in which they put forward a sensational claim that from 1978-2011, the death rate of Parkinson patients quadrupled thanks to the inclusion of carbidopa in their meds. They trace this toxicity to the fact that carbidopa binds irreversibly to vitamin B6. No doubt many in the Parkinson community have wondered about this claim, but lacked the scientific background to check its veracity. In this site, Hikoi has expressed skepticism about Hinz's indictment, and inquired whether any reputable experts worldwide have supported this idea.
Alexis Peterson, the biochemically-trained wife of Alex Tessor (ballet master and PD patient) has now chimed in on this topic, putting Hinz's paper under a critical lens.
Unfortunately, parts of her argument--especially the biochemical ones--are over my head. Perhaps there is some smart cookie in this community who can simplify her arguments for yokels like me. The net result of her aspersions is that she raises some healthy doubt about Hinz's thesis. (But for me, since I don't understand/agree with all parts of her argument, and since I have been benefiting from the Hinz protocol, I am not fully convinced. In my opinion, the jury is still out, and I await a more definitive analysis.)
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Remember that if you look hard enough, you can f ind "research" out t here that c an prove or disprove anything you like. For example, fats are bad for you / fats are good for you. We must do our own math and make a decision.
I choose to take Marty Hinz's word for it because there are people out there with Carbidopa induced dyskinesia, which I think might be irreversible, and I dont want to take a chance that I could lose control and flail around like Michael J Fox does on TV. So, I choose Mucuna and EGCG as my source of L-Dopa and peripheral Aromatic L-Amino Acid Decarboxylase inhibitor.
Dr Cosentini wrote to me this AM, "To obtain the complete regression of the motor symptoms it is necessary to add the right dose of levodopa which will never give so-called late complications."
That sounds encouraging. Presumably he refers to standard levodopa drugs which always include carbidopa/benserazide? And the "right dose" of levodopa, If such a thing exists, is not written on the sky. It can only be found by painstaking trial and error.
I too have used only mucuna 98% for the past 5 months or so and 15 other herbs and the past 2 1/2 weeks have developed dyskinesia, but I think Dr Cosentini is right as I've been playing with the dosage trying to get it right I've been seeing some difference but alot of juggling work. I'm glad you guys are talking about this. Thanks😊
shows that, indeed, just as you say, the levodopa (LD) itself, whether or not it is contained in Mucuna Pruriens (MP) can cause dyskinesias. However, the following passage from this report shows that the dopa decarboxyase inhibitors (DDCI), such as carbidopa and benserazide, contribute much more heavily to the dyskinesias than the levodopa:
"Interestingly, the adjunct of DDCIs was reported to yield earlier and more severe dyskinesias despite the 60%–80% reduction in levodopa dose. These observations may contribute to explain the lower rates of dyskinesias we found with levodopa alone (MP-Hd=High dose and LD−DDCI) than with combined levodopa plus DDCI (LD+DDCI and MP+DDCI), despite the higher levodopa dose."
In other words, the addition of DDCIs reduces the levodopa dose by 2.5 -5 times; but notwithstanding this, the inclusion of DDCIs increases the severity of dyskinesias, Say we take a 25/100 Sinemet (i.e., CD and LD in a 1 to 4 ratio) as a typical dose. Then elementary algebra shows that the 25 mg of carbidopa (CD) is at least 1.5 to 4 times more effective at generating dyskinesias than the 100 mg of levodopa. On an equal gram-to-gram basis, the carbidopa is thus at least 6-16 times more effective than levodopa at generating dyskinesias. (Technical Note: for the simplest possible algebraic model, I assumed an additive, linear dose-response w/o any synergy -- cross-terms -- between the carbidopa and the levodopa.)
Thanks for this info dumpelkin. I tried very hard to follow both the paperand your response but Im mathematically challenged so not sure that i do either justice in my response. However i do have a couple of thoughts.
Carbidopa and benserizide (DDCI’s) aid levadopa getting to the right place through the blood brain barrier. I do not know or understand how they-do this but if they increase the efficacy of LDopa then could it not be that the enhanced levadopa iis responsible for increased dyskenesia with the DDCI’s as catalyst but not cause?
Could it be a chemical reaction when DDCI’ s combine with L Dopa in the body that is responsible? If so I dont know that the blame lies solely with the DDCI’s.
This all begs the question of whether it is the use of drugs that is the actual cause of dyskinesia and I dont believe it is. As has been discussed here many times before recent research points to it being due to disease progression not drug use.
