Being recently diagnosed with PD ( June 2019 ), I am confused. My first Neurologist prescribed Sinemet. 1 pill 2 x per day, upping this dosage after 2 weeks to 2 pills twice a day. I noticed a " fog clearing " after the first night. Encouraging. We sought a second opinion because of difficulties " connecting " with this doc. The second Neurologist confirmed the PD diagnosis, told me I was badly under-medicated and prescribed Rytary 3 pills 4 x per day. Ok...difference of opinion? Maybe? Confusing? YOU BET!! Confused on two ( 2 ) fronts. 1. Type of med - Sinemet - Dopamine or Rytary - Agonist , 2. Dosage? "...badly under-medicated..." Compare to ???
I'd like to understand the differences, risks, benefits of an Agonist and / or Dopamine? I have a follow up with #2 next week, so any and all insights, perspectives are welcome.
I'm not sure what questions I should be asking, paying attention to etc.
I am grateful to have found this site. Thank y'all in advance....Art
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TR8Man
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Rytary is an extended release version of carbidopa/levodopa. So it's in the same class as sinemet.
You should ask your neuro abour the pros and cons of agonists v dopamine replacement.
There was a view held by some that holding off from dopamine replacement would help keep motor complications (dyskinesia and other side effects) at bay for longer, but the research on this seems inconclusive.
Dopamine agonists can have behavioural side effects like being addicted to sex and shopping etc.
Perhaps a good question to ask is whether the Dr sees any merit in trying dopamine agonists before the dopamine replacememt?
Usally first is a dopamine agonist is used, then dopa. The watershed is the 60th live year, from then on dopa. Some patients begin with selegeline type drugs. DAs have probably a disease modifying effect,with a lower rate of dyskinesias ìn later disease, but side effect can be very, very severe. The old ones, the ergolinic are sometimes followed by a retroperitoneal fibrosis. One should prefer non ergolinic DA, f. E. Ropinirol or pramipexol. The side effects on the psyche are sometimes quite uncomfortable, like bying or sex addiction. Apomorphine is a very strong aphrodisiac effect. I felt this effect in a more comfortable manner and buying can be rűckabgewickelt. So you should not be too s anxious. but informing your relatives seems to make sense.
Dopamine agonists are associated with severe adverse effects such as impulse control disorder – compulsive gambling, sex, shopping, or eating. Some seniors have lost their retirement as a result. Dopamine agonist can also cause orthostatic hypotension - loss of blood pressure upon standing.
While it is clear there is not a consensus on whether or not to begin levodopa therapy at the time of diagnosis or when symptoms interfere with the quality of life, I, personally, am operating on the belief that if I start C/L therapy many years after diagnosis, I will start at a lower dose than where I would be had I started at the time of diagnosis and I have not heard an explanation as to why that is not delaying the probability of dyskinesia.
" I will start at a lower dose than where I would be had I started at the time of diagnosis"
I agree that this is logical in the context of some drugs, are you sure that it applies to CL? My understanding is that required increases of CL are the result of disease progression rather than the building of a tolerance, and that you will therefore need the same amount in year 10 whether you took it in years 1 through 9 or not. I don't remember whether I've seen studies on this or not, though I would think that if it was that simple, there would be a consensus in the research that starting later is better.
I agree that waiting until it interferes with QOL seems sensible either way, though. What seems foolish to me is people struggling with poor QOL yet not taking CL because of possible future side effects. A lot of things might happen before then, like you might die of something else, or there might be a cure.
I agree, none of us should endure a significantly impaired QOL for fear of dyskinesia.
We are all in a different circumstance and have a different threshold of tolerance. I'm retired, don't have to conceal it and not much concerned with what other people think, so I have more latitude to work around my tremors, balance, and gait issues.
I hope I don't die on the way home from my FUS PTT.
That a person would take the same dose at the 9 year mark whether or not they had been taking it from the beginning is the rationale for not delaying, but I'm expecting that in practice, it won't work like that.
I'm 10 years in, often take a Sinemet at bedtime and sometimes when going out averaging 5 to 10 per week. At the rate I've been going, I expect a realistic rate of increase in the frequency of dosing to to put me at 5 or 6 pills/day in 2 years. It just does not seem realistic to me that had I started at 3 or 4 pills per day, my dosing would increase so gradually that I would be at 5 or 6 pills a day after 12 years. For all intents and purposes, spread over 12 years, that's not really an increase.
TR8Man's doctor wants him, as a newly diagnosed person, to start at 3 pills, 4 times a day, which is 1200 mg/day. If he sticks with that doctor, he'll be at about 30 to 40 pills a day in 12 years. Good luck with that.
