People with Parkinson’s may be at greater risk of more severe cases of Covid19, because we tend to have lower levels of Regulatory T cells.
I don't want to alarm people here, but I think this may be a valid concern.
1) Check out this quote from a recent article about Vitamin D and Covid19.
“T regulatory lymphocytes (TRegs) are a principal defense against uncontrolled inflammation. The number of TRegs has been found to be markedly lower in patients with severe COVID-19 infection whereas elevated TReg levels have been found to be associated with a reduced level of respiratory viral disease.”
Disclaimer: I don't know if any studies looking directly at people with Parkinson's disease who have contracted the coronavirus. I also don't as yet know anybody who's made the above connection. But I'm just putting two and two together.
As the second source says, T cells can be anti-inflammatory, like Treg and Th2. Or they can be pro-inflammatory, like Th1 and Th17.
We tend to have less Treg (anti-inflammatory) and also Th 17 (pro-inflammatory). We tend to have more of the pro-inflammatory TH1
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ElliotGreen
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There are many studies like this that associate worse inflammation with more severe Covid 19 disease. I suspect that inflammation is being unfairly blamed – that there is more inflammation because of higher viral load, and that this is the root of the problem.
You know I value your perspective park_bear, but in this case I disagree.
I think there's a good deal of evidence that excessive inflammation is a real problem, and related to why some people have worse cases.
There is the above mentioned correlation (that people with lower amounts of the anti-inflammatory Treg cells tend to have worse cases of Covid). Likewise, there is the correlation between low levels of vitamin D and bad cases of Covid. Also see this article, "Inflammation: the key factor that explains vulnerability to severe COVID."
Inflammation can help explain why certain subpopulations are more vulnerable to severe cases of Covid, people such as men, older people, obese people.
I can't really imagine a scenario where instead, the tendency towards more severe Covid cases for the subpopulations would be explained by higher viral loads.
Some children are also having problems, where they get "COVID-19-associated multisystem inflammatory conditions". This is specifically to do with inflammation. thelancet.com/journals/lani...
"It induces the expression of antimicrobial peptides that can decrease viral replication and also reduces the level of pro-inflammatory cytokines while enhancing the level of anti-inflammatory cytokines."
" By counterbalancing the activity of the renin-angiotensin system, angiotensin-converting enzyme 2, which is the fusion receptor of the virus, plays a protective role against the development of complications of this viral infection. Vitamin D can induce the expression of angiotensin-converting enzyme 2".
Given these different beneficial effects of vitamin D we must look at additional data to sort out whether inflammation is a cause or an effect.
Cytokine storm is closely correlated with viral load:
"Findings: The Result showed that cases with RNAaemia [viral RNA in blood stream] were exclusively confirmed in critically ill patients group and appeared to reflect the illness severity. Further more, the inflammatory cytokine IL-6 levels were significantly elevated in critically ill patients, which is almost 10-folds higher than those in other patients. More importantly, the extremely high IL-6 level was closely correlated with the incidence of RNAaemia (R=0.902) and the vital signs of COVID-19 patients (R= -0.682). Interpretation: Serum SARS-CoV-2 viral load (RNAaemia) is strongly associated with cytokine storm and can be used to predict the poor prognosis of COVID-19 patients. Moreover, our results strongly suggest that cytokine IL-6 should be considered as a therapeutic target in critically ill patients with excessive inflammatory response."
Here is a study of what happened to mice with inadequate vitamin C after being exposed to influenza virus - they all died, versus mice with adequate vitamin C survived. The mice that died had a dysfunctional immune response which failed to control the virus early on:
"The defects on the production of type I IFNs ... are closely related to the inflammatory responses due to the failure of controlling virus replication at the initial stage of its infection"
I do not dispute that inappropriate inflammation is destructive in severe Covid 19 cases. I am pointing out that this results from failure to control the virus infection early on. The key to a good outcome is an immune system that controls virus replication promptly. Once it does get out of hand patients end up with both a high viral load and high cytokines. At that point I agree it does become necessary to mitigate the cytokines.
Conclusion: Everyone should ensure that they have abundant plasma levels of vitamin C and vitamin D.
Good information, and food for thought. This stuff is really complicated. Obviously, there is more going on than just inflammation. I am pleased to learn that vitamin D can have antiviral effects.
However, I think you missed something. You mention vitamin D's modulation of the renin-angiotensin system as if it were separate from actions which lessen inflammation. But what is happening here? Parts of the renin-angiotensin system are pro-inflammatory, and vitamin D is acting to turn that down. This isn't a counterexample.
"Recent work has shown that angiotensin II (Ang II) has significant proinflammatory actions in the vascular wall, inducing the production of reactive oxygen species, inflammatory cytokines, and adhesion molecules."
As described in the paper you cited, "vitamin D can induce the expression of angiotensin-converting enzyme 2 (ACE2)".
ACE2 acts to neutralize the different functions of Ang II.
Therefore, vitamin D is being anti-inflammatory in this case.
As for the issue of viral load, I'm not surprised that viral load is correlated with Covid symptom severity, but the degree of correlation is a little bit surprising.
But I think the main question here is, why are some subpopulations (older people, men, overweight people, and other susceptible folks) faring worse with Covid?
1) I DON'T think it's because they are somehow being exposed more, and having a higher viral load because of that.
2) You seem to be suggesting that they are worse at fighting off the virus, so the virus replicates more in their bodies, and that's why they have a higher viral load.