Of course once you have dyskenesia it will be triggered e=ery time you take the medication but it is not present if or when you are not medicated.
Hikoi, I will try to respond to the interesting points you raise:
A) " . . . if they increase the efficacy of LDopa then could it not be that the enhanced levadopa iis responsible for increased dyskenesia with the DDCI’s as catalyst but not cause?" -- Probably not. The reason is that whether we use mucuna or "lab-processed" L-Dopa, we need the same amount of L-Dopa reaching the brain to subdue our symptoms. The relative amounts of L-Dopa getting through the BBB are different, but the absolute amounts are nearly the same.
B) "Could it be a chemical reaction when DDCI’ s combine with L Dopa in the body that is responsible? If so I dont know that the blame lies solely with the DDCI’s."
--The easiest way for me to respond here is with a bit of math, so please bear with me while I try to explain it simply.
Let's suppose you create a numerical scale for the maximum intensity Dys of dyskinesias (in a specific patient, at a particular time in their progression) produced by taking PD meds. For concreteness, suppose for example that mild, moderate, and intense dyskinesias correspond , respectively, to Dys scores from 0-0.9, 1-1.9, and above 2. Now let's say 100 mg of L- Dopa (by itself) leads to a Dys score of L, and 25 mg of carbidopa (by itself, no added L- Dopa) yields a Dys score of C. Now note that according to the assumption of "linear dose-response," L and C are each proportional to the dose given. So, for 50 mg of carbidopa, Dys increases to 2C.
Then how bad will the dyskinesias be if we give him both the carbidopa and the L-Dopa? The simplest guess ("additive" ) would be
Dys = L + C. . . . (1)
i.e. the responses simply add on top of each other. Note that with mucuna (w/o carbidopa), we need typically to supply 4 times more L-dopa because more of it gets metabolized before crossing the Blood Brain Barrier, so Dys = 4L. But the latter value of Dys is smaller than the former, according to the quote cited above: "Interestingly, the adjunct of DDCIs was reported to yield earlier and more severe dyskinesias despite the 60%–80% reduction in levodopa dose. " We can express this by L+C > 4L. This implies C>3L, or "the carbidopa is at least 3 times worse for dyskinesias than the L-Dopa."
A more sophisticated and realistic model than equation (1) allows for interaction or "synergy" between L and C by including a term s LC, where s is any positive real number (e.g., 0.3, 4.2, 7, etc.) Then our equation takes the form
Dys = L + s L C + C. . . . (2)
The synergy term allows for a mutual reinforcement between carbidopa and l-Dopa. As above, we can compare this to Dys = 4L from mucuna to get
L + s L C + C >4L. . . . (3)
Subtracting L from both sides, and solving for C, C > 3L/(1+sL).
So, Hikoi--thank you for your patience if you gave read this far! Here's the payoff: the cross-term sLC represents your phrase " DDCI’ s combine with L Dopa in the body. " You are 100% correct: if this crossterm is large, then it will give a large Dys even though C and L are small. For example, suppose s = 8; then (3) becomes
L + 8 L C + C > 4L. . . . (4)
For an example, some values satisfying this are L = C = 0.5 (both dyskinesias are mild). Plugging into (4), we get
0.5 +8x0.5x0.5 + 0.5 = 3 > 4x0.5 = 2,
which is true. As you say, Hikoi, carbidopa by itself is then "not to blame." But placing or removing blame is irrelevant. The dyskinesia is still severe (Dys>2) !
C) "This all begs the question of whether it is the use of drugs that is the actual cause of dyskinesia and I don't believe it is. As has been discussed here many times before recent research points to it being due to disease progression not drug use. "
That may be true, but it only distracts from what we can control. Medicating with carbidopa, it seems we are worse off with regard to dyskinesias.
Thankyou for trying to explain but now my brain is aching from the effoer. What may be clear and simple to a retired physics professor is like another language to us mere mortals! 😉
Let me say I have no problem with mucuna, i havent personally tried it because i get my meds free and I see no reason to start paying if I dont need to. It is also not convenient to source and use as is demonstrated here by the continual questions.
Back to the original claim that carbidopa has raised the death rate in the US. I’m sorry but I cant take it seriously, i find it beyond belief that this would only be happening in the US and that Hinz appears to be the beckon of hope pointing this out. I still see no proof that carbidopa is the villain painted by Hinz. Hinz ethics do not sit comfortably with me either.
