As a physician and geneticist-in-training studying the human genetics of COVID-19, I remain cautious about where the pandemic will go from here. At this point in the pandemic, there are few if any policies requiring one to wear a mask in public areas. Many hospitals still have masking policies, appropriately, although Quebec has recently lifted its mask mandate from public transportation.

Individuals riding the at-times crowded buses have no legal obligation to wear a mask to protect themselves and others from COVID-19. This is the case even when there is poor ventilation, such as when windows are closed when it rains. Fortunately, I see that there are still a reasonable number of individuals opting to mask up in crowded areas, even when it is not required.

This article is not about arguing whether restrictions were lifted too soon. Let me know in the comments your thoughts on restrictions being lifted. Given much less politicization of public health measures in Canada versus the United States, even in the Nationalist-led province of Quebec, I trust that the decision was made with close guidance from public health experts. The reasoning appears sound, given that there are more opportunities for ventilation in the warmer months, and a large proportion of Canadians are fully vaccinated against COVID-19 (83%, per OurWorldInData). This article is about individuals considering wearing a mask even when they are not obligated to in crowded public areas.

As the case, hospitalized, and death statistics demonstrate, COVID-19 is still with us. While some argue that COVID today is milder than at the beginning of the pandemic, individuals with comorbidities or risk factors for severe disease can still get very ill, even when fully vaccinated with access to therapeutic agents like Paxlovid. The best treatment for COVID-19 is not getting it all. Voluntarily continuing prevention measures when they make sense, such as when one is in a crowded bus where others may be at higher risk of severe disease than you, could save a life. Wearing a mask for 15–30 minutes is a pretty minor inconvenience. Considering how much good it can do, it seems like a good trade-off to me.

In summary, we have an opportunity to relax with the COVID-19 pandemic. We can expect it to again rise to prominence this coming winter. There are steps that we can do, at minimal inconvenience to ourselves, that will protect ourselves, our loved ones, and our neighbors. If you liked this article, be sure to give me some claps, it will help more see my writing so we can all think more deeply about health together.

The post Why I Still Wear a Mask appeared first on Medika Life.

The United States Centers for Disease Control offers that one in five adult Covid survivors under the age of 65 in the United States has experienced at least one health condition that is a part of so-called long-Covid.

For those 65 and older, the statistics are even more disturbing: One in four will suffer from chronic symptoms associated with a COVID-19 infection.

Today, we explore the phenomenon of long COVID. We’ll look at some of the conditions associated with the condition and new findings.

Long COVID: Scope of the problem

I increasingly hear of individuals previously infected with SARS-CoV-2, the virus that causes COVID-19, reporting persistent symptoms (or the onset of long-term ones) four weeks or more after their acute infection.

We refer to such chronic COVID symptoms as post-COVID conditions or long COVID.Post-COVID ConditionsImportant update: Healthcare facilities CDC has updated select ways to operate healthcare systems effectively in…www.cdc.gov

The United States Centers for Disease Control evaluated electronic health record data for March 2020 through November 2021. The researchers looked at persons at least 18 years old.

The researchers assessed the incidence of 26 conditions (often attributable to post-COVID) among those with a previous COVID-19 diagnosis and matched patients with evidence of COVID-19 in the electronic health record.

The investigators divided the population by age (18 to 64 versus 65 years or older).

Here are the study findings:

• Among adults, 28 percent experienced a condition thought to be COVID-19 infection; in the control group, 16 percent reported such symptoms.
• The conditions affected several body systems, including cardiovascular, pulmonary, hematologic, renal, endocrine, gastrointestinal, musculoskeletal, neurologic, and psychiatric.
• For both age categories in the COVID group, the highest risk ratios were for lung clots (acute pulmonary embolism) and respiratory symptoms, with over double the risk of the control group.

Long COVID: Symptoms

People who experience post-COVID conditions most commonly report:

General symptoms

• Tiredness or fatigue that interferes with daily life
• Symptoms that get worse after physical or mental effort (also known as “post-exertional malaise”)
• Fever

Respiratory and heart symptoms

• Difficulty breathing or shortness of breath
• Cough
• Chest pain
• Fast-beating or pounding heart (also known as heart palpitations)

Neurological symptoms

• Difficulty thinking or concentrating (sometimes referred to as “brain fog”)
• Headache
• Sleep problems
• Dizziness when you stand up (lightheadedness)
• Pins-and-needles feelings
• Change in smell or taste
• Depression or anxiety

Digestive symptoms

• Diarrhea
• Stomach pain

Other symptoms

• Joint or muscle pain
• Rash
• Changes in menstrual cycles

The US Centers for Disease Control warns that if you have a long COVID condition, you may develop or continue to have symptoms that are challenging to explain or manage. The symptoms may be similar to those with chronic fatigue syndrome and other poorly understood chronic conditions that happen after other types of infection.

Long COVID: Who is more likely to experience it?

Some groups may be affected more by long COVID, including those who experience more severe COVID-19 illness (especially true for those hospitalized or needing intensive care).

Those with pre-existing health conditions may also be more likely to suffer from long COVID symptoms than those who did not get a COVID-19 vaccine.

