bookmark_borderLong COVID Update: 3 Years of Living With It

by Daniel Brouse
March 7, 2023

COVID=19

In February of 2020, I contracted SARS-CoV-2. By May of 2020, I recognized a pattern of recurring symptoms including: difficulty breathing, congestion, cough, stomach aches, diarrhea, loss of taste and smell, temperature deregulation, night sweats, nightmares, vivid dreams, dizziness, brain fog, headaches, muscle aches, earaches, and peripheral neuropathy.

Over the next year, I was able to treat most of these symptoms with nicotinic acid; however, reducing the niacin dosage yielded increased symptoms. It was only after becoming fully vaccinated in 2021 (post-infection vaccination) that I appear to have been cured of most of the above symptoms. Approximately ninety days after my second dose of the COVID vaccine I was able to reduce my niacin dosage with no ill side effects.

The problem with long COVID is many aspects of the condition(s) do not readily present themselves. In my case, COVID appears to have permanently:
1) increased hypertension
2) increased blood sugar
3) increased cholesterol

If you have had COVID, I highly recommend a medical physical and complete blood work. Though only 10% of people “present with symptoms”, it appears COVID will impact 99% of survivors in the long-term.

With vaccination, medication, and diet, I have been able to control all of my known conditions.

I’m coming to the conclusion that there are 2 main things going on: 1) persistent virus 2) epigenetic changes

1) SARS-CoV-2 can live in organs for an indefinite period of time. Even after testing negative for weeks, the virus can be active in the brain, heart, blood, etc.

2) There appear to be dozens of epigenetic modifications.  The changes are not uniform across the population due mainly to preexisting conditions and/or predispositions (eg family history).

In my case, it is likely I had both conditions.  The persistent COVID-19 was causing most of my readily apparent symptoms.  The niacin helped treat the NAD+ deficiency but did not help clear the virus. It was only after I was fully vaccinated that I was able to clear the virus.

On the other hand, the epigenetic changes appear to be of a permanent nature.  My genes are now programmed for increased hypertension, blood sugars, and cholesterol. Unfortunately, it is quite likely I have other undetected epigenetic modifications. I am looking to my family history and being extra diligent on cancer and other health screenings.

The BBC has produced a documentary entitled The long haul of long Covid that talks about COVID induced: cognitive impairment, fatigue, lactic acid, metabolic dysfunction, micro clots, hypertension, blood sugar, diabetes, asthma, allergies, overactive immune system, muscle and joint pain, arthritis, migraines, shortness of breath, and other chronic problems.

Three years after the official declaration of a pandemic, 65 million people – one in 10 who had Covid-19 – still have symptoms. Some are so ill they are yet to return to work.

The Economist’s health editor, Natasha Loder, examines the science behind long Covid and hears about the challenges as researchers try to unravel the cause behind a condition associated with around 200 symptoms.

Natasha gains insights about the disease from Dr Walter Koroshetz, co-director of the long Covid Recover study in the United States, pulmonologist Dr Lancelot Pinto in Mumbai, India, and long Covid expert Dr Waasila Jassat in Johannesburg, South Africa.

She also meets Dr Emma Wall at London’s Francis Crick Institute to hear about the UK’s long Covid drug trial and Dr Maria Teresa Ferretti, from the Women’s Brain Project, discusses why women are twice as likely to get long Covid than men.

Some Known COVID Chronic Conditions

* Persistent SARS-CoV-2 RNA in multiple organs and throughout the brain
* Destruction of Good Gut Bacteria Resulting in a Compromised Immune System
* Epigenetic Modifications (Changes to DNA)
* Change in Cell Fate
* Tryptophan Deficiency
* Dysfunctional Kynurenine Pathway
* Neurological Damage
* New-Onset Alzheimer’s Disease
* Exertional Intolerance, Oxygen Extraction, Reduced Exercise Capacity
* Down Regulating NAD+
* Up Regulating IDO
* Rogue Antibodies
* Insulin Reduction, Diabetes, High Cholesterol, Heart Disease and Stroke
* Increased Risk of Cancer
* Blood Clots
* Hypertension, Vascular Disorders, Myocarditis and Heart Disease
* Multisystem Inflammatory Syndrome in Children (MIS-C)
* Dysregulation of the innate immune system, i.e. “cytokine storm”