The context, MB is that according to my MDS, Rytary is supposed to be weaker than Sinemet and less “bio available” than Sinemet. By his calculations Sinemet is 4X stronger than Rytary in terms of immediate release.
The entire Rytary medication is too complicated. I am still adjusting after 9 months and I was up to 25 pills per day. Now I am at Three 100mg Sinemet and One 145mg capsule 5 times a day.
I am basically experimenting with doctor consent and family/care provider anger with the help of a virtual pharmacy at my house. I am Levodopa rich😅
TR8Man, I know that you meant to joke about it but unfortunately I have more bad news for you. Rytary is extra sensitive to food and stops working with the slightest little mistakes in timing.
My real solution? I stopped eating during the day and do intermittent fasting. This is not all that bad and many other people on this forum do such fasting as well.
I tend to lean towards your philosophy. I'm currently prescribed 3 x 100mg Levodopa a per day. At my last Consultant visit I suggested that I could skip the evening dose if I was simply at home watching TV, being inactive anyway. The Dr said he would prefer I keep taking the third dose because he was aiming for a regular or even medication profile. I understand that, but my instinct says that if I don't need it, why take it.
Against all advice, I have occasionally taken a day's Levodopa holiday. Been OK for me.
As we all know, some days are good some days is bad, so why take it if you don't need it I take it 'as needed.' I often skip one or several days. I don't know anything wrong with that.
This is a topic, when to start meds, we have disagreed about before isnt it. You were diagnosed in 2011 right?
I dont follow that TR8 would be on 30-40 pills a day at 12 years! Thats not how it works. Once they have found their optimum dose many people maintain the same regime for years.
I believe that most people who began Sinemet at the time of diagnosis, 10 years later are taking at minimum 8 per day and most likely 10 to 20 per day.
I believe the vast majority, probably 80% to 90%, do not remain at a constant dose for years at a time, but instead continue to increase their dose throughout the 10 years.
This is the study which supports your contention Horace. MB Anderson and I discussed this study two years ago and somehow he used it to justify his position, that witholding levadopa means he will start at a lower dose. Though he now takes some levadopa I think he is happy to put up with far more disability than I would.
The sub-Saharan study concludes that it is not the duration of therapy, but the increasing dose that induces dyskinesia. The problem with basing a decision regarding pharmaceuticals and a study is that it does not apply to everybody (in the cohort) because of the fact/truth is that any PWP can get dyskinesia from any dose of Sinemet for any time period, to wit, there is a person on this forum who commented not so long ago that she got dyskinesia from a minimum dose of Sinemet in 3 weeks.
So if a PWP is 1 of those people who cannot take Sinemet for an indefinite period without dyskinesia, and your doctor does not know that, it only makes sense to delay increasing the dose for as long as possible. (From 0 per day to 3 per day is an increase.)
Do you agree that starting at 1200 mg per day is unusually high?
Do you agree that the frequency of dyskinesia increases at around the 1000 mg per day threshold?
During the past decade, a number of large drug trials suggested that the initiation of levodopa therapy should be delayed to reduce the risk of motor complications in patients with Parkinson's disease. ...
The primary objective was to investigate whether the occurrence of motor complications is primarily related to the duration of levodopa therapy or to disease-related factors.
We conclude that motor fluctuations and dyskinesias are not associated with the duration of levodopa therapy, but rather with longer disease duration and higherlevodopa daily dose. Hence, the practice to withhold levodopa therapy with the objective of delaying the occurrence of motor complications is not justified.
I guess I was looking at the findings through the primary objective where it is not time on levadopa but disease progression (and hence increased levadopa) that correlates with dyskenesia.
“it is clear there is not a consensus on whether or not to begin levodopa therapy at the time of diagnosis or when symptoms interfere with the quality of life” I question this statement. There is a great deal of agreement among health professionals that QOL is to be maintained. Often diagnosis and symptom interference happen around the same time or within a year of diagnosis.
I also think you statement of belief that if you start levadopa therapy many years after diagnosis you will start at a lower dose... also cannot be applied generally. It may be true that you start on a lower dose but for most people the increase in medication levels would quickly reach that of those who started on meds earlier. It may also be true that you personally will stay on a low dose because of your concern about dyskensia but I don't believe you can generalise your particular beliefs to others.
You're probably right on this. I can really only speak for myself and my beliefs are just projection of my own strategies & theory.