People suffering from multisystem inflammatory syndrome (MIS) during or after COVID-19 illness appear more likely to have chronic COVID-related troubles, as do those from populations suffering from health inequities.

I’ll end with this: Long COVID is one more good reason to get a COVID-19 vaccine. People who are vaccinated but experience a breakthrough infection appear less likely to report post-COVID conditions, compared to people who are unvaccinated.

The scope of the long COVID problem is shocking to me. We need to develop additional tools to reduce the risk of long Covid.

The post One in Five With Adult Covid Develop Long COVID appeared first on Medika Life.

The German study looked at a cohort analysis from the “Disease Analyzer,” a national database from 1171 primary care physicians throughout Germany. The timeframe was March, 2020 to January, 2021, a time when few were vaccinated, and covered 8.8 million patients.

There were 35,865 individuals with documented COVID-19 during the study period. A control group with an equal number of individuals who had an acute upper respiratory infection (URI or “viral cold”) was matched for demographics and clinical characteristics. The two groups were similar for sex, age, health insurance index, month of COVID-19 or a URI and for comorbidities such as obesity, hypertension, hyperlipidemia, myocardial infarction and stroke. New onset diabetes was recorded from shortly after infection onset until July, 2021.

Type 2 diabetes, but not Type 1, was found to be increased among the Covid patients compared to the controls, 15.8 versus 12.3 per 1000 person years.

The graph above portrays the onset of diabetes over the 12 months observation period, the red line for those with a URI and the blue line for those with COVID-19. The absolute numbers are small but the difference, especially over time becomes clear.

The authors conclude that “COVID-19 confers an increased risk for Type 2 diabetes.”

The American study utilized the electronic medical record database of the Veterans Administration health system. They selected a cohort of about 181,000 individuals who had a positive test for Covid between March 1, 2020 and September 30, 2021 and who survived at least 30 days. They also created two control groups. The first or concurrent controls were about 4.2 million VA patients during the same timeframe and the second or historical controls were about 4.2 million veterans seen between March 1, 2018 and September 20, 2019, i.e., before the pandemic.

All of these individuals had no evidence of diabetes at the onset of the study period. The concurrent control group individuals had no positive tests for COVID-19 but it’s possible, in fact likely, that some had asymptomatic infection or were infected but never were seen in the VA system for their infection. All were followed for approximately one year. The numbers of individuals who developed diabetes were determined and compared between the Covid-19 patients and the two control groups.

All three groups were quite similar for multiple baseline characteristics. The average (but with wide ranges) age was about 61- 62 years, about three quarters were white, and 88% were male. The average BMI was 29. They were equally represented by blood pressure levels, cardiovascular disease, cerebrovascular disease, chronic lung disease, and dementia.

Taking the contemporary control group as a baseline, those who had COVID-19 had an excess of diabetes detected over the next 12 months.

Those individuals who at baseline had a higher diabetes risk score were substantially more likely to develop diabetes during those next 12 months. Diabetes onset was also more common among those who were greater than 65 years of age, those who had prediabetes as measured by HbA1c (a measure of blood sugar over time) and those with a BMI >30.

Those with more severe Covid-19 who were admitted to the hospital and those who were admitted to intensive care has substantially more diabetes develop than did those who had only mild Covid-19.

The risk for developing diabetes among the ~162,000 non-hospitalized individuals when considered as an excess burden above that of the concurrent control group was about eight per 1000 people at the end of 12 months. That may not sound like a big risk but it equates to about 1500 excess cases of diabetes among those not hospitalized with Covid, i.e., those with relatively mild Covid-19.

As the study authors noted, “Given the large and growing number of people infected with Covid-19…, these absolute numbers might translate into a substantial overall population level burden and could further strain an already overwhelmed healthcare system.”

These two reports demonstrate that diabetes is one more syndrome/disease that occurs after even mild Covid-19, another addition to the Long Covid pantheon. It is a reminder that even mild Covid-19 infection can lead to many later “Long Covid” syndromes and diseases. Patients and physicians need to be cognizant of the possibility that new onset diabetes might be related to prior Covid infection within the last year or so.

The post Diabetes Is Increased After Mild Covid-19 appeared first on Medika Life.

This article will examine all the most common symptoms in-depth and offer advice to those who are hesitant to seek out treatment.

What exactly is LCS and how do I know if I’ve got it?

The million-dollar question. With so many varying symptoms, ranging from leg pain and breathing difficulty to brain fog and depression, healthcare is still trying to get a proper feel for the after-effects of Covid in certain individuals. Here are a few key facts you should keep in mind.