3) I guess I'm pushing the line that the susceptible populations have an excessive inflammatory response, and that's where much of the harm is.
There's a good chance that it's a combination of 2 and 3.
I believe that PWP are at increased risk to Cpvid-19 because they have elevated levels of proinflammatory cytokines as well as elevated levels of oxidative stress along with reduced total antioxidant capacity (TAC). The normal system in PWPs is unable to overcome these deficits on its own as proven in the newer randomised, double blind, placebo controlled 10 mg melatonin/Parkinson's Disease study that I posted about here which also showed that melatonin reduced oxidative stress, reduced inflammatory markers, increased TAC and improved some PD symptoms in 12 weeks at just 10 mg / night as outlined here :
Covid-19 brings with it more of the same, reduced TAC, increased oxidative stress and increased inflammatory mediators. Based on Dr. Neel's results in over 400 patients, his high dose melatonin (HDM) treatment protocol (1 mg of melatonin per kilogram of body weight) using vitamin C and Vitamin D has managed to prevent the often deadly cytokine storm, pneumonia and consequently the need for a ventilator as outlined here :
Melatonin has also prevented the onset of acute respiratory distress syndrome (ARDS) and acute lung injury (ALI) in Dr. Neel's patients because of its highly protective effects of the lungs and its many inhibitory actions against many of the known negative effects of Covid-19 on the human organism. It is worth noting that melatonin increases tregs under inflammatory conditions and Covid-19 and PD are definitely inflammatory!
My personal opinion is that Dr. Neel's protocol is instituted relatively early and this is a major part of the reason for his huge success using HDM for his Covid-19 patients. He is not hindered by hospital standards that would send you home until you are having difficulty breathing before you can actually be admitted to the hospital. As soon as his patients exhibit known symptoms of Covid-19 and test positive for Covid-19, he starts them immediately on HDM.
Another example of the successful use of HDM in patients at high risk is its recent use in a Texas convalescent facility that had no deaths from Covid-19 in patients after HDM was started. Unfortunately, the first two patients died prior to the facility starting the use of HDM under Dr. Neels guidance. Generally these convalescent facilities seem like a breeding ground for death once Covid-19 enters the facility. I think this bodes well for PWP.
The best test of HDM is yet to come, once the multi-hospital study in Manila, Philippines is completed next month, if they stay on schedule. In this second study with a larger patient group (350 patients) and lower dosing than Dr. Neel is currently using in Texas, they will only be treating patients with Covid-19 who also have pneumonia. I think this study requirement is just begging for the study to fail as these are patients who are proving very difficult to treat and frequently die with multiple complications due to Covid-19 and pneumonia. Less so now, compared to at the very beginning of Covid-19, but still a really tough group to treat. If they prove HDM successful in this study, then I believe it will also show similar results for PWP who are treated early, such as in that time period where hospitals might tell you to come back when you are having difficulty breathing.
This recent study(June/2020) is in agreement with the idea of using melatonin against Covid-19, but their hypothesized dose rate is approximately 8 times greater than what Dr. Neel is using on average (1mg per kilogram/day) at 8 mg/kg/day and higher for severe cases! To put that in perspective, if you weigh about 175 lbs or 80 kilos, you would have to take about 640 mg of melatonin per day for severe Covid-19 infection!!!
wellll since > 80% of us die from respiratory complications that puts us right in line with a deep respiratory covid type virus. exacerbated imuno-response......etc....
my lungs are 48% vital capacity from rigid chest wall etc. that gives me a trip to the ER for a cold..........respiratory issues plague pwp. they just dont often know it........or the dr doesnt have a clue. cheers. hsng tough.
The way I am reading your sources is that Parkinson's patients are not in greater danger of contracting COVID-19, but are in greater danger of developing Acute Respiratory Distress Syndrome (ARDS) once they have contracted the illness.
Inflammation is a central aspect of Parkinson's; it is an inflammatory autoimmune process that gradually consumes the neurons in the nigrostriatal area of the brain, resulting eventually in the appearance of the motor symptoms which typically trigger diagnosis.
And inflammation anywhere in the body increases the chances of inflammation everywhere in the body. So I would say that it does seem reasonable to believe that PD patients could be more susceptible to developing ARDS once they have contracted COVID-19.
I read an interesting review article just published this past April, which describes the evidence that the supplement curcumin can reduce the likelihood of contracting ARDS. It also shows that curcumin is an antiviral that has been shown to suppress other corona viruses (not specifically COVID-19, but it is reasonable to suspect that it could also suppress that type of corona virus). Curcumin is also arguably helpful in suppressing the autoimmmune inflammation of Parkinson's, and it also reduces the tendency of alpha-synuclein to aggregate into the more toxic fibrils that eventually form Lewy bodies.
Here is a post containing a link to that review article, along with some additional information:
Studies show ( I refer to the Saturday edition of the National Post ) that people in their 20 and 30 's are suffering from anxiety attacks and depression, while older people are taking it in their stride , without the mental health problems even though they are more susceptible to the virus and can suffer more severity The elderly seem to take a more active defensive roll such as removing themselves from all opportunities to come in contact and believe in their ability to overcome and survive. Yes if we get it we will be in big trouble, so don't get it.
The grandchildren are back to school, my children are working and me and my wife are isolating again with just the two of us in the bubble. Cozy bubble
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