I had been taken one 50/200 at bedtime usually 5 times a week and then 5 to 10, 25/100 daytime doses per week. A few weeks ago I began increasing that to perhaps 10 to 15 per week.
Still, there is a cohort which is not addressed and that is that group of people who more quickly are vulnerable to dyskinesia on lower doses. Since neither me nor a doctor can know if I might be 1 of those, so if I am in that category, might my delay of increased dosing address that?
PS. Plus, this whole 'quality of life' thing is pretty squishy, isn't it? I mean, it takes a person about 2 seconds looking at me to know I have some neurological problem, i.e., both arms shake, my jaw tremors, my walk is slow and awkward, I limp, I lean to the right, blah, blah, blah -- but I'm a happy camper. I'm enjoying my life. So, why should I risk all the consequences and side effects of levodopa therapy?
...risk all the consequences and side effects? I dont know what you think the side effects and consequences are in taking levadopa? What is likely to happen to you?
I can understand there being differences on the issue of when to start carbidopa levodopa, but when you say, "I don't know what you think the side effects and consequences are in taking levodopa?" it sounds like your challenging the premise that there are side effects??
Surely you are not doing that, are you?
Commentaries on this forum discuss most of these below.
From WebMD
Carbidopa-Levodopa Side Effects by Likelihood and Severity
•A Feeling Of Restlessness With Inability To Sit Still
•Orthostatic Hypotension, A Form Of Low Blood Pressure
If experienced, these tend to have a Less Severe expression
•A Type Of Abnormal Movement Disorder Called Dyskinesia
•Anxious Feelings
•Constipation
•Difficulty Sleeping
•Head Pain
•Loss Of Muscle Coordination
•Mental Status Changes
•Nausea
•Vomiting
INFREQUENT side effects
________________________________________
If experienced, these tend to have a Severe expression
•Involuntary Eyelid Twitching
If experienced, these tend to have a Less Severe expression
•A Painful Condition That Affects The Nerves In The Legs And Arms Called Peripheral Neuropathy
•Abnormal Color Of Urine
•Abnormal Dreams
•Blurred Vision
•Confusion
•Decreased Appetite
•Depression
•Diarrhea
•Dizziness
•Dry Mouth
•Generalized Weakness
•Indigestion
•Low Energy
•Temporary Redness Of Face And Neck
•Twitching
RARE side effects
________________________________________
If experienced, these tend to have a Severe expression
•A Heart Attack
•A High Alanine Transaminase Level
•A High Aspartate Transaminase Level
•A Type Of Blood Disorder Where The Red Blood Cells Burst
•Abnormal Heart Rhythm
•Accidental Falls
•An Inability To Control Impulsive Behavior
•An Ulcer Of The Duodenum
•Anemia
•Decreased Blood Platelets
•Extrapyramidal Disease, A Type Of Movement Disorder
•High Amount Of Bilirubin In The Blood
•High Blood Pressure
•Inflammation Of The Skin With Blisters
•Low Levels Of White Blood Cells
•Mental Problems From Taking The Drug
•Priapism, A Prolonged Erection Of The Penis
•Rapid Deep Breathing
•Suicidal Behavior
•Suicidal Thoughts
If experienced, these tend to have a Less Severe expression
•A Feeling Of General Discomfort Called Malaise
•A Sore Throat
•A Sudden Onset Of Sleep
•An Extreme Sense Of Wellbeing Called Euphoria
•An Inability To Completely Empty The Bladder
•An Increased Interest In Having Sexual Intercourse
Along with its needed effects, carbidopa/levodopa may cause some unwanted effects. Although not all of these side effects may occur, if they do occur they may need medical attention.