• Long Haul Covid, PASC, LCS, or CCS is a very real thing. It is now a recognized and documented medical consequence of coronavirus infection in some people. The exact percentage of people who will suffer from LCS is still unknown. This report from the CDC offers a new perspective and actual figures, but it’s too early yet to call these figures definitive and the CDC’s goal in publishing these is to draw your doctor’s attention to the incidence of LCS as becoming more commonplace.
• A study published in December of 2020, entitled Characterizing Long COVID in an International Cohort: 7 Months of Symptoms and Their Impact (links to a PDF file ) is based on survey results from more than 3,700 self-described COVID “Long Haulers” in 56 countries. They show nearly half couldn’t work full time six months after unexpectedly developing prolonged symptoms of COVID-19. A small percentage of respondents, thankfully, seemed to have bounced back from brief bouts of Long COVID, though time will tell whether they have fully recovered.
• There is no clear age group or demographic more likely to suffer from LCS. Some evidence exists to suggest that if you have pre-existing lung/heart/other conditions, these may increase your risk for developing LCS but the jury is still out on this. What is clear is that no age group is exempt from developing LCS.
• Good news. You aren’t losing your mind. This is an important point to grasp for most who start experiencing symptoms. Brain fog, depression, cognitive impairment and even waking dream states can all be caused by LCS and can have a profound impact on your mental health and thought patterns. Not seeking out help will increase your levels of stress and simply contribute to the worsening of symptoms.
• Not all medical practitioners will recognize your symptoms as LCS. Ensure your care provider is up to speed on the signs and symptoms of the condition, but don’t step into the public trap of self-diagnosis. Keep an open mind and discuss ALL your symptoms openly with your health care provider.
• What makes this condition so difficult to diagnose with certainty is that you may tick a number of boxes and not actually have LCS. Your doctor is the only person properly qualified to properly assess your condition and we’d recommend examining LCS extensively as a potential cause of any new mental health symptoms you may be experiencing, particularly if you’ve recently had a brush with the coronavirus.
• You may even have had a mild Covid infection and not been aware of it or simply passed it off as mild flu or sniffles. To play it safe, if you’re exhibiting some of the symptoms below, go in and have yourself checked out properly. A test that looks for coronavirus antibodies can help identify an earlier infection if you’re uncertain you’ve had Covid or haven’t recently had a PCR test.

So, about those symptoms. Pull up a chair, it’s a long and growing list and you can expect additional symptoms to be added to this list over the coming months and some to fall away as our understanding of the condition improves.

LCS Symptoms

In the 2020 study referenced above, the following was found among 3,762 respondents from 56 countries. We’ve used this report as the basis for this article as it encompasses the broadest set of symptoms we’ve seen described and contains more detail than other reports.

Prevalence of 205 symptoms in 10 organ systems was estimated in this cohort, with 66 symptoms traced over seven months. Respondents experienced symptoms in an average of 9.08 (95% confidence interval 9.04 to 9.13) organ systems. The most frequent symptoms reported after month 6 were: fatigue (77.7%, 74.9% to 80.3%), post-exertional malaise (72.2%, 69.3% to 75.0%), and cognitive dysfunction (55.4%, 52.4% to 58.8%). These three symptoms were also the three most commonly reported overall

To best describe the findings in this cohort we’ve dissected the graphs published in the report and reproduced them below, as per the reports license Attribution-NonCommercial 4.0 International (CC BY-NC 4.0). We’ll start with the neuropsychiatric symptoms (brain and mood-related). Bars represent the percentage of respondents who experienced each symptom at any point in their illness and are divided into nine sub-categories. When all rows in a given panel use the same denominator, the first row, labeled “All,” indicates the percentage of respondents who experienced any symptoms in that category. Error bars are 95% confidence intervals. Base scale is prevalence (in percentage)

Nest, we’ll move on to the non-neuropsychiatric symptoms. In other words, everything to do with the rest of the body, but excluding the brain. Bars represent the percentage of respondents who experienced each symptom at any point in their illness. Symptoms are categorized by the affected organ systems. When all rows in a given panel use the same denominator, the first row, labeled “All,” indicates the percentage of respondents who experienced any symptoms in that category. Error bars are 95% confidence intervals.

As the lists of possible symptoms are lengthy, we’ve summarized them below and you can view prevalence for each in the linked report. To simplify finding your symptoms, we have again separated these as per the report and graphics above, neuropsychiatric symptoms are shown first followed by non-neuropsychiatric.

List of neuropsychiatric symptoms for LCS

Brain fog/Cognitive dysfunction and memory impairment symptoms

• poor attention or concentration (74.8%)
• difficulty thinking (64.9%)
• difficulty with executive functioning (planning, organizing, figuring out the sequence of actions, abstracting) (57.6%)
• difficulty problem-solving or decision-making (54.1%)
• slowed thoughts (49.1%)
• short-term memory loss (64.8%)
• long-term memory loss (36.12%)
• forgetting how to do routine tasks (12.0%)
• unable to make new long-term memories (7.3%)

Memory symptoms, cognitive dysfunction, and the impact of these on daily life were experienced at the same frequency across all age groups. Of those who experienced memory and/or cognitive dysfunction symptoms and had a brain MRI, 87% of the brain MRIs (n=345, of 397 who were tested) came back without abnormalities.

Speech and language symptoms

• problems with word retrieval (46.3%)
• difficulty communicating verbally (29.2%)
• difficulty reading/processing written text (24.8%)
• difficulty processing/understanding others. (23.8%)

Those who spoke two or more languages had changes to their non-primary language. Speech and language symptoms occurred in 13.0% of respondents in the first week, increasing to 40.1% experiencing these issues in month 4. 38.0%of respondents with symptoms for over 6 months reported speech and language symptoms in month 7.