MORE ON COVID: COVID-19 / SARS-CoV-2 / Novel Coronavirus

The Long COVID NAD+ Plus Immune System Diet

COVID: Heart-disease Risk Soars

COVID-19: Increased Risk of Autoimmune Diseases

COVID-19 Compromises Your Immune System (Immunocompromised)

COVID-19: reinfection increases risks of death, hospitalization and damage to multiple organs

COVID-19: Aging Accelerant

Long-COVID: 4 Out of 5 Experiencing Limitations in Daily Activities

Long-COVID: What We Know About Long Haulers Syndrome

bookmark_borderCOVID: Hypertension, Heart-disease Risk Soars

by Daniel Brouse

There have been many documented cases of Sars-Cov-2 causing heart problems including Myocarditis (inflammation of the heart.) Johns Hopkins Medicine says, “Coronavirus infection also affects the inner surfaces of veins and arteries, which can cause blood vessel inflammation, damage to very small vessels and blood clots, all of which can compromise blood flow to the heart or other parts of the body.”

Long term studies have now shown a significant long term risk of heart disease. In the Nature article, Heart-disease risk soars after COVID — even with a mild case, the authors report:

Massive study shows a long-term, substantial rise in risk of cardiovascular disease, including heart attack and stroke, after a SARS-CoV-2 infection.

What’s more, the risk was elevated even for those who were under 65 years of age and lacked risk factors, such as obesity or diabetes.
“It doesn’t matter if you are young or old, it doesn’t matter if you smoked, or you didn’t,” says study co-author Ziyad Al-Aly at Washington University in St. Louis, Missouri, and the chief of research and development for the Veterans Affairs (VA) St. Louis Health Care System. “The risk was there.”

“I am actually surprised by these findings that cardiovascular complications of COVID can last so long,” Hossein Ardehali, a cardiologist at Northwestern University in Chicago, Illinois.

Data from the Smidt Heart Institute at Cedars-Sinai found that deaths from heart attacks rose significantly during pandemic surges. “The dramatic rise in heart attacks during the pandemic has reversed what was a prior decades-long steady improvement in cardiac deaths,” said Yee Hui Yeo, MD, first author of the study. “We are still learning the many ways by which COVID-19 affects the body, regardless of age, gender, ethnicity or race.”

Post-COVID individuals should be on the lookout for heart related issues. Studies have shown an increase risk of hypertension. The study Does COVID-19 Cause Hypertension? concluded, “These findings suggest that COVID-19 increases systolic and diastolic BP and may cause new onset hypertension.”

The Journal Nature published the study Long COVID and hypertension-related disorders. “As a sequel to our previous report in 2020 which reviewed the association of COVID-19 and hypertension, we summarize the possible influences of long COVID on hypertension-related organs, including the cardiovascular system, kidney, and endocrine system, as well as the pathophysiological mechanisms associated with the disorders.” The study concludes, “Evidence suggests that long COVID affects the clinical course of hypertension-related disorders, such as CVD, kidney diseases, and endocrine diseases. Studies thus far also indicate that long COVID has greater impacts on older population and women.”

A niacin supplement (nicotinic acid) is recommended to help reduce the severity of long term complications.

ALSO SEE: COVID: Long COVID Update: Living With It

Insulin Reduction, Diabetes, High Cholesterol, Heart Disease and Stroke
COVID, Long-COVID, and Blood Clots

MORE Scientific Research on COVID-19 / SARS-CoV-2

bookmark_borderCOVID-19: Increased Risk of Autoimmune Diseases

by Daniel Brouse

Not only is COVID-19 known to cause immune system disorders, post-COVID also increases the risk of autoimmune disease.

There are multiple ways COVID has been shown to weaken the immune system (Immunocompromised) including: Destruction of Good Gut Bacteria Resulting in a Compromised Immune System, Dysfunctional Kynurenine Pathway, Down Regulating NAD+, Up Regulating IDO, Rogue Antibodies, Exacerbates Underlying Conditions, and Post–COVID-19 Associated with Immune Cell Infiltration and Altered Gene Expression.