Check with your doctor immediately if any of the following side effects occur while taking carbidopa / levodopa:
More common
•Twitching, twisting, uncontrolled repetitive movements of the tongue, lips, face, arms, or legs
Less common
•Bladder pain
•bloody or cloudy urine
•chest pain
•confusion
•difficult, burning, or painful urination
•discouragement
•feeling sad or empty
•frequent urge to urinate
•inability to move the eyes
•increased blinking or spasms of the eyelid
•irritability
•lack of appetite
•loss of interest or pleasure
•lower back or side pain
•seeing, hearing, or feeling things that are not there
•sticking out of tongue
•tiredness
•trouble concentrating
•trouble in breathing, speaking, or swallowing
•trouble sleeping
•uncontrolled twisting movements of the neck, trunk, arms, or legs
•unusual facial expressions
Incidence not known
•Anxiety
•black, tarry stools
•bluish color
•blurred vision
•changes in skin color
•chest discomfort
•chills
•convulsions
•cough or hoarseness
•dizziness, faintness, or lightheadedness when getting up suddenly from a lying or sitting position
•dry mouth
•false beliefs that cannot be changed by facts
•fast, irregular, pounding, or racing heartbeat or pulse
•feelings about hurting oneself or others
•fever with or without chills
•general feeling of tiredness or weakness
•high fever
•hyperventilation
•increased in sexual ability, desire, drive, or performance
•increased interest in sexual intercourse
•increased sweating
•large, hive-like swelling on the face, eyelids, lips, tongue, throat, hands, legs, feet, or sex organs
•loss of bladder control
•lower back or side pain
•nausea
•pain
•pain or discomfort in the arms, jaw, back, or neck
•restlessness
•seeing, hearing, or feeling things that are not there
•severe muscle stiffness
•shaking
•sore throat
•sores, ulcers, or white spots on the lips or in the mouth
•swelling of the foot or leg
•swollen glands
•tenderness
•tiredness
•unusual bleeding or bruising
•unusual tiredness or weakness
•unusually pale skin
•vomiting
Some side effects of carbidopa / levodopa may occur that usually do not need medical attention. These side effects may go away during treatment as your body adjusts to the medicine. Also, your health care professional may be able to tell you about ways to prevent or reduce some of these side effects. Check with your health care professional if any of the following side effects continue or are bothersome or if you have any questions about them:
Less common
•Acid or sour stomach
•back or shoulder pain
•belching
•body aches or pain
•burning, crawling, itching, numbness, prickling, "pins and needles", or tingling feelings
•diarrhea
•difficulty having a bowel movement (stool)
•ear congestion
•headache
•heartburn
•indigestion
•loss of voice
•muscle cramps
•nasal congestion
•runny nose
•sneezing
•stomach discomfort, upset, or pain
•unusual dreams
•weight loss
Incidence not known
•Abdominal or stomach distress
•bad, unusual, or unpleasant (after) taste
•belching
•change in taste
•dark sweat
•double vision
•enlarged pupils
•feeling of warmth
•hair loss or thinning of the hair
•lack or loss of strength
•redness of the face, neck, arms, and occasionally, upper chest
The most common adverse reactions reported include nausea, dizziness, headache, insomnia, abnormal dreams, dry mouth, dyskinesia, anxiety, constipation, vomiting, and orthostatic hypotension.[Ref]
Nervous system
Very common (10% or more): Headache (up to 17%), dyskinesia (up to 16.5%), dizziness (up to 12%)
Common (1% to 10%): Confusion, dystonia, on-off phenomena, hypoesthesia, polyneuropathy, tremor, dysgeusia, bradykinesia
Uncommon (0.1% to 1%): Paresthesia, ataxia, gait disturbance, convulsion
Rare (less than 0.1%): Malignant, neuroleptic syndrome
Frequency not reported: Chorea, somnolence, memory impairment, sense of stimulation
Postmarketing reports: Polyneuropathy[Ref]
Psychiatric
Very common (10% or more): Anxiety, insomnia, depression (up to 11%)
Common (1% to 10%): Hallucinations, psychosis, abnormal dreams, sleep disorder, agitation, impulsive behavior, sleep attacks
Uncommon (0.1% to 1%): Suicide, dementia, disorientation, euphoric mood, fear
Common (1% to 10%): Ischemic events, orthostatic hypotension, peripheral edema, hypertension, syncope, irregular heart rate, hypotension
Uncommon (0.1% to 1%): Palpitations, phlebitis
Frequency not reported: Chest pain, myocardial infarction[Ref]
Cardiovascular ischemic events occurred in 2.4% (7 of 289) patients receiving carbidopa-levodopa extended-release capsules compared to 1.1% (1 of 92) of patients receiving placebo in early Parkinson's disease clinical trials. In advanced Parkinson's disease, 0.7 % (3 of 450) patients experienced cardiovascular ischemic events. These patients had a previous history of ischemic heart disease or risk factors for ischemic heart disease.[Ref]
Dermatologic
Common (1% to 10%): Excessive granulation tissue, rash, contact dermatitis, hyperhidrosis, pruritus
Uncommon (0.1% to 1%): Alopecia, erythema, urticaria
Rare (less than 0.1%): Sweat discoloration, angioedema
Insertion site complication was reported in 57% of patients who received this drug compared with 44% of patients who received a PEG-J tube without receiving treatment. The most common adverse reactions associated with naso-jejunal (NJ) insertion were oropharyngeal pain, abdominal distention, abdominal pain, abdominal discomfort, pain, throat irritation, gastrointestinal injury, esophageal hemorrhage, anxiety, dysphagia, and vomiting. The most common adverse reactions associated with PEG-J insertion included upper abdominal pain, duodenal ulcer, duodenal ulcer hemorrhage, erosive duodenitis, erosive gastritis, gastrointestinal hemorrhage, intussusception, peritonitis, post-operative abscess, and small intestine ulcer.[Ref]
Very common (10% or more): Insertion site complication, incision site erythema (19%), post-operative wound infection
Common (1% to 10%): Incision site cellulitis, post procedural infection, device dislocation, device occlusion
Uncommon (0.1% to 1%): Postoperative abscess, bezoar, ischemic colitis
Postmarketing reports: Gastric perforation, gastrointestinal perforation, small intestinal ischemia, small intestinal perforation[Ref]
Yes written for a litigious US market I would say.