Sensorimotor symptoms

• numbness
• coldness in a body part
• tingling/pins and needles
• electric zap
• facial paralysis
• facial pressure/numbness, and weakness

Tingling, prickling, and/or pins and needles were the most common at 49% of respondents. Refer to Supplemental Table S3 (shown below) for the most commonly affected anatomical locations.

Sleep-related symptoms

78.6% of respondents experienced difficulty with sleep. The table below lists each type of sleep symptom, as well as the percentage of respondents with that symptom who also listed it as pre-existing (before COVID-19 infection).

Headaches

Headaches were reported by 77.0% of participants, with the most common manifestations being ocular 40.9%, diffuse 35.0%, and temporal 34.0%. 24.0% of respondents reported headaches after thinking/mental exertion and 23.0% experienced migraines. Of those experiencing migraines, 56.4% did not list migraines as a pre-existing condition. 46% of all respondents reported headaches during week 1, 54% of respondents experiencing symptoms in month 4 reported headaches in month 4, and 50% of respondents experiencing symptoms in month 7/reported headaches in month 7.

Emotion and mood

• Anxiety (the most common psychological symptom reported at 57.9%)
• Irritability (51.0%)
• Depression (47.3%)
• Apathy (39.2%)
• Mood lability, assessed by “mood swings” and “difficulty controlling emotions (46%)
• Suicidality (11.6%)
• Mania and hypomania (2,6 AND 3.4% respectively)

Of those who reported anxiety, 61.4% had no anxiety disorder prior to COVID. Of those who reported depression, 55.0% had no depressive disorder prior to COVID.

Taste and smell

• Loss of smell ((35.9%)
• Loss of taste (33.7%)
• Altered sense of taste (25.1%)
• Phantom smells (i.e. olfactory hallucinations or phantosmia) (23.2%)
• Altered sense of smell (19.8%)

Phantom smells were accompanied by a write-in question asking for a description of the smells, in which the most common words were “smoke,” “burning,” “cigarette,” and “meat.” Changes to smell and taste were more likely to occur earlier in the illness course, with 33.2% occurring in week 1. 25.2% of respondents with symptoms for over 6 months experienced changes to taste and smell in month 7.

Hallucinations

The most common hallucination reported was olfactory hallucinations 23.2%, mentioned above. Visual hallucinations were reported by 10.4% of respondents, auditory hallucinations by 6.5%, and tactile hallucinations by 3.1%.

List of non-neuropsychiatric symptoms for LCS

Systemic

• Fatigue (98.3%)
• Weakness (44.5%
• Elevated temperature below 100.4F (58.2%)
• Fever above 100.4F (30.8%)

3.0% (113 respondents) experienced a continuous fever (>100.4F) for 3 or more months, and 15.0% (563 respondents) experienced an elevated temperature, continuously, for 3 or more months. Skin sensations of burning, itching, or tingling without a rash were reported by 47.8% of respondents.

Reproductive/Genitourinary/Endocrine

• Menstrual/period issues (36.1% of respondents with active menstrual cycle)
• Abnormally irregular periods (26.1%,)
• Abnormally heavy periods/clotting (19.7%)
• Post-menopausal bleeding/spotting among cis females over 49 (4.5%)
• Early menopause among cis females in their 40s (3.0%)
• Extreme thirst (35.8%)
• Bladder control (14.1%)

Sexual dysfunction occurred across genders, experienced by 14.6% of male respondents, 8.0% of female respondents, and 15.9% of nonbinary respondents. 10.9% of cis male participants and 3.2% of nonbinary participants reported pain in testicles.

Cardiovascular (heart and circulation)

• Heart palpitations (67.4%)
• Tachycardia (61.4%)
• Pain/burning in the chest (53.1%)
• Fainting (12.9%)

Cardiovascular symptoms were more common over the first 2 months than in later months. Even so, 40.1% of respondents with symptoms for over 6 months experienced heart palpitations, 33.7% experienced tachycardia, and 23.7% experienced pain/burning in the chest in month 7.

Postural Orthostatic Tachycardia Syndrome (POTS)

To screen for POTS, participants were asked whether they had the ability to measure their heart rate, if their heart rate changed based upon posture, and if standing resulted in an increase of over 30 BPM. Of the 2,308 patients who reported tachycardia, 72.8% (1680) reported being able to measure their heart rate. Of those, 52.4% (570) reported an increase in heart rate of at least 30 BPM on standing.

Musculoskeletal

• Chest tightness (74.8%)
• Muscle aches (69.1%)
• Joint pain (52.2%)

Musculoskeletal symptoms were common in this cohort, seen in 93.9%. In month 7, chest tightness affected 32.9% of month 7 respondents and muscle aches affected 43.7% of month 7 respondents

Immunologic and Autoimmune

• Heightened reaction to old allergies (12.1%)
• New allergies (9.3%)
• New or unexpected anaphylaxis reactions were notable at 4.1%

20.3% of respondents (n=765) reported experiencing changes in sensitivity to medications,

Reactivation and test results for latent disease

Since being infected with SARS-CoV-2, 2.8% of respondents reported experiencing shingles (varicella-zoster reactivation), 6.9% reported current/recent EBV infection, 1.7% reported current/recent Lyme infection, and 1.4% reported current/recent CMV infection. Detailed results are shown in the table below.

