Below is a lengthy article titled 'Citicoline: pharmacological and clinical review, 2022 update'.
Some of you may have seen it earlier. Apologies if this is a duplication.
It has references to many studies regarding Citicoline. I am interested in the section 'Other clinical experiences' which has references to PD studies.
I request everyone here to take your time and read through the article and references, and share your thoughts on the same.
"Although potentiation of levodopa may not be explained by an ac-
tivation of tyrosine hydroxylase, this effect appears
to be related to an improved release of dopamine
synthetized from exogenous levodopa."
The main Section on Parkinson starts at page 59 of the PDF. Almost all of the studies cited used either intravenous or intramuscular administration, thereby avoiding the potential production of cardiotoxic TMA, and avoiding any absorption issues. Not clear how well these results carry over to oral administration. Of note:
"Authors found significant differences be-
tween citicoline and placebo at the controls per-
formed after 14 and 21 days of treatment in all pa-
rameters assessed by the Webster and Northwest-
ern University disability scales. They also noted
that patients treated with citicoline experienced a
significant worsening 45 days after the medication
was discontinued [This explains my current experience]...
In patients with more than two years of levodopa treat-
I don't have the expertise to correctly interpret these studies. From what I understood, Citicoline seems to be safe and beneficial, but I may be wrong.
I started citicoline in January of this year, and stopped around the second or third week of January. Just recently I've experienced an exacerbation of my Parkinson symptoms.
Park Bear, if there was a tip jar on the counter, I would put money in it for you, for all of the editing and sage wisdom you offer each time. 👍👍🙂
So are you back on Citicoline? Noted you said you went off of it in late January, and here we are in March and your symptoms got worse. Do you think there is a residual effect it could have?
Per the above citation and comments, it would appear citicoline is responsible for my worsened symptoms. I have just restarted at a lower dosage. My advice: if you have not started it, don't. If you are taking it, don't quit.
Well noted in regards to not starting Citicoline, and my current C/L intake is 25/100 three times per day. But I, like many others on this forum, are looking for ways to reduce that intake. This seems to offer some solution, but maybe not.
Seems to me the jury is still out in regards to this product.
I’m sorry to hear that your symptoms have worsened. My hwp also took the CDP Citicoline during the month of January. He stopped taking it around the last of the month. Can you tell me what symptoms have gotten worse for you? I am wondering if we will experience the same as you….
Sorry to hear that things have deteriorated, but I suspect the 1985 paper does not say what you think it's saying.
A different interpretation: PD symptoms got better on citicoline and then - simply - reverted when they came off it. This is true for most all beneficial interventions, of course. And, this is surely how the authors of the review see things.
Secades and Gareri would surely not - as they do below - trumpet the benefits of citicoline if they thought that starting and stopping treatment caused a fundamental deterioration above and beyond that which would be experienced in the absence of treatment.
"Authors found significant differences between citicoline and placebo at the controls performed after 14 and 21 days of treatment in all parameters assessed by the Webster and Northwestern University disability scales. They also noted that patients treated with citicoline experienced a significant worsening 45 days after the medication was discontinued, thus showing the efficacy of citicoline as adjuvant treatment to levodopa in patients with Parkinson’s disease."
Many PD citicoline trials have happened since '85. Pretty sure they would not have been given the green light if the '85 study was saying what you think it's saying.
It is commonplace for investigators of a particular treatment to become invested in good results. In any case what you have bolded is merely a restatement that citicoline helped while it was being used.
Be that as it may, what I have experienced is not merely a reversion to the prior efficacy of conversion of levodopa to dopamine, but a dramatic decrease far below the prior efficacy. To compensate I have upped my levodopa dosage to much more than my prior regimen.
I'm hoping this is merely a temporary effect. We shall see.
My personal experience of progression has been a gradually decreasing tolerance of levodopa medication due to dyskinesia. What I have been experiencing since quitting citicoline is a rapidly increasing tolerance apparently due to inefficiency of conversion of levodopa to dopamine.
Aye, it's a restament but that's sorta immaterial...It's existence is the thing. I do not think that statement is made if the authors interpret the 85 study as you do.
Anyways, I have contacted Secades to see what he says, and I wish you all the best.
At this point my take on what is going on is that my brain's ability to convert levodopa to dopamine has taken a dive. My normal, pre-citicoline dosage of levodopa has been inadequate to get me out of off time. By substantially increasing the dosage I seem to be doing better. This is likely to be a moving target because I've restarted citicoline, at half the prior dosage, and plan to taper slowly if and when it takes effect.
Citicoline and choline are thought to raise TMA and TMAO levels which, health wise will be counter productive to the heart and other areas of the body. If you are going to take it, it would be wise to also take vitamin D to try and counter the elevated TMAO levels. Moving your 25 OH d level up into the upper half of the reference range of 30 to 100 ng/ml may be a good idea. If you have PD, you should be taking vitamin D anyway as I discussed here :
' After 3 months of supplementation with cholecalciferol 2000 IU/day in obese people, a decrease in the level of leptin and TMAO as well as an increase in the level of NO and VEGF-A was observed. '
This study suggests a similar effect in animals via vitamin D manipulation of the gut microbiome in a positive way :
' Vitamin D supplementation significantly reduced plasma TMA and TMAO levels in mice fed a high-choline diet. Furthermore, gut microbiota composition was regulated, and the Firmicutes/Bacteroidetes ratio was reduced by vitamin D. Spearman correlation analysis indicated that Bacteroides and Akkermansia were negatively correlated with plasma TMAO in the HC and HCD3 groups. Our study provides a novel avenue for the prevention and treatment of CVD with vitamin D.
I have discussed the value of melatonin at length for PwP and for health in general on this forum. Melatonin is also another useful consideration to not only lower TMAO, but also to reduce some of the causes of elevated TMAO levels and inhibit the negative consequences on the organs of which, melatonin is protective of the major organs.
If you are of the mind that one or two more supplements are too much, then a reasonable alternative is to get a daily dose of sunshine to increase your vitamin D and melatonin levels for free!
If you are looking for a much more potent reducer of TMAO (-35%), berberine would be it and it is also useful in PD.
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