Everything has side effects. I was curious what it is that frightens you enough to make you so adverse to taking regular sinemet. If it is dyskinesia I would think you are not in the age range to worry.
I can play the list game too but it means nothing to me. Many of those side effects are also caused by PD not just meds.
Presume you have checked out all the meds you might take. This is for paracetomol.
From Drugs A to Z
Paracetamol Side Effects
Generic Name: acetaminophen
Medically reviewed by Drugs.com. Last updated on Feb 7, 2019
Note: This document contains side effect information about acetaminophen. Some of the dosage forms listed on this page may not apply to the brand name Paracetamol.
Along with its needed effects, acetaminophen (the active ingredient contained in Paracetamol) may cause some unwanted effects. Although not all of these side effects may occur, if they do occur they may need medical attention.
Check with your doctor immediately if any of the following side effects occur while taking acetaminophen:
Rare
Bloody or black, tarry stools
bloody or cloudy urine
fever with or without chills (not present before treatment and not caused by the condition being treated)
pain in the lower back and/or side (severe and/or sharp)
pinpoint red spots on the skin
skin rash, hives, or itching
sore throat (not present before treatment and not caused by the condition being treated)
sores, ulcers, or white spots on the lips or in the mouth
sudden decrease in the amount of urine
unusual bleeding or bruising
unusual tiredness or weakness
yellow eyes or skin
Get emergency help immediately if any of the following symptoms of overdose occur while taking acetaminophen:
Symptoms of overdose
Diarrhea
increased sweating
loss of appetite
nausea or vomiting
stomach cramps or pain
swelling, pain, or tenderness in the upper abdomen or stomach area
The most commonly reported adverse reactions have included nausea, vomiting, constipation. Injection site pain and injection site reaction have been reported with the IV product.[Ref]
Hepatic
Common (1% to 10%): Increased aspartate aminotransferase
Rare (less than 0.1%): Increased hepatic transaminases
Frequency not reported: Liver failure[Ref]
Gastrointestinal
Very common (10% or more): Nausea (up to 34%), Vomiting (up to 15%)
Common (1% to 10%): Abdominal pain, diarrhea, constipation, dyspepsia, enlarged abdomen
Common (1% to 10%): Anemia, postoperative hemorrhage
Very rare (less than 0.01%): Thrombocytopenia, leucopenia, neutropenia[Ref]
Dermatologic
Common (1% to 10%): Rash, pruritus
Rare (less than 0.1%): Serious skin reactions such as acute generalized exanthematous pustulosis, Stevens-Johnson syndrome, and toxic epidermal necrolysis
Very rare (less than 0.01%): Pemphigoid reaction, pustular rash, Lyell syndrome[Ref]
Respiratory
Common (1% to 10%): Dyspnea, abnormal breath sounds, pulmonary edema, hypoxia, pleural effusion, stridor, wheezing, coughing[Ref]
Cardiovascular
Common (1% to 10%): Peripheral edema, hypertension, hypotension, tachycardia, chest pain[Ref]
Metabolic
Common (1% to 10%): Hypokalemia, hyperglycemia[Ref]
Nervous system
Common (1% to 10%): Headache, dizziness
Frequency not reported: Dystonia
Musculoskeletal
Common (1% to 10%): Muscle spasms, trismus
Psychiatric
Common (1% to 10%): Insomnia, anxiety
Genitourinary
Common (1% to 10%): Oliguria
Local
Common (1% to 10%): Infusion site pain, injection site reactions
I'm 73. Is that within the age range that I shouldn't worry about dyskinesia.
It feels like I'm being admonished for trying to avoid dyskinesia.
As a general rule, because the molecules of synthesized pharmaceuticals are not found in food or made by us, I try as much as possible to keep them out of my body.
