In this article, we look at the largest and longest study on the neurological effects of COVID and the underlying reason that COVID-19 harms our nervous system. By addressing the underlying cause, we may be able to change the situation and possibly extend our lives. This is how COVID attacks the brain and how to reverse damage.
Recent large-scale research on the neuropsychiatric effects of COVID-19 infection was published in the medical journal Lancet Psychiatry.
Seven researchers from Cambridge University and Oxford University in the UK, led by Oxford University psychiatrist Professor Paul Harrison, examined retrospective cohort studies for this research (read below).
There were 62 medical institutions involved in the studies, which were conducted across four continents (occurring in the United States, Australia, the United Kingdom, Spain, Bulgaria, India, Malaysia, and Taiwan). The studies were carried out between January 2020 and April 2022, a span of two years and three months.
The researchers found more than 1.28 million cases of COVID-19 infection from the electronic medical records of roughly 89 million patients, and compared them to a cohort of non-COVID patients who had other respiratory disease. In other words, they had the same age, gender, occupation, risk factors for diseases, and vaccination status as the experimental group did at the same time. The experimental and control groups each had more than 1.2 million patients.
There has never been a study of COVID-19 cases with such successful concurrent control.
The analysis assessed 14 neurological and psychiatric COVID-19 infection sequelae’s two-year time-varying hazard ratios. These conditions included:
- Brain fog, dementia, Parkinson’s, and insomnia
- Anxiety disorders, mood disorders, and psychosis
- Epilepsy, encephalitis, intracranial hemorrhage, and ischemic stroke
- Guillain-Barré syndrome, neurological root and plexus disorders, and neuromuscular joint and muscle disorders
The mean age of the 1,284,437 patients with the COVID-19 infection was 42.5 years; they ranged in age from children to the elderly.
This analysis has given us a great deal of useful knowledge.
Higher Mortality Risk in COVID Group Than Control Group
Initially, six months after diagnosis, the majority of the 14 neurological and psychiatric illnesses maintained a considerably elevated morbidity risk among COVID patients than non-COVID patients.
Second, even two years later, the threat of cognitive problems (brain fog), dementia, psychosis, Guillain-Barré syndrome, and epilepsy stayed elevated, with far-reaching health implications.
To illustrate the situation, consider dementia, a common symptom.
When the cumulative occurrence of dementia in the COVID-infected group was compared to the patient population with other respiratory illnesses (i.e. the control group), it was discovered that the probability of dementia was substantially greater in the first group at six months of diagnosis than in the control group.
At the end of the two-year follow-up period, this threat remained higher in the first group than in the control group.
Brain fog is another common symptom, and its hazard ratio remained greater than that of the control group both six months after diagnosis and two years later.
After one to two months, the likelihood of common mental disorders like mood and anxiety disorders returned to normal.
In older individuals over 65, the threat of psychosis, neuromuscular diseases, dementia, and brain fog is substantially greater. There were as many as 32 percent of elderly patients who experienced any of these neurological and psychiatric sequelae over the course of two years, and 34.1 percent of those elderly patients who experienced these neuro-psycho sequelae passed away during the two-year follow-up.
Notably, over the two-year follow-up period, mortality rates for older adults with dementia, brain fog, or epilepsy were 71%, 61%, and 83%, respectively.
It is clear from the information above that a serious illness is present. In other words, the onset of dementia and brain fog in the ongoing care of these elderly patients heralds a rather dismal prognosis for them.
The Severity of Sequelae Varies Among Different Variants
Additionally, during the extensive follow-up period, the researchers also examined data from various COVID-19 variants, including Alpha, Delta, and Omicron. Other studies have rarely offered this kind of distinctive data.
The majority of neurological or psychological sequelae, such as ischemic stroke, epilepsy, brain fog, insomnia, and anxiety, as well as patient mortality are significantly more likely to occur in the majority of cases of the Delta variant.
The incidence or mortality have not changed as a result of the Alpha variant.