You seem to have a deep concern about developing dyskenesias, would that be accurate. Actually your chances are minimal given (what I think is) your age and age at onset.
Hikoi, Thank you for taking a run at it. Right now I am not overly concerned with dyskinesias. They have not yet hit me. Instead right now, I am distressed by some crazy-making dystonia/cramps manifesting in my right foot, which was previously untouched by the disease. Maybe if I ignore it, it will go away. This blasted disease sure doesn't give us any vacations! All victories are hard won!
I havent given up on your explanation (with 2 immediate family members with physics degrees) .... the biggest challenge will be remembering to follow it up.
Dystonia is most unpleasant, do you know if yours is on or off dystonia (or biphasic). I had mild foot dystonia many years before diagnosis but it has hardly bothered me since treatment.
I wonder how Hinz claims would stack up if presented as a case study for evidence based practice.
Just as there is a distrust of Big Pharmas motives by many here i believe there should be an equal distrust and a healthy scepticism of the motives of the multi million healing industry.
Hinz and his associates would like us to believe that a long list of diseases and conditions are related to neurotransmitter dysfunction and can be helped with dietary supplements sold by CHK Nutrition. Here's why I am skeptical:
The scientific community recognizes a few rare inherited neurotransmitter diseases that involve inborn errors of metabolism or transport [41]. These are not included on the lists that Hinz's network has published.
Some of the disorders on Hinz's lists involve neurotransmitter problems, but I have been unable to find any research that supports the methods he recommends to treat them. The journal articles he has cited certainly do not.
Before posting this article, I asked Hinz whether any controlled clinical trial has ever demonstrated a favorable health outcome produced by one of his protocols. He replied that there are none.
As far as I can tell, DBS's test methodology has not been independently validated as a useful diagnostic test. When I asked Hinz for citations to any relevant studies, he sent none but said that his articles served that purpose because they had been "independently verified by the peer-reviewers and the publishing company."
If Hinz's treatment methods were valid, he should be able to cite dozens of well-designed clinical trials that validate them. Despite extensive searching on PubMed and with Google, I have found none.
Yes, that is what I am about to say. At the first time when I do research, I was also confused about L dopa and thought it was macuna. But I found L dopa referee to lab created form while macuna called natural L dopa instead.
I stop all prescribed med for my husband and take natural form of L dopa( Macuna)
Improvement and quality life is much better and reversed;
1. No more problem in the toilet
2. Have his sense of smell back- which is incredible.
3. Can Eat, Sleep and have better emotion
4.homocysten value came down to normal. ( I use blood test to improve him)
4. Dyskinesia also reduce, he can dress up by himself and he do not use wheelchair anymore.
Interpretation of research paper is very important and can lead to misunderstanding.
Research on L dopa= lab dopa made by pharmaceuticals Indus.
Research on Macuna = natural L dopa
It is not right to read lab created lDopa effect and conclude that it is the same as natural dopa effect.
I was very worried when I saw the post and was thinking was me alone? Until I see this reply, thanks .
Thanks Hikoi , He was under Senimet and all conventional med prescribed by his neuro doctor. Then He had strong constipation that took him an hours in the morning routine. Then, he could not eat and became depressed. Doctor gave him stronger medication for depression which make him worse and start to have hallucination like hearing another me somewhere. One night he woke up screaming because of muscle spasm at night and he could not recognize me at all.
I was very sad.
In that darkness night, I revise what he was only taken is only medicine and the more he become worse, I gave him more medicine. Therefore, I decided to stop all med he had and move to natural L-Dopa. It took the whole month in December last year to face a very severe withdraw symptom and adjust to new dosage of natural l-Dopa Macuna for him. However, after Macuna replacement done, he start to smell food I cook as well as my hand cream. I was amaze. We are in Japan, so it was very difficult to have Macuna here. However, I have been research for sometimes and ask my friend in US to send to me.
I use now l-Dopa mix with MCT oil and use syring to put it under his tong.
Before using Now brand, my cat came to ask for the powder and lick from my spoon, she make a very happy face as if it is a cat nip. Then I test on myself before I gave to my husband. Now I use Zandopa. because it is easier and make less sleepy.
(you can imagin how he was so severely in bad condition. I though I may lost him but because of PubMed, I dare to follow the procedure and adjust it on my own way)
Effectively, I can see the result in one week of Macuna adminstration.
However, withdraw symptom from various med he took was so scary. But it go away in one or two weeks.