How low of a dose of c/l can cause involuntary movements??Are involuntary shoulder shrugs and tightening of abdominal muscles considered a side effect of c/l? If so can it be reversed ? Thanks
I don't know about shoulders shrugs or tightening of abdominal muscles, but any dose of c/l can cause dyskinesia, although typically more than 800 mg - 1,000mg/day, for several years, increases the likelihood.
MBA it could be that your delay in increasing meds may shield you from dyskinesia but the biggest factor that I notice is age at onset of PD. Young onset (diagnosed before 50 yrs) often get worst dyskinesia eg MJF and Tom Isaacs.
If one does get dyskinesia then decreasing the dose of levadopa often stops it.
Intermittent dosing was discourage when I was first diagnosed as the pulsatilla effect was considered to contribute to side effects.
So, if you're going to get it, you'll get it whether or not you control your symptoms in earlier years with levodopa, so you might as well.
Well, that's pretty discouraging.
It makes a certain amount of sense, though, saying that the problems are caused by the depletion of dopamine and since PD pharmaceuticals have no effect on that, whatever one is going to get, they're going to get with or without levodopa.
But, aren't we living in a day and age when facts don't matter and one shouldn't let science and truth inform their decisions? Life is so much easier when you can live in your own universe.
Oh please.! Was that the death rate throughout the world or just in the US? Just the US right? If so how come it only happened there and look who brought it to our attention-, why the guy who says stop lev/carb and take amino acids which I will sell you at great expense.
See my reply to Parkie below. There are other data beyond Marty Hinz which draw that conclusion.
Most PWP take carbidopa/levodopa, consider it essential, and are well served by it. I totally support everyone's need to take it, but there are numerous other consequences & considerations in addition to dyskinesia such as an increase homocysteine levels and, perhaps, damage to DNA, etc.
Oops. I looked for a reference and even though I didn't find one, I repeated the post.
My bad.
I just saw Winnie the Pooh's comments, which are always right on, and those of MarionP and sure enough, there is Hinz once again sneaking around and camouflaging his identity.
"My husband takes carbidopa, I learned about carbidopa in medical school, but I haven't ever felt the need to dig too deeply into the mechanisms underlying carbadopa’s effects… until a few days ago when I was given the following article:"
The title alone made me skeptical
“The Parkinson’s disease death rate: carbidopa and vitamin B6.”
To summarize what I found:
The death rate chart is incredibly misleading, and there was significant data manipulation to create the graph
There is no convincing data indicating that carbidopa causes increased death rates
Vitamin B6 biochemistry is complicated, and is affected by L-dopa and carbidopa (and genetics, epigenetics, other drugs, nutrition, etc.)
Supplements selling “natural” L-dopa are still L-dopa… whether it’s made in a lab or a plant, it’s the same compound.
My husband took his carbidopa/levodopa this morning"
I am not a fan of Marty Hinz and don't rely on his study.
Do you know the author of this article?
Published October 11, 2019 in the Journal of Parkinson's Disease.
Department of Neurology, Amsterdam UMC, University of Amsterdam, Amsterdam Neuroscience, Meibergdreef, AZ Amsterdam, The Netherlands
Department of Neurology, Radboud University Medical Center, Donders Institute for Brain, Cognition and Behavior, Nijmegen, The Netherlands
"Results:
Overall mortality increased with age, male sex, higher levodopa equivalent dose, and presence of mild cognitive impairment. PD-related mortality increased with earlier onset of Parkinson’s disease, higher levodopa equivalent dose, and mild cognitive impairment."
Department of Biochemistry and Molecular Pharmacology, West Virginia University Medical School, Morgantown, WV, USA
"However, a combination therapy (carbidopa/levodopa) presently heavily used today to treat Parkinson’s disease rather than decreasing death rate as was observed with L-DOPA alone actually increases the PD death rate 4 fold. ... We propose that this is likely why this drug combination is shortening lives of people with PD. "
So the first reference is about a shortened life span for pwp. Not a surprise, it is after all a multi systems condition and incudes denervationof the heart and unstable bp amongst heaps of other problems.
The second reference lost me in the first sentence “The treatment of Parkinson’s Disease (PD) has evolved from drugs that are mostly symptomatic to substances which if used correctly can actually slow down the progression of the disease”. No supporting evidence or references. It recommeds Ltyrosine . No thanks.
Alexis has extensive training in ballet, medicine, and science, which together bring a unique expertise to Parkinson's on the Move.