Autoimmunity does not mean the same thing as immunocompromised.   When you are immunocompromised, your immune system is under-performing.  If you are immunocompromised, you have a weakened immune system with a reduced ability to fight infections and other diseases. Autoimmune diseases are usually associated with an overactive immune system that mistakenly attacks healthy cells.  COVID can cause both immunocompromised conditions and autoimmunity diseases. “COVID-19 itself shares some similarities with systemic autoimmune rheumatic diseases, which could be a challenge for diagnostics.”

The matched cohort study Incident autoimmune diseases in association with a SARS-CoV-2 infection found:
Incident autoimmune diseases in association with a SARS-CoV-2 infection
“We found a 42.63% higher likelihood of acquiring autoimmunity for patients who had suffered from COVID-19.”

Conclusions SARS-CoV-2 infection is associated with an increased risk of developing new-onset autoimmune diseases after the acute phase of infection.

A study published in the journal Lancet Risk of autoimmune diseases in patients with COVID-19 found:

“After matching, the COVID-19 cohort exhibited significantly higher risks of rheumatoid arthritis, ankylosing spondylitis, systemic lupus erythematosus, dermatopolymyositis, systemic sclerosis, Sjögren’s syndrome, mixed connective tissue disease, Behçet’s disease, polymyalgia rheumatica, vasculitis, psoriasi, inflammatory bowel disease, celiac disease, type 1 diabetes mellitus and mortality.”

The study, titled “Iron Dysregulation and Inflammatory Stress Erythropoiesis Associated with Long-Term Outcome of COVID-19,” reveals that Long-COVID is linked to elevated levels of C-reactive protein and prolonged elevation of cytokines compared to healthy controls. Iron dysregulation is a common occurrence after infections, as the body swiftly moves iron out of the bloodstream to prevent it from becoming a potential breeding ground for harmful bacteria. The study suggests that defects in iron homeostasis, dysregulated erythropoiesis, and immune dysfunction resulting from COVID-19 may contribute to inefficient oxygen transport, inflammatory imbalances, and persistent symptoms. The information on autoimmune diseases emphasizes that an excessive release of cytokines, which are signaling molecules involved in immune responses, can lead to an exaggerated inflammatory response. This heightened inflammation has the potential to damage tissues and contribute to autoimmune diseases, where the immune system mistakenly attacks healthy cells.

The study: Iron dysregulation and inflammatory stress erythropoiesis associates with long-term outcome of COVID-19

Also see: COVID-19 Compromises Your Immune System (Immunocompromised)

COVID-19 Index

bookmark_borderCOVID-19 Compromises Your Immune System (Immunocompromised)

By Daniel Brouse

SARS-CoV-2 and the results of COVID-19 cause long-term immune system dysfunction. That is to say COVID results in a compromised immune system.

* SARS-CoV-2 infection weakens immune-cell response
The magnitude and quality of a key immune cell’s response to vaccination with two doses of the Pfizer-BioNTech COVID-19 vaccine were considerably lower in people with prior SARS-CoV-2 infection compared to people without prior infection, a study has found. In addition, the level of this key immune cell that targets the SARS-CoV-2 spike protein was substantially lower in unvaccinated people with COVID-19 than in vaccinated people who had never been infected. Importantly, people who recover from SARS-CoV-2 infection and then get vaccinated are more protected than people who are unvaccinated. These findings suggest that the virus damages an important immune-cell response.

* Destruction of Good Gut Bacteria Resulting in a Compromised Immune System
Gut microbiome composition was significantly altered in patients with COVID-19 compared with non-COVID-19 individuals.

* Dysfunctional Kynurenine Pathway
“Targeted and untargeted metabolomics analyses identified altered tryptophan metabolism into the kynurenine pathway, which regulates inflammation and immunity.”

* Down Regulating NAD+
“NAD regulates the inflammatory response in immune and non-immune cells through Sirtuins. Epigenetic regulation of histones and non-histone proteins is induced by sirtuins and is essential for the development, reprogramming, and differentiation of the immune system and its related pathologies. A deregulation of the NAD+ levels has been associated with metabolic diseases and aging-related diseases, including neurodegeneration, defective immune responses, and cancer.”