HEENT (Head, ears, eyes, nose, throat)

28 symptoms were defined as symptoms of the head, ears, eyes, nose, and throat (graphic above). All respondents experienced at least one HEENT symptom. A sore throat was the most prevalent symptom (59.5%) which was reported almost twice as often as the next most prevalent symptom, blurred vision (35.7%). Within this category, symptoms involving vision were as common as other organs. Notably, 1.0% of participants reported a total loss of vision (no data on the extension and duration of vision loss were collected).

Ear and hearing issues (including hearing loss), other eye issues, and tinnitus (ringing in the ears) became more common over the duration studied. Tinnitus, for example, increased from 11.5% of all respondents reporting it in week 1 to 26.2% of respondents with symptoms for over 6 months reporting it in month 7.

Pulmonary and Respiratory (lungs)

• Shortness of breath (77.4%)
• Dry cough at (66.2%)
• Breathing difficulty with normal oxygen levels (60.4%)
• Rattling of breath (17.0%)

Dry cough was reported by half of the respondents in week 1 (50.6%) and week 2 (50.0%) and decreased to 20.1% of respondents with symptoms for over 6 months in month 7. Shortness of breath and breathing difficulties with normal oxygen increased from week 1 to week 2 and had a relatively slow decline after month 2. Shortness of breath remained prevalent in 37.9% of respondents with symptoms in month 7.

Gastrointestinal (stomach)

• Diarrhea (59.7%)
• Loss of appetite (51.6%)
• Nausea (47.8%,)

Of respondents experiencing symptoms after month 6, 20.5% reported diarrhea and 13.7% reported a loss of appetite in month 7.

Dermatologic (skin)

• Itchy skin (31.2%)
• Skin rashes (27.8%)
• Petechiae (17.8%
• COVID toe (13.0%)

COVID toe, petechiae, and skin rashes were most likely to be reported in months 2 through 4 and decreased thereafter.

Post-exertional malaise

The survey asked participants whether they have experienced “worsening or relapse of symptoms after physical or mental activity during COVID-19 recovery”. Borrowing from Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) terminology, this is referred to as postexertional malaise (PEM). 89.1% of participants reported experiencing either physical or mental PEM.

• Of the respondents who experience PEM triggered by physical exertion, 49.6% experience it the following day, 42.5% experience it the same day, and 28.7% experience PEM immediately after.
• Of the respondents who experience PEM triggered by mental exertion, 42.2% experience it the same day, and 31.4% experience it immediately after.

For some respondents the time PEM started varied. A high number of the respondents with PEM (68.3%) indicated that the PEM lasted for a few days. For physical exertion, the mean severity rating was 7.71, and for mental exertion, the mean severity rating was 5.47.

Recovery and long term prognosis for LCS

Now you know the possible effects of LCS the next question on everyone’s mind is an obvious one. Is this permanent or do people recover, and if they do, what sort of time frames are we looking at.

These are both difficult questions, particularly as we are still only getting to grips with the condition and we don’t have a long enough frame of reference yet to answer the question definitively. Obviously, the degree to which your organs have been affected, pre-existing conditions, and the type of symptoms you exhibit all play a role. Let’s look again at the cohort from the report above.

Relapses: triggers & experience

Patients with Long COVID can experience relapsing-remitting symptoms. A minimum of 85.9% of respondents reported experiencing relapses. Respondents characterized their relapses as occurring in an irregular pattern (52.8%) and in response to a specific trigger (52.4%). The most common triggers of relapses, or of general worsening of symptoms, that respondents reported were

• Physical activity (70.7%)
• Stress (58.9%)
• Exercise (54.39%)
• Mental activity (46.2%
• More than a third of menstruating participants experienced relapses during (34.3%) or before menstruation (35.2%).

Heat and alcohol were other triggers of relapse. Triggers that were written in by respondents included food with sugar and high histamines (reported by 70 respondents); lack of sleep or rest (64 respondents); cold air (39 respondents); overworking or schoolwork (28 respondents); smoke, pollution, and chemical odors (24 respondents).

Approximately half (51.7%) of respondents indicated that their symptoms have slowly improved over time, while 8.9% indicated that their symptoms have gradually worsened and 10.8% have had symptoms rapidly worsen over time.

Remaining symptoms after 6 months

Only 164 out of 3762 participants (4.4%) experienced a temporary break in symptoms. The remaining participants reported symptoms continuously, until symptom resolution or up to taking the survey. A total of 2454 (65.2%) respondents were experiencing symptoms for at least 6 months. For this population, the top remaining symptoms after 6 months were primarily a combination of systemic and neurological symptoms. Over 50% experienced the following symptoms:

• Fatigue (80.0%)
• Post-exertional malaise (73.3%)
• Cognitive dysfunction (58.4%)
• Sensorimotor symptoms (55.7%)
• Headaches (53.6%)
• Memory issues (51.0%)

In addition, between 30%-50% of respondents were experiencing the following symptoms after 6 months of symptoms:

• insomnia
• heart palpitations
• muscle aches
• shortness of breath
• dizziness and balance issues
• sleep and language issues
• joint pain
• tachycardia
• other sleep issues.

How is LCS affected by pre-existing conditions?

