COVID survivors may be at a greater risk of developing Parkinson’s disease–like symptoms, researchers warn. What you need to know to protect your healthfinance.yahoo.com/news/covi...
"The virus was able to infect cells from all the aforementioned organs. But it did a particularly good job of infiltrating some types of neurons in the brain that produce dopamine—a neurotransmitter responsible for feelings of pleasure, motivation, memory, sleep, and movement.
Once infected, such cells can lose their ability to grow and divide, researchers found. The cells also stop producing dopamine and instead send out signals that cause inflammation.
Because a loss of dopamine-producing neurons is associated with Parkinson’s disease—a slowly developing neurodegenerative condition that leads to tremors and, often, dementia—people who’ve been infected with COVID are at an increased risk of developing symptoms of the disorder at some point in their lives, the researchers wrote.
“We keep discovering new cell types that can be infected by the virus,” Dr. Shuibing Chen, professor of chemical biology in surgery at Weill Cornell Medicine and lead author on the study, tells Fortune. “We’re still trying to understand how it damages them. We need to keep the work ongoing, keep watching to see what happens.”
Regardless, the virus’s detrimental effect on dopamine neurons may explain neurologic symptoms in those with an active COVID infection, like headache, loss of smell, and a persistent unpleasant taste in the mouth, according to researchers.
It may also explain more immediate neurologic symptoms of long COVID, like brain fog, sleep issues, depression, and anxiety.
However grim the findings, the team’s study resulted in some positive news: ALS drug riluzole, diabetes drug metformin, and cancer drug imatinib appear to prevent the aforementioned type of neurons from becoming infected with COVID and, thus, losing their ability to function properly."
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' Investigators in the Smidt Heart Institute at Cedars-Sinai have confirmed that people who have had COVID-19 have an increased risk for new-onset diabetes—the most significant contributor to cardiovascular disease. '
Further people with diabetes are at increased risk for Parkinson's disease and cardiovascular disease as discussed here :
' Diabetes mellitus and Parkinson’s disease are both aging-associated diseases that are turning into epidemics worldwide. Diabetes mellitus and insulin resistance not only increase the possibility of developing Parkinson’s disease but can also determine the prognosis and progression of Parkinsonian symptoms. '
Both diabetes and PD increase the risk for cardiovascular disease (CVD), the number one cause of death in the world . People with diabetes are two to four times more likely to develop CVD as discussed here :
' People with diabetes are 2 to 4 times more likely than others to develop cardiovascular disease. Because this risk is so high, cardiovascular disease remains the most common cause of death in people with diabetes. '
People with PD are at increased risk for CVD as discussed here :
Here is a relevant quote that is my limit for doom and gloom in one post :
' Parkinson's disease (PD) is one of the most common neurodegenerative illnesses, and is a major healthcare burden with prodigious consequences on life-quality, morbidity, and survival. Cardiovascular diseases are the leading cause of mortality worldwide and growing evidence frequently reports their co-existence with PD. Cardiac dysautonomia due to autonomic nervous system malfunction is the most prevalent type of cardiovascular manifestation in these patients, comprising orthostatic and postprandial hypotension, along with supine and postural hypertension. Moreover, many studies have endorsed the risk of patients with PD to develop ischemic heart disease, heart failure and even arrhythmias, but the underlying mechanisms are not entirely clear. As importantly, the medication used in treating PD, such as levodopa, dopamine agonists or anticholinergic agents, is also responsible for cardiovascular adverse reactions, but further studies are required to elucidate the underlying mechanisms. The purpose of this review was to provide a comprehensive overview of current available data regarding the overlapping cardiovascular disease in patients with PD. '
On the upside I could make multiple suggestions for long covid, diabetes and CVD and of course melatonin for PD and CVD.