Following Omicron variant infection, the prevalence of a number of neuropsychiatric sequelae, including dementia, mood disorders, and neurogenic disorders, increased significantly. There was no rise in patient mortality, though.
Why Do Neuropsychiatric Impairments Persist for 2 Years After Infection?
We can view from the data above that even two years after a COVID-19 infection, there was a relentlessly high prevalence of some neuropsychiatric sequelae than in the control group.
This shows that the SARS-CoV-2 virus is distinct from other viruses because it is difficult for a patient to recover after suffering a neuropsychiatric injury.
There is a lot of research being done in this area, and it has long been a subject of fascination to researchers.
Two articles, one in the journal Science in January 2022 and the other in the journal Nature in July 2022, claim that the SARS-CoV-2 virus can harm nerve cells in the body through at least seven different mechanisms, some of which may persist long after an acute infection.
- It causes the apoptosis of neuronal progenitor cells directly.
- Endothelial diseases can cause damage or fragility of the cerebral blood vessels, thrombotic events, or leaks by attacking the blood vessels of the brain and causing ischemia and hypoxia.
- It causes autoimmune reactions: Autoimmunity not only attacks the virus, but it can also attack the components of one’s own neurons, including the external protective layer of nerves (myelin), which functions similarly to the insulation skin of electronic wires. Our nerves will be unable to transmit neuronal signals as quickly as before if myelin is destroyed. That is one of the reasons we think, respond, and move more slowly.
- Inflammation of the nervous system: Inflammation causes damage to our regular nerve cells.
- Mitochondrial nerve cell damage: Our mitochondrial cells are our powerhouse. Nerves end up losing their power source when it is compromised. Our cells will be unable to function normally.
- Impairments in nerve cell lipid metabolism: lipids make up 60% of the brain. Lipid disorders are directly related to neuronal system dysfunction.
- Autophagic activity inhibition: Autophagy is a process by which nerve cells renew themselves and remove waste. The autophagy process functions similarly to our intrinsic waste recycling system. The inhibitory effects on the autophagic process will result in more garbage and an inefficient garbage processing system, ultimately hastening the aging process of brain cells.
It is clear that COVID-19 infection has a wide-ranging and profound effect on the brain and nervous system. This harm is extensive, persistent, and very challenging to repair.
It is important to note one phenomenon. In other words, the study reported that the prevalence of anxiety and mood disorders was temporarily elevated in COVID-19 patients, indicating that these symptoms may be brought on by some transitory triggers. The mechanisms of neuronal apoptosis and loss due to brain fog and/or dementia are different from the causes of such mood disorders and anxiety.
Mild COVID-19 Infections Can Also Alter the Brain
Even a minor COVID-19 infection can change the brain, according to a March 2022 study that was published in Nature.
The UK Biobank’s bio-specimens from nearly 800 participants—half of whom had COVID infection and the other half did not—were used in this study by Oxford University neuroscientists. Ninety-six percent of them did not require hospitalization, indicating that the majority had only mild infections.
Before and after the infection, magnetic resonance imaging of the brain was performed on these subjects.
Three significant structural alterations in their brain were identified by the researchers after an analysis.
First, COVID-infected respondents had a substantial reduction in brain size, also referred to as atrophy, implying an uptick in dementia incidence. The average additional loss of brain volume in COVID-infected patients was 0.2 percent to 2 percent higher than in the control group.
Second, the orbitofrontal cortex (connected with decision making processes) and the gray matter thickness of the parahippocampal gyrus (affiliated with cognition, emotion, and memory) were lost to a greater extent, indicating an increased danger of brain fog.
Third, there was substantial damage to regions associated with the olfactory cortex.
More pertinently, this implies that the brain damage caused by the SARS-CoV-2 virus is unrelated to the severity of the illness. Even in mild forms, structural and functional brain abnormalities can take place.
As previously stated, Omicron infection does not have a high rate of serious disease or mortality, implying that there are many mild cases. However, as mentioned in the previous study, it can cause long COVID, the sequelae of COVID-19 infection, including dementia and neurological diseases.