Again, let’s examine the data from the cohort. Most patients (83%) reported at least one pre-existing condition. The most commonly reported pre-existing conditions were;

• Seasonal allergies (36.3%)
• Environmental allergies (24.1%)
• Migraines (18.7%)
• Asthma (17.1%)

Other conditions of note include acid reflux (12.2%), irritable bowel syndrome (12.9%), vitamin D deficiency (11.8%), obesity (10.7%), hypertension (9.1%), hyperlipidemia (7.4%), and myalgic encephalomyelitis / chronic fatigue syndrome (2.5%).

In the United States, the prevalence of asthma in the general population is 7.7%. While this cohort is not representative of the U.S. population, the prevalence of asthma (17.07%) should be noted.

Making it personal, the voices of respondents

We’ve added these, not to concern you, but to allow you a deeper understanding of the extent to which LCS can affect your life and if you’re experiencing these symptoms, to assure you, you not losing your mind. We strongly urge you to seek help from a trusted medical practitioner who is knowledgeable in the field of LCS.

On Cognitive Dysfunction and Memory Loss

“mother has started to help me take the medications I’m on because I can’t remember if I’ve taken them immediately after having the bottle in my hand”

“was trying to fill out a mortgage application form and couldn’t remember our rent. I put £3750 a month. My partner said, no it’s £1375. So I put £13750. My partner said no, so I tried several more times — I was just guessing numbers”

“sitting on the toilet to pee and had to stop for a second to think if I was really there and not about to pee myself or the bed”

“don’t remember what I did in March or April up until the last week of April. I had almost nothing on my schedule. I don’t know what I did”

“put food on the gas stove and walked away for over an hour, only noticing when they were smoking/burning”

“forget how to do normal routines like running a meeting at work”

“felt lost driving and had to stop and find my position in a GPS to be able to drive back home. It’s a route I have done hundreds of times”

“have trouble comprehending new ideas”

“can’t hold multiple trains of thought […] If I tell myself I have to water my plants, I must do it before another thought comes into my mind because otherwise, I will forget”

“can’t follow plots in movies or tv shows, have to write everything down, have to remember to look at notes”

“had to terminate many phone calls because I could no longer comprehend the speakers nor communicate clearly with them”

“used to do the New York Times crossword puzzle every single day and I can’t even manage the mini ones now”

“can’t focus on reading complex texts, and it makes me feel very tired to do that”

“Found that I had become dyslexic — and knew it was happening at the time, could not remember how to spell words — also found I was missing words from sentences and sometimes writing things that did not make sense”

Should I see a psychiatrist or psychologist first?

Medika’s advice on this is no. Your first port of call should be a doctor qualified to recognize the symptoms of LCS. The right provider can assist you with an appropriate treatment strategy without necessarily resorting to psychotropic drugs and antidepressants which can have serious long-term implications for your mental health.

First, explore the probable diagnosis of LCS with a qualified medical practitioner, particularly if you’re experiencing a number of the symptoms listed above.

If you would like to share your personal experiences of LCS, we encourage you to use the form below and we’ll add your voice to the conversation.

The post The Complete A to Z of Long Haul Covid Symptoms. What you Need to Know appeared first on Medika Life.

Among 3,171 nonhospitalized adult COVID-19 patients, 69% had one or more outpatient visits 28–180 days after the diagnosis. Two-thirds had a visit for a new primary diagnosis, and approximately one-third had a new specialist visit. Symptoms potentially related to COVID-19 were common new visit diagnoses. Visits for these symptoms decreased after 60 days but for some patients continued through 120–180 days.

It is as important for patients and the public to be aware of the potential for follow on symptoms. Let’s examine the report in a little more detail and see what this potentially means for patients that may have been asymptomatic or only experienced light symptoms with their initial coronavirus infection.

It’s also important to note that for obvious reasons with our attention diverted to fighting the spread of the virus, healthcare needs in the months after Covid diagnosis among nonhospitalized adults have not been well studied. The figures below were drawn from a sample of 3,171 adults, none of whom had been hospitalized. Their electronic health record (EHR) data from health care visits in the 28–180 days after a diagnosis of COVID-19 at an integrated health care system was analyzed and showed the following.

• Among 3,171 nonhospitalized adults who had COVID-19, 69% had one or more outpatient visits during the follow-up period of 28–180-days.
• Compared with patients without an outpatient visit, a higher percentage of those who did have an outpatient visit were aged ≥50 years, were women, were non-Hispanic Black, and had underlying health conditions.
• Among adults with outpatient visits, 68% had a visit for a new primary diagnosis, and 38% had a new specialist visit.
• Active COVID-19 diagnoses* (10%) and symptoms potentially related to COVID-19 (3%–7%) were among the top 20 new visit diagnoses; rates of visits for these diagnoses declined from 2–24 visits per 10,000 person-days 28–59 days after COVID-19 diagnosis to 1–4 visits per 10,000 person-days 120–180 days after diagnosis.

The report concludes

The presence of diagnoses of COVID-19 and related symptoms in the 28–180 days following acute illness suggests that some nonhospitalized adults, including those with asymptomatic or mild acute illness, likely have continued health care needs months after diagnosis. Clinicians and health systems should be aware of post-COVID conditions among patients who are not initially hospitalized for acute COVID-19 disease.