' Oxidative stress is a pivotal point in the pathophysiology of COVID-19 and presumably also in Long-COVID. Inflammation and oxidative stress are mutually reinforcing each other, thus contributing to the systemic hyper-inflammatory state and coagulopathy which are cardinal pathological mechanisms of severe stages. COVID-19 patients, like other critically ill patients e.g. with pneumonia, very often show severe deficiency of the antioxidant vitamin C. '
' A FSS complete response was reached in 62 (53.5%) patients in treatment group and in two (3.5%) patients in control group. A reduction in FSS core < 20% from baseline at T1 (non-response) was observed in 11 patients in the treatment group (9.5%) and in 15 patients in the control group (25.9%) (p < 0.0001). To date, this is the first study that tests the efficacy of coenzyme Q10 and alpha lipoic acid in chronic Covid syndrome. Primary and secondary outcomes were met. '
' This survey is the first to show the beneficial effects of the combination of l-Arginine and Vitamin C in Long-COVID. Our investigation was based on a robust rationale, i.e. targeting endothelial dysfunction in Long-COVID. Indeed, endothelial cell infection with consecutive inflammatory cell recruitment and endothelial dysfunction could explain the impaired microcirculation observed across vascular beds in COVID-19, triggering vasoconstriction, ischemia, and a pro-coagulant state [92], [93], [94], [95]. Consistent with our view, several investigators had proposed that endotheliitis could be a critical mechanism underlying systemic impaired microcirculatory function observed in different vascular beds in patients experiencing Long-COVID symptoms [92], [96]. '
' This methoxyindole is found in all forms of life that express aerobic respiration; melatonin's primary function is cytoprotection, displaying anti-inflammatory, antioxidant, and immunostimulant effects [29, 30] which together endow it with highly potent neuroprotective properties [31]. The anti-inflammatory action of melatonin involves a variety of mechanisms [32]. One of them is Sirtuin-1 induction, which decreases the polarization of macrophages toward a proinflammatory profile [33]. Suppression of nuclear factor (NF)-κB activation [34, 35] and stimulation of nuclear erythroid 2-related factor 2 are also detected after exposure to melatonin [36]. Melatonin reduces proinflammatory cytokines (tumor necrosis (TN)F-α, interleukin (IL)-1β, IL-6, and IL-8) and increases anti-inflammatory cytokines such as IL-10 [33, 37]. '
' The antioxidant and scavenging effects of melatonin on free radicals in both the cytoplasm and the cell nucleus are mainly independent of receptors [38]. To fulfill this, melatonin not only acts as a free radical scavenger but also gives rise to a cascade of molecules with high antioxidant activity. It also acts as an indirect antioxidant, enhancing the production of antioxidant enzymes while inhibiting that of prooxidant enzymes [39]. In addition, some antiapoptotic and cytoprotective effects are seen under ischemia, presumably due to melatonin's stabilizing activity of the mitochondrial membrane [40]. '
' Thus, melatonin can reduce the damage resulting from sepsis mediated by COVID-19 through different mechanisms, I.e., by reversing the Warburg-type metabolism and transforming proinflammatory M1 macrophages into anti-inflammatory M2 macrophages [43], by mitigating the production of HIF-1α [44], by suppressing NF-κB [45], and by inhibiting NLRP3 inflammasome [46]. Circulating secreted phospholipase-A2 (Group IIA) correlated with the severity of COVID-19 disease [47]; hence, cyclooxygenase inhibition by melatonin [48, 49] is another potential mechanism by which the methoxyindole may inhibit viral infection. '
' It may well be true that higher doses of melatonin would be more beneficial in the COVID pandemic condition. For example, in a retrospective cross-sectional study of a closed population of 110 old adult patients treated with a mean melatonin daily dose of 46 mg for at least 12 months prior to the availability of COVID-19 vaccination, there was no death in the face of a lethality rate of 10.5% in the local population of elders suffering acute COVID-19 disease [64]. Indeed, animal studies support the use of high doses of melatonin to prevent infection in murine COVID-19 models [65]. From several animal studies, the human equivalent dose HED) of melatonin was calculated by allometry for a 75 kg adult [46]. Allometry is commonly employed for determining initial doses used in Phase I human clinical drug trials [66]. '