Of course, research has shown that Omicron infections cause half as many long COVID as Delta infections do. The number of long COVID patients due to Omicron is not necessarily less than that of the prior variants, despite the significant increase in the infected population.
The Brain Has the Ability to Regenerate: Long COVID Can Be Reversed
Every disease has at least one cause, and it might be intricate. The disease may be treated or even reversed if the underlying cause(s) can be identified and eliminated.
What is causing the COVID-19 infection’s neurological harm?
We have been reading a lot of literature and keeping up with the neurological and psychological aspects of COVID-19 for a while now. We have also done neurology research in the past. Our understanding and conclusion are that while the SARS-CoV-2 virus affects the human nervous system in seven different ways, the lethal attack of the virus on neural stem cells is the most serious.
In other words, the SARS-CoV-2 virus’s attack on neural stem cells results in the destruction of the brain’s neural cell regeneration mechanism, which is the main issue.
Even if the brain appears to have sustained severe damage, it can still be repaired. Researchers have found that the human brain is capable of self-repair and regeneration.
It was once believed that the brain could not regenerate, and this belief was expressed in textbooks. Since 1960, researchers have provided compelling evidence that adult animals’ or adults’ own brain nerve cells can regenerate.
As an illustration, researchers have discovered that the hippocampal region generates 600–700 new neurons every day. Considering that the brain contains 100 billion cells overall, 600–700 cells may not seem like a lot. But it also demonstrates that the brain can regenerate, which is a crucial mechanism for preserving brain plasticity and resilience.
And it is this mechanism that the SARS-CoV-2 virus targets, as well as this ability to regenerate, which it suppresses. We must therefore examine the issue of neurological sequelae following COVID-19 infection from the point of view of regeneration in order to find a solution.
The subventricular zone/olfactory bulb (which are connected together) and the parahippocampal gyrus are the primary sites of nerve cell regeneration.
The olfactory bulb and parahippocampal gyrus are attacked by the SARS-CoV-2 virus.
These two areas act as nerve cell manufacturing plants in our bodies and are crucial for nerve cell regeneration. In other words, the SARS-CoV-2 virus attacks the brain’s core, which is in charge of nerve cell regeneration. This is why the consequences of the COVID-19 infection’s nerve damage last so long and are so severe.
So, how long does it take for nerve cells to regenerate?
One would hope that this process moves as quickly as possible. In fact, regeneration of nerve cells is not slow. It takes three days for neural stem cells to generate neural progenitor cells, two weeks for them to distinguish into naive nerve cells (i.e. immature neurons), and four weeks for them to mature. As a result, the entire process typically takes at least six to seven weeks.
Ultra-simple Aerobic Exercise for Nerve Cell Regeneration
Nerve cell regeneration is a popular study topic these days. Numerous scientists are employing methods such as neural stem cell implantation and neurotrophic factors, but their applicability and effects are severely limited.
We read a lot of books to find methods that are both convenient and accessible while also being effective in helping the mind and body. There are many more natural methods, which we will discuss later when we have the opportunity.
We are going to show you one of the most basic, cost-free, and simple ways to regenerate neurons that anyone can do. This method involves regular, consistent, relaxing, and voluntary aerobic exercise.
Exercise has been shown to increase blood flow to the heart, lungs, and even the brain. However, a lot of people are unaware that adult adults can encourage the regeneration of brain nerve cells through regular aerobic exercise.
First, let us look at the results of an animal experiment.
Adult mice were split into two groups in a study at the Salk Institute for Biological Sciences in California. The control group’s cages lacked running wheels and other conducive exercise features, whereas the experimental group’s did. It was discovered that adult mice’s regeneration of hippocampal dentate gyrus nerve cells was significantly increased after four weeks of voluntary and unwinding exercise.
Three to four times as many new nerve cells had grown in the experimental group of mice than in the control group.
Additionally, the exercise hastened the growth of their regenerative neurons.