What this means to you

If you know you contracted the coronavirus in the last few months and you’ve developed any annoying and persistent symptoms, leg pain, headaches, lethargy, breathing issues, unusual and sudden bouts of depression, etc, that cannot be explained by a pre-existing condition, make sure you get to a doctor and explain to them that you recently tested positive for the virus.

The post 68 Percent of Patients With Mild COVID-19 Get New Diagnosis Within 6 Months appeared first on Medika Life.

Even if you’re not a medical expert, you must have heard the term Blood-Brain Barrier (BBB) and Central Nervous System (CNS) being used over and over in the last few months. Covid, we are told, can get into your head and I’m not referring to the mental stress of avoiding infection or being quarantined, but rather the real virus itself that causes covid. SARS-CoV2 can infect cells, nerves, and synapses in your brain.

This isn’t some superpower the covid virus possesses, but rather a trait shared by many of the coronaviruses that have preceded it. A growing body of literature demonstrates that neurotropism (a virus that is capable of infecting nerve cells) is a common feature of coronaviruses. Aside from common symptoms of covid, some neurological complications following SARS-CoV-2 infection include confusion, cerebrovascular diseases, ataxia, hypogeusia, hyposmia, neuralgia, and seizures. There are reports of brain edema⁵, partial neurodegeneration⁶, even encephalitis⁷ in severe cases of COVID-19.

Our brains are the computers that operate all the systems in our bodies. Breathing, blood flow, neural responses, pretty much everything your body can do or does, is controlled by the brain. For this reason, it’s well protected against invaders which may damage its delicate systems. Brain cells, unlike other cells in our body, can also not be replaced, so this is another good reason to try and keep the brain isolated and protected.

One method of protection for the brain is the Blood-Brain Barrier (BBB) mentioned earlier. It’s really good at keeping out viral invaders, but as we are discovering, it isn’t bulletproof. Certain viruses would seem to be able to cross this barrier. Let’s first establish what the SARS-CoV2 virus is and how it operates.

MOA and understanding the coronavirus family

Coronaviruses (CoVs) refer to a family of enveloped, positive-sense, single-stranded, and highly diverse RNA viruses. There are four genera (alpha, beta, gamma, and delta), among which α-coronavirus and β-coronavirus attract more attention because of their ability to cross animal-human barriers and emerge to become major human pathogens.

SARS-CoV-2 is the seventh member of the coronavirus family we’ve discovered. We know from previous evidence that these viruses infect humans. Of the seven, NL63-CoV, HKU1-CoV, 229E-CoV, and OC43-CoV, typically cause common cold symptoms, while SARS-CoV, MERS-CoV, and now the SARS-CoV-2 are responsible respectively for the SARS pandemic in 2002 and 2003, MERS in 2012, and the current COVID-19 pandemic.¹

SARS-CoV-2 is a betacoronavirus that shares almost 80% sequence identity with SARS-CoV and 50% sequence identity with MERS-CoV². Similar to SARS-CoV, SARS-CoV-2 binds to the enzymatic domain of the angiotensin-converting enzyme 2 (ACE-2) receptor exposed on the surface of several cell types, including alveolar cells, intestinal epithelial cells, endothelial cells, kidney cells, monocytes/macrophages, as well as neuroepithelial cells and neurons³.

After spike (S) protein binding to ACE-2 receptor, a subsequent cleavage by transmembrane protease serine 2, cathepsin, or furin, probably induces the endocytosis and translocation of SARS-CoV-2 into endosomes⁴ or a direct viral envelope fusion with host cell membrane for cell entry.

What we don’t know

There is no described direct mechanism of SARS-CoV-2 neuroinvasiveness currently in the medical literature. In simple English, we still don’t understand exactly how the virus manages to get through the body’s defenses to reach the brain. However, we do know that coronaviruses are not always limited to the respiratory system, but they can reach the central nervous system (CNS), inducing neurological impairments.

We have suspicions about the possible mechanisms the virus might be employing to breach our defenses but none have as yet been confirmed. As the covid virus shares much of its genetic makeup with the SARS and MERS viruses, perhaps we can look to studies of these viruses for clues, as both are known to also attack the CNS.

Breaching the castle walls

Essentially, there are three theories put forward currently to explain the CoV2 virus’s ability to reach the brain. All three mechanisms show merit and the issue is the subject of ongoing research across the planet. This matters because before you can successfully attempt to block a mechanism or ingress point, you need to figure out which one is being used.

Our starting point, as always, should be the known. It is known that coronaviruses are not always limited to the respiratory system, but they can reach the CNS, inducing neurological impairments. This neuroinvasive capacity is well established for most beta coronaviruses, including SARS-CoV⁸, MERS-CoV⁹, 229E-CoV¹⁰, OC43-CoV¹¹, and HEV¹².

The how isn’t that important to our understanding of the impacts of the virus on our brains, but for those interested in exploring the mechanisms further, here are the potential routes under investigation. If this isn’t your cup of tea, skip over it and scroll down to ‘What happening to our brains’.