' As stated above, the deficits in attention, memory, verbal processing, and problem-solving seen in patients complaining of brain fog resemble MCI, the initial phase of Alzheimer's disease (AD) [22]. The underlying neuroinflammation in this condition (Figure 1) could be effectively controlled by melatonin, as shown by studies in cell lines linked to AD, in which melatonin reverses abnormalities in the Wnt/β-catenin, insulin, and Notch signaling pathways, proteostasis disruption and abnormal autophagic integrity (reviewed in Refs. [67, 68, 69, 70, 71]). '
' The beneficial effects of melatonin on fibromyalgia (associated commonly with ME/CFS) were first described in one of our laboratories [90]. Since then, several studies have confirmed the initial findings (for a summary, see ref. [91]). A common pathogenic mechanism is suggested by the similarities among ME/CFS, fibromyalgia, and post-COVID syndrome. The multiplicity of pathophysiological abnormalities in ME/CFS patients opens the possibility of numerous potential therapeutic targets [24]. The several abnormalities described comprise increased oxidative stress, mitochondrial dysfunction, dysregulated bioenergetics, a proinflammatory state, the disruption of gut mucosal barriers, and autonomic nervous system disturbances related to autoimmunity [92] (Figure 2). The possible therapeutic options targeting these pathways include melatonin, coenzyme Q10, curcumin, molecular hydrogen, and N-acetylcysteine [24]. Among them, melatonin is the only compound that addresses all mentioned potential targets [24].'
In part, another cover story to hide or explain away vaxxine side effects. I've read many anecdotal stories of people being diagnosed with PD following the shot. And although I'll never know for sure i think my PD is a result of a Tetanus shot (DTap), as that's when my health changed as evidenced by my medical records.
Be careful, because i read making your bed can cause heart attacks.
That’s according to a new study published this month in the journal Cell. Researchers from Weill Cornell Medicine, Memorial Sloan Kettering Cancer Center, and Columbia University used human stem cells to create cells from various organs, including the lung, heart, and pancreas. The virus was able to infect cells from all the aforementioned organs. But it did a particularly good job of infiltrating some types of neurons in the brain that produce dopamine—a neurotransmitter responsible for feelings of pleasure, motivation, memory, sleep, and movement.
People bitch and moan about the lack of progress in scientific research, then when three different organizations band to together to undertake complex research that presents interesting information, responses include: "nah it was the vax - i read it on facebook" 🙄
My story is, I received the covid shot and my right arm went into immediate shoulder impingement a few months later frozen shoulder then I started to develop a right arm tremor. I had a bad cold virus that winter for about 4 weeks. About a month later I started to develop foot pain in my right foot then a limp followed. Six months later I was diagnosed with Parkinsons, bartonella (a co-infection of lyme disease from a tick bite) and mono all at the same time. It was kind of a nightmare.I feel pretty good now and I'm still trying to figure out what happened to me. I'm waiting to see a move disorder specialist. I have an appointment with a craniosacral DO to help with resetting my nervous system and alignment.
I have a feeling alot more will be coming out about covid and the covid shot. I just found another person who had thier left arm freeze up after the shot then developed PD.
We are on track in the US for 90,000 new cases of PD this year.
After years of research with the disease I don't have much doubt that it's not a particular event or something that is the cause of the Parkinson's diagnosis. Rather it is waiting to happen to you and it's just by chance that the person has dodged the bullet until the moment it happens.
Hope it makes sense. At least it helps you to not blame yourself for the choices you have made or intend to make in the future as long as they are informed and good faith choices.
For instance, they say that smoking is believed to prevent Parkinson's. Even if it is true, which I have doubts about, would you blame yourself if you never smoked?
I know I can't blame myself. The crazy thing is, my whole life,I have tried to eat really healthy and exercise,since my early 20's.I have been extremely disciplined about it. It helps me now because now I need it to survive this disease.
Thank you for the list! There is alot of information here. I'll look into it. At the time my Naturopath put me on something to clear it up. I can't remember what it was but it cleared it up .
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