I use Ashwaghanda to help his mood with those herb tea (stag like 3-4 bags in one cup ) and Restore Gold to help his nerve . Also Benfothiamine to protect his physical nerve first and CoQ10 for heart and blood circulation. I fix problem one by one and then using his blood test and fix from the blood result. Now his blood test ok. He also can walk and feeling hungry. Now we are in the phase to improve his weight and rehabilitation.
I wish I can tell more how I have him and his smile back and wish all Parkinson people who suffer can have their happiness back like my husband. I went to see Liver doctor and have him clean blood by glutathione and receive Vitamin B by IV. Liver doctor was very impressed with his recovery and about to use our way to treat other patients too. However, I am working on how to transit from conventional to natural carefully since the withdraw effect was very scary and quite risky -it need to be handle with professional care. I did it at that time because I was crazy and scare that I may loose him, but other patient , I need to give more careful information. After doctor and me can find solution about transition way, I will post for you more.
Dear Hikol, while we transit to natural L-Dopa, I use high dose of Natural L-Dopa(Macuna) in order to stop those emergencies situation of muscle spasm, screaming, bad vivid dreams that occur 3 times a night first. Then after the incidents controlled I reduce an amount to half and then take another two week to learn to adjust the dosage that suit for him. The depressive med he have to stop was Rivotril and I think Haddol too. ( yes you were right that haloperidol) we finally stop all and he getting much better.
We also reduce his dyskinesia by using high dose of Rutin and now dyskinesia disappeared.
How long all of this?
December 2-3 start reduce all medication
December 12 all med stop stay with only MCT and Fava bean
December 15 Test Natural L-Dopa
December 16 he can smile feeling much better.
December 17 Cope with depletion, start to test around the clock dosage.
18-24 Adjust dosage and reduce episode severity and quantity.
December 25 Episode zero, no more cough , start to walk by himself.
February start IV blood cleansing phase. Can walk properly .
Thankyou for all your trouble Yo1ku. It is wonderful you have taken such good care of your husband and you have him back. He sounds like he was badly over medicated. If he had been on Hadol which I read somewhere, then he could have had drug inducd Parkinsons too.
I think there are parts of mucuna that are helpful that we havent discovered yet. I know some dctors have researched it but not alot.
I am fortunate that i am quite well controlled on ordinary meds after 10 years taking them. People dont know I have Parkinsons unless I tell them.
You are so lucky that you can manage and get along well with your medication. People have different adaptation to medication. We were running around from neuro 1 -2- 3 and change medication in order to make him better. I still wish my tough experience can be any useful to help others who can not get along with medication easily like him.
Hi my husband has just been put on Madopar 100/25 3 x a day. He has not improved yet but he has only been on in for 10 days. I ve always thought he might be better on Mucuna but I m nervous about the doses he needs to take etc. Is there any where where we can get advice pls? Thanks
Prevents L-Dopa from being metabolized peripherally, thereby leaving more to be utilized within the brain. This is why sinemet uses less l-dopa to be effective. The carbidopa is the decarbolase. It was originally combined with l-dopa to reduce nausea caused by high doses of l-dopa.
This reminds me of something discussed yesterday, does levodopa cause skin cancer or does Parkinsons in itself cause it? Are high homocysteine levels found in PWP or does carbadopa raise it? Is it dosage dependent or does it depend on the what shape the patient is in? (I have a neighbour who has done well on statins compared to how it affects other people)
Lot of questions, but with anything pharma it'll treat symptoms as best it can, but there will most likely be side effects, the more you take, the older you are, the longer you take it. That's the depressing reality of 'evidence-based' medicine which will never cure.
I havent seen any proof that carbidopa causes high homocysteine levels.
People on Hinz protocol are likely to take more ldopa in the form of Mucuna than those on sinemet because you need more to be effective. This means they may well have higher homocysteine levels than for those on sinenet treatment.
Thanks, Dumpelkin. Alexis Peterson's death rate chart, for the period shown, 1999-2015, corresponds to Hinz's. The difference is she isolates the increase in death rate to the over 85 age group.
B6 utilization by high dose levodopa advocated by Hinz is not the only problem with it:
"Nonetheless it is well known that the use of levodopa to alleviate symptoms of Parkinson’s leads to hyperhomocysteinemia, and that patients with the highest levels of homocysteine deteriorate faster than those with lower homocysteine titres." worldnewsmd.com/Documents/n...
"L-DOPA-induced hyperhomocysteinemia in Parkinson's disease: Elephant in the room:
L-DOPA therapy increases homocysteine level in Parkinson's disease.The toxicity of homocysteine to dopaminergic neuron is direct and specific. L-DOPA-induced hyperhomocysteinemia might be responsible for L-DOPA-induced dyskinesia. Hyperhomocysteinemia could be a putative contributor of the side-effects of L-DOPA." doi.org/10.1016/j.bbagen.20...
"In addition PN [peripheral neuropathy] may also result from or be aggravated by levodopa-related metabolic derangements, including depletion of vitamin B12 and B6 levels [confirming Alexis Peterson's analysis] and elevation of both methylmalonic acid (MMA) and homocysteine (HCy) levels [2–4]. The neuropathic effects of vitamin B6 and B12 deficiency are well recognized (as is the association of the latter with elevated MMA levels), and hyperhomocysteinaemia may itself be potentially neurotoxic [5]. The severity of PN in PD patients is positively correlated with lifetime levodopa exposure [3]. PN associated with oral levodopa treatment in PD is typically sensory, of axonal type and either asymptomatic or mildly symptomatic in severity [1–3]. However, isolated reports exist of severe, disabling PN occurring in the context of long-term, high dose oral levodopa use [6]" onlinelibrary.wiley.com/doi...
refs:
2. Rajabally YA, Martey J. Neuropathy in Parkinson’s dis- ease: prevalence and determinants. Neurology 2011; 77: 1947 – 1950.
3. Toth C, Sutton Brown M, Furtado S, Suchowersky O, Zochodne D. Neuropathy as a potential complication of levodopa use in Parkinson’s disease. Mov Disord 2008; 23: 1850 – 1859.
4. Urban P, Wellach I, Faiss S, et al. Subacute axonal neu- ropathy in Parkinson’s disease with cobalamin and vita- min B6 deficiency under duodopa therapy. Mov Disord 2010; 25: 1748 – 1752.
5. M € uller T, van Laar T, Cornblath DR, et al. Peripheral neuropathy in Parkinson’s disease: levodopa exposure and implications for duodenal delivery. Parkinsonism Relat Disord 2013; 19: 501.
6. Kimber T, Blumbergs P, Thompson P. Severe ataxic polyneuropathy associated with chronic levodopa use in Parkinson’s disease. Parkinsonism Relat Disord 2013; 19: 847 – 849
Park_Bear, That sounds scary! You seem to be coming down in favor of using carbidopa because it lowers the amount of levodopa needed? However, another approach would be use the Hinz approach, thereby consuming larger amts of levodopa from mucuna, but controlling the homocysteine with folic acid, B6 and B12. From Google:
"What decreases homocysteine levels?
The amount you need also depends on your current homocysteine level. One study found homocysteine scores were reduced by 17% on high-dose folic acid alone, 19% on vitamin B12 alone, 57% on folic acid plus B12, and 60% on folic acid, B12 and B6.[1] All this was achieved in three weeks! Oct 29, 2016" google.com/search?q=control...
Again, from Life Enhancement:
"The key to controlling runaway homocysteine levels is to convert the amino acid back to the harmless amino acid methionine, from whence it came, a normal process known as remethylation. To accomplish remethylation, the body requires adequate amounts of folic acid (folate), vitamin B12 and vitamin B6, and sometimes betaine (trimethylglycine). In the absence of these cofactors, homocysteine can easily accumulate to toxic levels." life-enhancement.com/magazi...
Which approach do you favor? As I recall, you take a small amount of Sinemet ER.
In the meantime, you got me worried enough I am going to have my homocysteine levels checked!
There are enough things to worry about with our Parkinson’s.. No need to add up more and more. Just control homocysteine levels every six months and use homocysteine defense pills. There are good ready combinations which do the job..
The carbidopa is known to be the more toxic ingredient found in the Sinemet; but don't we need it to get the L-dopa (and ultimately the dopamine) into the brain (via BBB)?
Carbidopa is most commonly used as a method to inhibit the activity of dopamine decarboxylase. This is an enzyme that breaks down L-Dopa in the periphery and converts it to dopamine. This results in the newly formed dopamine being unable to cross the blood–brain barrier and the effectiveness of L-Dopa treatments is greatly decreased. Carbidopa reduces the amount of levodopa required to produce a given response by about 75% and, when administered with levodopa, increases both plasma levels and the plasma half-life of levodopa; this results in less undesirable side effects such as dyskinesia.
If we only use Mucuna Pruriens, how do we get the L-dopa thru the BBB? I read from most users that they just take much less Sinemet along with the Mucuna powder to do the job. The Carbidopa still is required and it is obtained thru the lower dosage of Sinemet taken.
Ultimately, you are saying that taking Mucuna powder with much less Sinemet is much healthier than continuing to increase the sinemet (with Carbidopa being the poison) medication. The B6 is readily absorbed by the Carbidopa, again making it our major menace in this war.
Do I have this correct? or have I missed your point?
His advice, in summary: take B6 and carbidopa well separated in time. Then both will remain effective in your body. If you take Sinemet every 2 hours, it will be more difficult to avoid an overlap, but perhaps the best way is to take the B6 at bedtime?
As for your question, "how do people who use mucuna (w/o carbidopa) get enough levodopa past the BBB?," the answer is simply that they use copious amounts of mucuna. I can substantiate this by citing folks on the Hinz protocol as one well-defined example. My naturopath, Dr. Oler told me that most of his PD patients take 30-40 grams (not milligrams!) per day of mucuna. Since they are all required to use mucuna 40% (i.e., standardized to contain 40% L-dopa), this means they are ingesting 12-16 grams of levodopa per day! Even with 25 Sinemets of strength (25/100) per day, you're only ingesting 2.5 gm/day of L-dopa, a much smaller amount. Because of other supplements in the protocol, such as tyrosine and cysteine, these patients do not get nauseated from these large doses of L-dopa--at least once their dosage is properly adjusted.
3 years ago I attempted to get on the Hinz protocol with Dr Oler's help. It was out of desperation; I had tried several times to take Sinemet, but I couldn't tolerate even a small amount. My PD symptoms were ramping up, and I felt that I had to do something.
Over a 6 month period, I followed Dr Oler's instructions to the letter. He tried to find the best dose for me, but my reactions to his dose changes frustrated both of us. I couldn't tolerate the high doses of L-Tyrosine (yes, many grams not mg) and I never felt one small benefit to my symptoms.
In the end, it was less painful for me to give up on it and live without any L-dopa meds. Several months later, Rytary became available and I could tolerate it, so that's what I'm on now.
The huge number of pills (or powders) always made me nervous. Where is the study that shows that taking many grams of those various supplements (L-Tyrosine, L-Cysteine, etc.) is safe long-term? I've since learned that even B6 can be dangerous at too high a dose, and at the time I was taking 500mg daily. People who say that it's "natural" or based on "nutrition supplements" have to realize that taking that much of any supplement might have consequences.
Now, I believe that it does work for some. Just go into it with realistic expectations.
Yes, JAS9, very good point. Although each dose of the Hinz protocol currently gives me 5 hours of on time, I've noticed that an ordinary Sinemet tablet is much less effective than 3 years ago--slower to kick in , and lasts less time, I am wondering whether the large, gram-level, doses of Mucuna, hence of L-dopa, have spoiled my sensitivity to the ~10 X smaller amount of L-dopa in a Sinemet tablet. (I am trying to combine the standard drug with the Hinz approach because popping a Sinemet is far quicker and easier than weighing out the powders in the Hinz protocol.)
Interesting to see how each of us responds a little differently to various drugs both pharmaceutical and natural. Symptom reduction vs side effects such as tremors vs dyskinesia. I believe the placebo effect is a factor. If we believe in a drug, it has a better chance of working for us. The doctor diagnosed me 8 years ago. Drug discussion: 1. No cure, drugs for symptoms only 2. Will be side effects and symptom relief decreases as drug continued. When considering use of drug, ask "are symptoms a problem or just a nuisance?" Are side effects worse than nuisance symptoms? Is body's ability to fix itself reduced by "crutch" of drugs?
PD is an ideal disease for a gambler or a risk-loving type. In this disease, you have to make risky decisions all the way along the line. You can lesson the apparent strain by deferring to an authority figure such as a neuro or a naturopath. But that is also a personal decision. Since I'm not good at making high-stakes decisions, this is not a "fun" disease for me!
Sorry for the delayed response but after researching the issue I do not believe that Sinemet/carbidopa (or Madopar/benserazide) caused as increase in the PD death rate. The following article explains the anomaly:
Mortality from Parkinson's disease in England and Wales 1921-89.
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WHY IS CARBIDOPA USED IN COMBINATION WITH LEVODOPA IN DRUGS SUCH AS SINEMET?
What are your experiences with the consequences of a (tested) too low vitamin b6 level. 
park_bear made a very compelling argument for taking P5P (active B6)