* Up Regulating IDO
Indoleamine 2,3-dioxygenase (IDO) is an immune checkpoint molecule in the sense that it is an immunomodulatory enzyme produced by alternatively activated macrophages and other immunoregulatory cells. IDO is known to suppress T and NK cells, generate Tregs and myeloid-derived suppressor cells, and also supports angiogenesis.

* Rogue Antibodies
Autoantibodies are antibodies (immune proteins) that mistakenly attack a person’s own healthy tissues and organs. SARS-CoV-2 infection, is associated with many different clinical features that are commonly found in autoimmune diseases, including arthralgias, myalgias, fatigue, sicca, and rashes.

* Dysregulation of the innate immune system, i.e. “cytokine storm”
It is important to note that the severity of disease in humans is not determined only by virus replication but also by the host immune response to the infection, which may lead to dysregulation of the innate immune system, i.e. “cytokine storm” (Omicron SARS-CoV-2 can infect faster and better)

* Reinfection Greater Risks & Exacerbates Underlying Conditions
The evidence shows that reinfection further increases risks of death, hospitalization and damage to multiple organ systems. COVID exacerbates underlying conditions including pulmonary, cardiovascular, hematological, diabetes, gastrointestinal, kidney, mental heal<th, musculoskeletal and neurological disorders

* Post–COVID-19 Associated with Immune Cell Infiltration and Altered Gene Expression
COVID causes long-term immune dysfunction. “These findings indicate that T cell–mediated inflammation persists in the olfactory epithelium long after SARS-CoV-2 has been eliminated from the tissue, suggesting a mechanism for long-term post–COVID-19 smell loss.”

* Elevated Cytokines and Low Iron
Defects in iron homeostasis, dysregulated erythropoiesis contribute to inefficient oxygen transport, inflammatory imbalances, and persistent symptoms. The information on autoimmune diseases emphasizes that an excessive release of cytokines, which are signaling molecules involved in immune responses, can lead to an exaggerated inflammatory response. This heightened inflammation has the potential to damage tissues and contribute to autoimmune diseases, where the immune system mistakenly attacks healthy cells.

Also see: COVID-19: Increased Risk of Autoimmune Diseases

COVID-19 Index

bookmark_borderCOVID-19: reinfection increases risks of death, hospitalization and damage to multiple organs

The study Acute and postacute sequelae associated with SARS-CoV-2 reinfection was published in the Journal Nature.

* The evidence shows that reinfection further increases risks of death, hospitalization and damage to multiple organ systems
* COVID exacerbates underlying conditions including pulmonary, cardiovascular, hematological, diabetes, gastrointestinal, kidney, mental health, musculoskeletal and neurological disorders

First infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is associated with increased risk of acute and postacute death and sequelae in various organ systems. Compared to no reinfection, reinfection contributed additional risks of death, hospitalization, and sequelae including pulmonary, cardiovascular, hematological, diabetes, gastrointestinal, kidney, mental health, musculoskeletal and neurological disorders. The risks were evident regardless of vaccination status. The risks were most pronounced in the acute phase but persisted in the postacute phase at 6 months. Compared to noninfected controls, cumulative risks and burdens of repeat infection increased according to the number of infections. Limitations included a cohort of mostly white males. The evidence shows that reinfection further increases risks of death, hospitalization and sequelae in multiple organ systems in the acute and postacute phase. Reducing overall burden of death and disease due to SARS-CoV-2 will require strategies for reinfection prevention.

MORE ON COVID: COVID-19 / SARS-CoV-2 / Novel Coronavirus

bookmark_borderCOVID-19: Aging Accelerant

In three separate studies of the kidneys, heart, and brain, COVID-19 has been found to act as an aging accelerant.

“Some of the theories for what may be causing long-COVID symptoms include the persistence of the virus. So, instead of the virus coming and going, it sticks around causing inflammation, auto-immune problems and changes in the microbiome,” Dr. Michael Peluso, an infectious disease specialist at the University of California, San Francisco said.