Researchers from Argentina published a study in Cell Reports in 2017. The experimental setup was comparable to that of the earlier research. The newly developed neurons in the exercising mice were found to be significantly more mature after 21 days of exercise, with dendrites that were four times longer and more branched than those in the sedentary (without running exercise conditions) mice.
In the graph, neurons from mice that were sedentary looked like tiny bean sprouts, while neurons from mice that were active looked like mature bean sprouts.
The electrophysiological function test revealed that sedentary mice’s granule cells lacked action potentials or function. The granule cells of the exercising mice discharged electricity repeatedly, showing that they were communicating with other neurons and transmitting information.
Only after a lengthy (three weeks) as opposed to a brief (one week) period of exercise does the development of nerve cells accelerate. The structure and functionality of the nerve cells have not yet changed significantly after one week.
So, must running be done in order to exercise effectively?
No, not always. Physical activities like walking, grocery shopping every day, and household chores are all good forms of exercise.
How much exercise should we get each day to promote neuroregeneration? Two studies can help us gain some understanding.
The first is a prospective observational cohort study that tracked the daily physical activity of 716 older adults without dementia over the course of four years.
After four years, 71 subjects developed clinical Alzheimer’s disease, a form of dementia, whereas those who engaged in high levels of daily physical activity had a risk of Alzheimer’s disease that was approximately 53% lower.
This study’s design was meticulous, and the analysis disregarded additional confounding variables, such as age, gender, education, social and cognitive activity, current level of motor function, depressive symptoms, chronic health conditions, and APOE allele status, that might affect the onset of dementia in old age.
In other words, both groups of older adults had an equal distribution of these confounding factors. The study came to the conclusion that a person’s level of daily physical activity was a reliable indicator of when dementia would start to affect them.
Another, more thorough study looked at the relationship between gray matter volume, physical activity, and cognitive impairment in 299 adults (with a mean age of 78 years).
Throughout this study, physical activity was measured as the number of blocks walked per week, and gray matter volume was a measure linked to brain regeneration.
From Q1 to Q4, the researchers divided the 299 subjects into four groups based on how much they exercised (Q1 group had the lowest activity, and Q4 group had the highest activity). The gray matter volume in the Q4 group was found to be significantly greater than those in the other three groups with lower levels of physical activity after 13 years of observation. Although there was no distinction in the gray matter volumes of the other three groups, this difference was statistically meaningful.
In addition, after 13 years, the Q4 cluster had a two-fold lower cognitive impairment risk compared to the other groups.
How much walking did the Q4 group do on a weekly basis?
Each week, they collectively walked 72 blocks (around 6 to 9 miles per week).
As a result, we can adjust how much exercise and workout we do based on our individual needs.
Therefore, considering that lockdowns were implemented during the COVID-19 pandemic and that some people were unable to exercise outside without restriction, it was not advantageous for their neuro-regeneration of the brain.
The Body Needs an Organic Balance of Movement and Stillness
It is simple to miss some health warning signs. In actuality, the human body and mind are intertwined.
The brain’s ability to repair itself and regenerate is aided by daily calming, relaxing, and voluntary exercise in addition to the need for nutrients like glucose and oxygen.
The advantages of sitting in meditation for the brain have been previously mentioned. The exercise advice is not necessarily in conflict with this. Movement and stillness must coexist in harmony for the human body to function as one organic equilibrium. Our brains gain a great deal from a dynamic equilibrium that can be achieved between our movement and stillness.
For this reason, we have consistently emphasized that the best aerobic exercise is the one that you enjoy. Each of us can set it up properly based on our personal and professional schedules.
The proverb “Walking a hundred steps after each meal can help you live to be 99 years old.” refers to the fact that this type of exercise is good for our intestines and digestion as well as our brain and nerve regeneration. It is simple, affordable, and organic. It might be able to stop aging and COVID’s neurological and psychological effects. Another illustration of how a single healthy habit can improve our health and even transform our lives is provided here.
Read the study below: