Hi! If you are here you are probably just like myself earlier, are looking for more knowledge around long covid to help yourself or your dear one. My name is Anastasia Mokienko, i live in Oslo Norway. I am a former researcher among other things I do. I have a PhD and I did a research on health care system in Norway. And I was so lucky and got long covid myself (LC). Since the disease is pretty novice, the health care providers across the world are still struggling to give any answers, at least in Norway they do, so I decided to update myself with the recent publications on the topic in hope to find something helpful for diagnostics and treatment. When I am thinking of diagnostics, I think about the root cause – why we get disautonomia, POTs, what happens to our blood, brain, cardio, vestibular, hormonal systems. The disease affects 75% women and as we know research on women has not been funded globally as much as it deserves. Most research projects were performed on men previously. Men as research subjects are easier to control, as there are no hormonal cycles. However those hormonal cycles and childbearing ability and autoimmunity is what some researchers believe, makes us, females, more prone to LC. Interestingly enough but the LC symptoms increase as well between ovulation and period. There is a theory that it could be connected to for example mast cell activation, oestrogen and reaction to histamine.
Below I have gathered a few articles that I found informative on different aspects of LC. It’s not complete yet, but you already may find something useful. And I keep adding more. You are welcome to dig in them and connect to me to discuss as well. It would be nice to make a research article in collaboration knitting things together.
Soon I will as well make a post about my own LC journey and symptoms, what helped me and what not. Keep tuned.
In this page I plan little by little to list out the research and articles that I find to be relevant and share links with you. The page will be open to public as I work on it. Since I have long covid myself i am working on it max 30 min a day, please come back later for the updates. You can also stay in touch through my instagram of fb pages. Feel free to write me say hi and leave your email to receive updates.
If you are a fellow researcher – please write me. I’d love to do something together.
As well I hope when I’m bit more recovered – I will do some short trainings for long COVID patients for activating parasympathetic nerve system. Stay tuned or ask me if it’s already out.
A must to read for every physician and patient- Review of long COVID findings:
«There are several hypothesized mechanisms for long COVID pathogenesis, including immune dysregulation, microbiota disruption, autoimmunity, clotting and endothelial abnormality, and dysfunctional neurological signalling. EBV, Epstein–Barr virus; HHV-6, human herpesvirus 6»
«Tests …such as total immunoglobulin tests, natural killer cell function tests, the tilt table or NASA lean test, the four-point salivary cortisol test, reactivated herpesvirus panels, small fibre neuropathy biopsy, and tests looking for abnormal brain perfusion96, should instead be prioritized.»
Estrogene, histamine: The Curious Link Between Estrogen, Mast Cells, and Histamine https://www.larabriden.com/the-curious-link-between-estrogen-and-histamine-intolerance/
Chronotropic incompetence (CI)
is generally defined as the inability to increase the heart rate (HR) adequately during exercise to match cardiac output to metabolic demands.
«PoTS is diagnosed if your heart rate increases by 30 beats a minute (bpm) or more (40bpm in those aged 12 to 19) usually within 10 minutes of standing. This increase continues for more than 30 seconds and is accompanied by other symptoms of PoTS.»
POTs: «We’ll review a groundbreaking new study funded by Dysautonomia International that found reduced cartilage and connective tissue biomarkers in POTS, as well as evidence of increased coagulation and inflammation.»
“The current proposed pathology for POTS is an inability to regulate blood volume. Researchers suspect that vasomotor denervation causes dilation of the blood vessels, leading to reduced preload to the heart, which triggers an increase in the central sympathetic nervous system response. Resulting symptoms are likely related to inadequate blood circulation and overcompensation by the sympathetic nervous system.”
Heart rate frequency
“hjertefrekvensvariasjonen registrerer spesifikke endringer i tid mellom påfølgende hjerteslag. Og tid mellom slag måles i millisekunder (ms) og er kjent som «RR-intervall» eller «inter-beat-intervall (IBI).”
“The sinus node discharge rate depends on a basic intrinsic or constitutional rate for that person as modulated by the speeding influences of sympathetic nervous system firing and the slowing influences of parasympathetic system (vagus nerve) firing upon the sinus node. Thus, a second-by-second recording of heart rate provides a second-by-second record of a balance between sympathetic and parasympathetic nervous system influences on the heart.”
“Reports using HRV to link autonomic dysfunction with infection. Proposed mechanisms of viral infection induced autonomic dysfunction include invasion of the central nervous system and the direct viral, toxin-mediated or immune-mediated involvement of the peripheral and autonomic nervous system
The vagus nerve seems to inform the brain about a peripheral inflammation. As a result, the production of cortisol (causing suppressing the inflammation) is activated through the hypothalamic–pituitary–adrenal axis. The Authors also pointed out that due to the descending efferent vagal-to-sympathetic neural conversion, a subclass of T-cells secrete acetylcholine and the production of inflammatory cytokines by splenic macrophages is limited. When the vagus activity is low, then the inflammatory response can even lead to a ‘cytokine storm’. However, in physiological response, the vagus ‘controls’ the inflammation process.