“You can start thinking about getting COVID as almost an accelerant to aging. The viral infection accelerates the aging process in people,” said Dr. Ziyad Al-Aly, director of the Clinical Epidemiology Center at Washington University in St. Louis and the chief of research and education service at Veterans Affairs St. Louis Health Care System.

Dr. Al-Aly researched data from millions of people across the country. The studies on kidney outcomes in long COVID, long COVID in the brain and long COVID in the heart had similar patterns.

“We have seen that people are losing about three to four percent kidney function in the year following that infection. That usually happens with three to four years of aging,” Al-Aly said.

Long-term cardiovascular outcomes of COVID-19

Long-term neurologic outcomes of COVID-19

Kidney Outcomes in Long COVID

MORE ON COVID: COVID-19 / SARS-CoV-2 / Novel Coronavirus

bookmark_borderLong-COVID: 4 Out of 5 Experiencing Limitations in Daily Activities

The CDC Panel Report Long COVID Panel Survey found:

* 81% of adults with ongoing symptoms of COVID lasting three months or longer — or four out of five adults — are experiencing limitations in their daily activities compared to before they had the virus. (Economic implications include work force participation and long-term health care costs.)

* Young adults between ages 18 and 29 had the highest share of people currently with long COVID who have trouble performing daily tasks, at 86.3%. What will the long-term costs and quality of life be when these people are in their 50’s,60’s, and if they get to live into their 70’s?

Long-COVID Survey
Long-COVID Survey

COVID-19 / SARS-CoV-2 / Novel Coronavirus

bookmark_borderCOVID-19 Significantly Higher Risk of Alzheimer’s

The risk of older people (over 65) developing Alzheimer’s disease over a one-year period nearly doubled following a COVID-19 diagnosis. The same researchers had previously found that individuals with dementia had a greater risk of contracting COVID-19 and being hospitalized and dying from the disease than those without dementia.

“Many people believe that for Alzheimer’s disease there is a combination of factors that work together to give you the cognitive impairment, and we were concerned that the kinds of things that happened during COVID-19 — the intense inflammation, and perhaps the kinds of direct action on the brain of the of the virus — might be a risk factor,” Dr. Davis, the study’s co-author, said. “So we went looking for that in our study.”

“We can say that they are associated, but we cannot infer causality,” she stressed.

“First, the pandemic presented serious delays for individuals seeking out medical diagnoses like Alzheimer’s disease, meaning these results could be driven by those who already had Alzheimer’s disease when they were infected but had not yet sought out a formal diagnosis,” Dr. Snyder, vice president of medical and scientific relations at the Alzheimer’s Association, explained.

“Alternatively, COVID-19 infection — which is linked to immune changes, including inflammation — may impact the onset of brain changes that are linked to Alzheimer’s disease and other dementia,” said Dr. Snyder. “However, because this study only showed an association through medical records, we cannot know what the underlying mechanisms driving this association are without more research.”

Association of COVID-19 with New-Onset Alzheimer’s Disease

COVID-19 / SARS-CoV-2 / Novel Coronavirus

bookmark_borderGut Microbiota (Good Gut Bacteria) and COVID-19

by Daniel Brouse

Good gut bacteria are the microorganisms (bacteria and archaea) that live in the digestive tract. The gut microbiota produces fermentation of non-digestible substrates like dietary fibres and endogenous intestinal mucus.

“Approximately 100 trillion micro-organisms (most of them bacteria, but also viruses, fungi, and protozoa) exist in the human gastrointestinal tract — the microbiome is now best thought of as a virtual organ of the body. he human genome consists of about 23 000 genes, whereas the microbiome encodes over three million genes producing thousands of metabolites, which replace many of the functions of the host, consequently influencing the host’s fitness, phenotype, and health,” according to the Role of the Gut Microbiota in Nutrition and Health. “Gut microbes are key to many aspects of human health including immune, metabolic, and neurobehavioural traits.”

Research published in the Journal Nature states, “The human oral and gut commensal microbes play vital roles in the development and maintenance of immune homeostasis.”

