the system into the competitive inhibition state.
When daily dopamine and dopamine amino acid requirements are higher than can be achieved in a normal or optimal diet, the state is known as a relative nutritional deficiency.
Past research documented the use of general decarboxylase inhibitors such as carbidopa and benserazide for the management of L-dopa-induced nausea. These drugs have no direct benefit in the management of Parkinson’s disease symptoms. The primary reason for administering carbidopa or benserazide is to decrease daily L-dopa dosing requirement, thereby decreasing L-dopa-induced nausea. During L-dopa monotherapy (administration without a decarboxylase inhibitor), these side effects may prevent the patient from ingesting enough L-dopa to control symptoms.
The enzyme L-aromatic amino acid decarboxylase (AAAD) catalyzes synthesis of serotonin and dopamine from 5-HTP and L-dopa, respectively. Through competitive inhibition of AAAD, carbidopa or benserazide compromises peripheral synthesis of serotonin and dopamine. This drug-induced inhibition of peripheral AAAD–L-dopa metabolism leaves more L-dopa unmetabolized and available to freely cross the blood–brain barrier into the central nervous system. As a result, when carbidopa or benserazide is administered, lower L-dopa daily intake values are required to achieve the same central nervous system results.
Carbidopa and benserazide also inhibit peripheral metabolism of 5-HTP to serotonin and can cause a drug-induced depletion of peripheral serotonin. Dopamine is metabolized to norepinephrine, which, in turn, is metabolized to epinephrine. The inhibition of dopamine synthesis may also deplete norepinephrine and epinephrine. Physicians may fail to recognize the signs, symptoms, adverse reactions, and side effects that result from this drug-induced peripheral depletion of serotonin, dopamine, norepinephrine, and/or epinephrine by carbidopa. It is known that inhibition of AAAD with drugs may induce life-threatening side effects, including myocardial infarction, neuroleptic malignant syndrome, agranulocytosis, hemolytic and nonhemolytic anemia, gastrointestinal bleeding, thrombocytopenia, and hypokalemia
L-dopa-induced nausea can be nutritionally managed by addressing serotonin and dopamine imbalance. Proper administration of 5-HTP with L-dopa effectively controls nausea, eliminates the need for carbidopa, and, as they are no longer required, removes the signs, symptoms, side effects, or adverse reactions associated with carbidopa or benserazide in virtually all patients. With the removal of carbidopa, the risks and problems associated with peripheral depletion of the centrally acting monoamines are eliminated, which is a great safety advantage.
L-dopa is an amino acid that may be classified by the US Food and Drug Administration (FDA) as a drug, a medical food, or a nutritional supplement, depending upon the application. As a nutritional supplement, L-dopa is classified by the FDA as Generally Recognized As Safe (GRAS), with a side effect profile safe enough to allow for over-the-counter sales. The combination of L-dopa with carbidopa is only classified as a drug; it is not listed as GRAS by the FDA. Currently, in the US, if a patient experiences a carbidopa side effect, the only available form of L-dopa without carbidopa is a nutritional supplement product containing standardized L-dopa. (MUCUNA, Velvet bean) L-Dopa is also found in broad beans, Fava beans, although obviously not in standardized doses!
few physicians are aware of the availability of the nutritional supplement form of standardized L-dopa over the counter in the US, and even fewer understand the management of L-dopa-induced nausea without the use of carbidopa.
The current standard of care for Parkinson’s disease is based on the endogenous state perspective. There is no consideration that nausea is caused by the imbalance between the serotonin and dopamine systems. The depletions of serotonin, thiols, L-tyrosine, L-tryptophan, and other monoamines associated with the clinical course of Parkinson’s disease, L-dopa monotherapy, and the use of general decarboxylase inhibitors are not addressed
Under the current standard of care, the etiology of the signs and symptoms associated with these depletions is not adequately recognized, understood, or controlled. Standard treatment of Parkinson’s disease under endogenous conditions is to simply increase L-dopa/carbidopa if symptoms of Parkinson’s disease are not optimally under control.
Competitive inhibition research has identified the causes of the depletion and previously published the steps required to increase the synthesis in a properly balanced manner, leading to optimal functional results. The properly balanced competitive inhibition approach avoids the extensive depletion of serotonin, thiols, L-tyrosine, and L-tryptophan that is known to exist with L-dopa monotherapy. It also eliminates the nausea dosing barrier that may occur when L-dopa is administered without the need for a general decarboxylase inhibitor.
PD is classified as a “progressive neurodegeneration” (PN) disease. With PD, irreversible brain damage involving the post-synaptic substantia nigra dopamine neurons induces fine motor control dysfunction (herein referred to as “electrical damage”).
PD electrical damage dysfunction is classically limited to the post-synaptic dopamine neurons. Electrical flow, regulating fine motor control, flows from the pre-synaptic neurons, across the synapse, then through the post-synaptic neurons. It is the novel primary hypothesis that if PD symptoms from post-synaptic neuron damage develop, then compromise at any point in the electrical event chain, to include outside the post-synaptic dopamine neuron focus, may exacerbate and mimic PD symptoms and/or disease progression.
In PD patients, reversible Relative Nutritional Deficiencies may induce PD symptoms which may be inappropriately managed when treated as Progressive Neurodegeneration. If a dysfunction resulting from nutrient depletion exists, then one or more underlying RNDs is always present.
At least give Marty a high five like you did for Bergman and Lieurance, your esteemed chiropractors. You lifted Marty's stuff word for word without a single quotation mark or mention of him. Well done.
Neither of the chiropractors you mention are in the same league with Marty or Perlmutter. But of course, just my opinion.
I know it was a long, wordy, multi-part reply, but, yes indeed, I did say, "quoting Dr Marty Hinz", before I copied his paper almost word for word. Sorry about the confusion, I just like to share what I learn. Perhaps too much!
as for Dr Bergman, i love watching his lectures on youtube, and I will say that he is a fantastic lecturer, but his approach to treating PD still falls a little short in the real world. There is another Chiro named Dr. John Lieurance of Sarasota Florida who has inspiring videos of intra nasal balloon techniques and glutathione therapy curing PD, as does Dr Grain Brain Perlmutter. Again, these techniques are a bit impractical and or too little too late. My good friend Reedboat nails it with the "5 pillars" of neuro-protection: exercise, diet, nutrition, good quality sleep, and stress reduction. All of this will certainly help, and WE ARE NOT DOOMED, although I agree, sometime it looks pretty bleak in there. Depression and anhedonia re THE WORST of our long list of symptoms.
To me, the bottom line is that we are HERE, on HU, to help and support each other with our personal experiences. Not to bicker or put each other down.Not to discourage. This is our online SUPPORT GROUP, educate each other, ask questions, give opinions, learn, take chances, bare your soul, spew your thoughts! Scroll on by if you dont care for something you see. Elaborate if you do.
I love you all in a special way, in that we have one thing in common that we all wish we did NOT have in common.
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