One of the clinical endpoints of the present study could be the development of a methodology for monitoring post-COVID patients, including the analysis of HRV performed by Holter monitoring. In order to validate the application of HRV measures, we suggest performing studies in groups of patients affected by COVID-19 several months after infection. In our report, the study group was characterized by a mild (or asymptomatic) course of the disease, which may indicate that the statistically significant HRV parameters are sensitive markers for a long-term monitoring of convalescent patients.”
Data gathering and explanation
“Our findings indicate that long COVID leads to sympathetic excitation influence and parasympathetic reduction. The excitation can increase the heart rate and blood pressure and predispose to cardiovascular complications. Short-term HRV analysis showed good reproducibility to verify the cardiac autonomic involvement.”
Free version of preprint is here: Cardiac Autonomic Function in Long COVID-19 Using Heart Rate Variability: An Observational Cross-Sectional Study[v1] | Preprints
Easy explained HRV: Heart Rate Variability | The Ultimate Guide to HRV | WHOOP
Resting heart rate
Brain and long COVID
Norsk forskning: Norwegian research project
Inflammation in the brain
• Inflammation in the brain and nerve cell damage are associated with symptoms of anxiety in long COVID-19 patients, a study finds.
• Both hospitalized and non-hospitalized COVID-19 survivors with symptoms of anxiety showed cognitive impairment and high levels of the biomarkers of brain inflammation.
• The evidence may help validate the experiences of people experiencing neurological symptoms of long COVID-19 and point towards better diagnostic strategies.
Long covid diagnostics
“COVID EBV activation and load + complete blood count (CBC), electrolytes, metabolites, hepatic function panels, cardiac biomarkers, thyroid panels and D-dimer “ : (11 things doctors have learned about long COVID)
“The team found that blood vessels of those with presumed long COVID were changing rapidly after a confirmed COVID-19 infection. They also found that patients with long COVID had 14 elevated blood biomarkers associate with blood vessels. With the help of machine learning, they discovered that two biomarkers called ANG-1 and P-SEL could be used to classify long COVID with 96 per cent accuracy.”
Causes of long COVID
WHO clinical guidelines
Anti COVID drug
Paxclovir and T-cells
Norsk: Rehabilitering i Norge
Norsk: Korona medisin paxlovir
Muscles and COVID
“…the progressive reports of aggressive skeletal muscle complications associated with COVID-19, mainly sarcopenia, cachexia, rhabdomyolysis, peripheral neuropathy, and Guillain-Barré syndrome. It is believed that these conditions are prompted predominantly by the cytokine storm triggered by SARS-CoV-2, but a few studies have also indicated an association with ACE2 downregulation, hypoxia, direct viral invasion into the skeletal muscle, and physical inactivity.”
Viral provoked anxiety
Lungs – OBS!
People with long-lasting symptoms of breathlessness after COVID-19 infection may have damage to their lungs that does not show up using routine diagnostic scans, according to a small UK study.
Supplements and mitochondria
Clinical trials have shown the utility of using oral replacement supplements, such as l-carnitine, alpha-lipoic acid (α-lipoic acid [1,2-dithiolane-3-pentanoic acid]), coenzyme Q10 (CoQ10 [ubiquinone]), reduced nicotinamide adenine dinucleotide (NADH), membrane phospholipids
Cold and mitochondria
Exercise and cold exposure promoted increased expression of mitochondrial biogenesis- related genes in soleus muscle.
Mitochondria and D-Ribose
If the mitochondria aren’t receiving enough oxygen, then mitochondrial enhancers might not make a difference. If a hydrogen sulfide imbalance is the issue, then that will have to be dealt with. If free radicals are a problem, then enhancing the mitochondria – the source of many free radicals in the body – could make things worse
D-Ribose levels decline during the low oxygen states which may be present in ME/CFS and FM. When those conditions are present, cells turn to bringing two ADP molecules together to form ATP. The AMP left over is washed out – leaving the cell depleted in purines. Bob Naviaux found reduced purines in ME/CFS.
D-Ribose is able to enhance purine levels. Two non-placebo blinded studies from Dr. Teitelbaum suggest the D-Ribose may be helpful in a number of ways.
Podcasts Jason Hommel on his new book, The Copper Revolution
Koder i Norge
Fra 2023: «For å markere at noe er en følgetilstand etter en infeksjon skal man som regel bruke en kode fra gruppen Følgetilstander etter infeksjonssykdommer og parasittsykdommer (B90-B94). For covid-19 er det imidlertid innført en egen kode, U09.9 Postinfeksiøs tilstand etter covid-19.
Eksempel: vedvarende hodepine etter vaksinasjon: Kode 1: R51 Hodepine
Kode 2: U09.9 Postinfeksiøs tilstand etter covid-19»