In the study, Gut microbiota composition reflects disease severity and dysfunctional immune responses in patients with COVID-19, it was reported:
Although COVID-19 is primarily a respiratory illness, there is mounting evidence suggesting that the GI tract is involved in this disease. Gut microbiome composition was significantly altered in patients with COVID-19 compared with non-COVID-19 individuals. Moreover, this perturbed composition exhibited stratification with disease severity concordant with elevated concentrations of inflammatory cytokines and blood markers such as C reactive protein, lactate dehydrogenase, aspartate aminotransferase and gamma-glutamyl transferase. SARS-CoV-2 primarily infects the respiratory tract, however, pathophysiology of COVID-19 can be attributed to aberrant immune responses in clearing the virus.

Associations between gut microbiota composition, levels of cytokines and inflammatory markers in patients with COVID-19 suggest that the gut microbiome is involved in the magnitude of COVID-19 severity possibly via modulating host immune responses. Furthermore, the gut microbiota dysbiosis after disease resolution could contribute to persistent (long-COVID) symptoms, highlighting a need to understand how gut microorganisms are involved in inflammation and COVID-19.

2025 Update: COVID-19, the Aging Brain, and Gut Microbiome

With growing evidence that COVID-19 can persist in the body, especially the gut, and cause systemic effects, researchers are calling for greater awareness, ongoing monitoring, and expanded health support — not just for those with long COVID, but for the broader public as well.

About Good Gut Bacteria (Gut Microbiome)
About Persistent SARS-CoV-2 and COVID-19
COVID Chronic Conditions and Long-COVID

Science Based Information on COVID-19 / SARS-CoV-2 / Novel Coronavirus

bookmark_borderCOVID, Long-COVID, and Blood Clots

by Daniel Brouse

Originally, COVID-19 was thought to be a respiratory infection. It didn’t take long to discover that SARS-CoV-2 quickly enters the heart, blood stream, and can infect every organ.

Now we know that SARS-CoV-2 causes micro bloodclots that do not necessarily clear the system.

Resta Pretorius, a South African scientist, says, “When we speak about long COVID and microclots, I think we should just step back a second and speak about acute COVID. We have noted – we and others have noted that the vascular system and clotting is not working properly during acute COVID. So the dilemma with long COVID is that the percentage of individuals, up to 30%, never really get over the presence of these clotting abnormalities or physiological abnormalities when they are not infective anymore – so when they get over the normal five to 10 days of acute COVID. So during long COVID, these clots then just continue to be present.”

“Inside the microclots that are present in these individuals’ blood in circulation, there are various entrapped molecules, inflammatory molecules, that actually prevent the breakdown of the microclots. So although the body’s trying very hard to break down these clots with the normal physiological processes, molecules entrapped in the microclots actually prevent it from breaking down.”

“Now, that is a massive issue because if these microclots are in circulation, it damages the vasculature, or your blood vessels, and in that process, prevents the cells to receive enough oxygen, causing then a failure of the coagulation system of oxygen to your cells. And that can be linked to all of the lingering symptoms that have been noted in long COVID.”

The Results of Persistent clotting protein pathology in Long COVID/Post-Acute Sequelae of COVID-19 (PASC) is accompanied by increased levels of antiplasmin: We show that plasma samples from Long COVID/PASC still contain large anomalous (amyloid) deposits (microclots). We also show that these microclots in both acute COVID-19 and Long COVID/PASC plasma samples are resistant to fibrinolysis (compared to plasma from controls and T2DM), even after trypsinisation. After a second trypsinization, the persistent pellet deposits (microclots) were solubilized. We detected various inflammatory molecules that are substantially increased in both the supernatant and trapped in the solubilized pellet deposits of acute COVID-19 and Long COVID/PASC, versus the equivalent volume of fully digested fluid of the control samples and T2DM. Of particular interest was a substantial increase in α(2)-antiplasmin (α2AP), various fibrinogen chains, as well as Serum Amyloid A (SAA) that were trapped in the solubilized fibrinolytic-resistant pellet deposits.

ALSO SEE: COVID: Heart-disease Risk Soars

COVID-19: Chronic Conditions

MORE Scientific Research on COVID-19 / SARS-CoV-2