Alexis attended Boston College. She graduated with a B.S. in biochemistry, was a recipient of multiple awards and was inducted into Phi Beta Kappa.
She has researched enzymatic structure-function relationships, worked on engineering vascularized tissue modules, and has also worked on developing novel antibody therapeutics for cancer patients. During her research career, she has been a co-author on multiple peer-reviewed scientific publications, which can be seen here.
Alexander Tressor
Parkinson’s on the Move Website workouts and exercises are based on extensive training and experience in the fields of medicine, science, fitness, and dance, alongside the knowledge gained from Alexander Tressor’s personal battle against Parkinson’s for the past 11 years.
........
MBA,
Thank you for your links.
The first link concludes pd mortality increased with higher levodopa equivalent dose.
I don't see a corrolation with "data showing the death rate began increasing when carbidopa was added to levodopa". It seems natural to me that the longer you live with pd, the higher dose l/c you will be taking.
The second link uses Hinz's citation as if it was a fact. The author seems like a reputable doctor so it worried me enough to write him an email mentioning Alexis Peterson "Parkinson’s on the Move" comments, as well as the quackwatch link to Hinz quackwatch.org/11Ind/hinz.html
If I ever get a response, I will post it here.
That being said, I know some PWP using Hinz's protocole are having success and I am happy for them. Some feel they were ripped off. It's probably like the high dose B1 protocol, some respond and some don't. I don't mean to put down Hinz's protocole, I just very strongly feel the statement of 4 fold death rate with carbidopa is false.
I think claims made from Dr. Hinz are basically correct. It is true that death rate from Parkinson’s or any disease could be misleading. However, if you look at the USA government’s own death rate figures from 1960-1975-- the Parkinson’s death rate figures went down because it is a superior treatment. Then Merck Sharpe and Dohme Co. added carbidopa to levo- Dopa to prevent nausea from L-Dopa. From 1975-to today the death rate has ridden steadily to somewhere between 10 and 12 fold. This is a huge difference.
Since not much changed from 1975 to today- in thousands of people –what would explain such a huge difference. AS people age-their blood –brain barrier becomes leaky. This is very important in most neurological diseases. Most of the people who get Parkinson’s disease are people 65 and older.
Carbidopa is effective against nausea when it cannot get into the brain because its stops L-dopa from changing into dopamine by inhibition of Dopa decarboxylase in the periphery (outside the brain) preventing increases in nausea and changes in blood pressure. But when the blood brain barrier gets damaged via aging, carbidopa can get into the brain. What would happen if this occurs. Carbidopa would prevent the formation of dopamine in the brain. The lack of dopamine in the brain will kill a person. This depletion of dopamine production in the brain is the actual cause of Parkinson’s disease. Therefore, this is a most likely reason the death rate greatly increased when elderly people used the combination of l-dopa and carbidopa. There may be other reasons but it is likely the main reason.
The most recent research on Parkinson’s disease and Alzheimer’s disease at UCLA have actually observed blood –brain barrier leakage occurring in brains of elderly people and this obviously plays a major role in neurodegenerative disease. It is caused by chronic inflammation. We have found a terrific new ,safe plant drug that in combination with other antioxidant sustained release substances should protect against blood-brain barrier leakage. A combination of sustained release inosine and these other compounds should slow or even help prevent the diseas, if taken early enough in the disease progression.
Dr Hinz tried to find new sources of l-dopa, that would be helpful. My guess is he skirted the FDA too much and lost his license. It not because he was wrong, it is because he tried to help people and broke the law in doing so. Sometimes our government does stupid things and this continues to this day. They need to get politicians out of the FDA.
Sincerely.
Knox Van Dyke
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End of email reply
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My own comments:
I just spotted Hiko's comment above about Dr Van Dyke's publishing website.
With all this conflicting input, I have no idea what to believe.
I know there are a few members on this site that have some medical training. Please give your opinion.
Thanks for that PD on the Move blog entry. Pretty much sums up and reinforces my own skepticism RE Marty Hinz and his research. Hinz is scaring PD newbies away from C/L in favor of amino acid therapies of dubious value. This is beyond irresponsible. It’s dangerous, because people are making bad decisions based on misinformation.
I had trouble with Amantadine which made me foggy.
Just let your doctor make the decisions for now. You have perhaps not understood your body yet with the new issues you are facing. You will be thankful that you did.
After a few years, the roles are reversed. You will know your body and your responses the best and you can work with your doctor and decide on what you want!
Yes, to a point. I believe it is called a " practice " for a reason. If they were knew what they are doing it'd be called a " permanent ".....and they are " practicing " on Me...so, I get a vote...but I have to and will learn more. This is why we sought a second opinion...He was / is / had to be the smartest person in the room. Great! You are....how does this help us - my bride and me? I'm anxious today. Is that PD or my med's " wearing off "? To your point, I'll learn what my body is telling me. In any case, thank you so much for your willingness to share.
TR8Man/Art, I think the information i left out is cost and after effects.
Rytary is incredibly expensive without the right insurance and costs thousands of dollars depending on the dosage. Rytary is a patented, complex, unknown composition and poorly understood by all.
The medicine tends to stack up over the day and peaks at night which makes me a very angry, unhinged, verbally abusive idiot. You said you have a bride? Maybe not the best choice for you. Other people on this forum have shared similar issues with Rytary at the end of day.
You say your newly diagnosed, but your doctor says you're badly under medicated.
Those 2 things usually don't go together.
When were you diagnosed, how old are you, how good is your health excluding PD, and please describe your symptoms, i.e., do you have a significant tremor in both arms, is your balance and gait impaired, etc.?
I'm 65. Generally in good health. Keep in mind, the older I get, the better I was....No tremors. Rigity on my left side only, Gait issues - cog wheel movements, left arm doesn't swing naturally as I walk, left foot dragging, speech impaired, weak voice...Balance is affected - left leg weakness, brain fog....Yeah, but....Solved my migraine issue - 15 - 18 migraine days / month for DECADES!!! Nothing worked, until I did a sleep study - found I " shallowly breath "...Been on a CPAP since February 2019....Averaging less than one ( 1 ) migraine / month. Thank you Lord!!! First Neurologist recommended sleep study....Who knew I have Sleep Apnea? Shallow breathing contributes to Strokes....
Seems like you are taking quite a lot of meds if you have recently been diagnosed.
My neurologist put me on azilect straight away as it possibly slows progression. The next visit I went on a small dose of madapor (1/4 tablet 3 times a day). This has slowly increased to the level
I need to control my symptoms and live a full life.
Much to his annoyance I play around with my dose so I can get away with the minimum possible. It does cause some dyskinesia about 1 hour after taking, but I just walk it off (or sit and frantically rotate my feet!).
Another neurologist I went to told me that dopamine receptors die off if they don’t get enough dopamine and that ideally they should be ‘bathed’ in dopamine. This convinced me to take the meds as well as the fact I believe in living for the moment as best I can - who knows what is around the corner.
You must also exercise.
That said I am off to the beach for a swim - left arm not the best so am swimming in circles! 40C here today.
We went through this minefield of Parkinson’s meds when my husband was diagnosed in 2015.
Main symptoms stiffness on shoulders, stiffness with hands and some medical friends suggested to my husband, very nicely, that it could be PD.
It was confirmed by first Neuro who said he wasn’t keen on Agonists and started my husband on C/L which he has been taking since then, not increased much but now taking C/L 100/25 4 times a day and has stayed at that for a while sometimes adds in a half a dose extra a day, if he feels he need it.
On every visit to Neuro he asks how he feels and says ‘ you look under dosed’ to which my husband replies he does not want to take more C/L as he’s not keen on some of the dyskinesia, although he manages them.
This year we saw another Neuro at our request. He was much more approachable but at the end of the consultation he did say he thought my husband was under-dosed and has added in Azilect. He has not taken it yet so we shall see.
Also asked for Terazozin as my husband has BPH prostate and could swap meds to this as it has shown, from research help in lessening progression of Parkinson’s.
He takes lots of supplement s including B1, magnesium, NAC, Q10 amongst others. The new Neuro said supplements were fine to take.
It’s really hard if one specialist tells you one thing and another has a different idea. The side effects from C/ L were definitely minimal for my husband, but now does have some dyskinesia, in feet and legs. After 4 years. Hoping the Azilect will help so we ll add in and see.
You may want to read recent threads (of 2 or 3 weeks ago) about NAC. A lot of us were taking it, but recent news caused many of us to stop. I had been putting it in my smoothie for couple years, but apparently it exacerbates some symptoms.
Thanks for that advice about NAC. Both my husband and I were introduced to NAC by my brother, not for PD but for excess mucous with colds, hay fever and congestion as he had been given it in France to help get rid of a cold.
This was quite a few years ago. So it was a supplement we had used before.
My husband seemed to be coughing often in the evenings so he took NAC and hey presto it seemed to help it. So that is partly why he takes it, then it came up as a maybe help for PD, so he added it more frequently. Not noticed any problems so far with exacerbated symptoms.
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