Transcribial Route and Neuronal Transport Dissemination

Growing evidence shows that some coronaviruses first invade peripheral nerve terminals, then are anterograde/retrograde spread throughout the CNS via synapses, a well-documented neuroinvasive route for coronaviruses such as HEV67¹² and OC43-CoV¹¹. Among the peripheral nerves, the olfactory nerve is considered one of the strongest candidates for SARS-CoV-2 dissemination into the CNS because of its close localization to olfactory epithelium.

In the intranasal administration of SARS-CoV and MERS-CoV into transgenic mice, the viral CNS invasion is possible through the transcribial route, gaining direct access to the olfactory bulb, and then spreading to the thalamus and brainstem¹³. The exact mechanism of early CNS access is still unclear.

The covid virus may also be using peripheral nerves such as the vagus nerve, via which lungs and gut afferents reach the brainstem.

SARS-CoV-2 has been detected in COVID-19 patient feces. A recent in vitro study demonstrated the SARS-CoV-2 capacity to infect human intestinal epithelium¹⁴. The anterograde and retrograde viral transmission from duodenal cells to brainstem neurons has also been reported¹⁵. Therefore, it is possible that upon enterocyte SARS-CoV-2 infection, a further transmission to glial and neuronal cells within the enteric nervous system could reach the CNS via the vagus nerve.

Evidence regarding the enteric nervous system and the SARS-CoV-2 vagus nerve dissemination is almost null, and further research is required.

Hematogenous Route

The infection and damage of cells of epithelial barriers allow the virus entrance to the bloodstream and lymphatic system, spreading to multiple organs, including the brain¹⁶. The BBB is one of the most frequent viral entry routes to the CNS.

There are two possible mechanisms for SARS-CoV-2 spreading via this route, which involve the circulation of viral particles into the bloodstream: the infection and viral transcytosis across vascular endothelial cells, and the leukocytes infection and mobilization towards the BBB, a well-described mechanism termed Trojan horse.

Although experimental evidence regarding SARS-CoV-2 neuroinvasiveness is still lacking, post-mortem studies have shown the virus’s presence in the brain microvasculature, cerebrospinal fluid, and even neurons. Studies have also demonstrated that the ACE-2 receptor is expressed on neuron and glial cells of structures such as the olfactory epithelium, cortex, striatum, substantia nigra, and the brain stem¹⁷, thus supporting the SARS-CoV-2 potential to infect cells throughout the CNS.

So what is happening to our brains?

First off, a few facts. It is unclear if the neurological symptoms of COVID-19 result from cytokine storm-induced neuroinflammation or the infection of some brain areas. Irrespective, the CNS and immune system involvement might have remarkably neurologic long-term consequences, including the development of neuropsychiatric disorders. Expanding the research and science in this area is key to furthering our understanding.

Neurological Manifestation of COVID-19, short and long-term

It‘s been widely described that a broad spectrum of virus infection can spread through the body and eventually reach and affect the mammalian peripheral nervous system (PNS) and CNS when optimal conditions exist. For instance, the hypoxia promoted by respiratory distress has been associated with disturbed brain metabolism and a subsequent neurological manifestation¹⁸.

Evidence appears to support the neuroinvasive and neurotropism and possible long-term neurological sequelae of coronaviruses, including SARS-CoV and MERS-CoV¹⁹.

Emergent data from case reports and clinical studies demonstrate that covid patients exhibit some CNS and PNS complications, ranging from mild to fatal. The most frequent neurological symptoms are mostly nonspecific in the short term, such as loss of smell and taste, headache, malaise, myalgias, and dizziness. In contrast, moderate-to-severe cases developed acute cerebrovascular diseases, impaired consciousness, and skeletal muscle injury²⁰. These manifestations can be considered a direct virus effect in the CNS.

Unfortunately, your recovery from an acute infection does not promise a full viral clearance, and if the infection becomes chronic, it may result in long-term sequelae(an aftereffect of a disease), including chronic neurological impairment¹⁸. Some studies report the coronavirus persistence in the CNS and some neurologic and tissular affections¹⁹.

In mice surviving acute encephalitis caused by OC43-CoV, the viral RNA could be detected even six months post-infection; in correlation with the viral persistence, these mice also display a reduced locomotor activity, subjacent decreased density of hippocampal layers, and gliosis.

The RNA of MHV-CoV is detectable in the brain, even 10–12-month post-infection. Chronic-CNS demyelination persists as late as 90 days post-infection to scattered demyelinated axons at 16 months after infection²¹. Case reports support that neurotropic viral infection promotes an exacerbated inflammatory response leading to encephalitis or CNS-target autoimmune (i.e., demyelination) response in COVID-19 patients.

Guillain-Barre and Miller-Fisher cases are reported without SARS-CoV-2 detection in cerebrospinal samples, supporting the inflammatory response’s role in neurological manifestations.

Whether the dysregulated immune response remains after the illness resolves, neurological disorders can be developed, including dementia, depression, and anxiety. Additionally, hypoxia and cerebrovascular diseases reported in COVID-19 patients, particularly encephalitis and stroke, are expected to produce permanent or at least long-term neurological impairments for affected patients.

A cohort study reported an altered mental status, reflecting neurological and psychiatric, such as encephalopathy, encephalitis, psychosis, and dementia-like syndrome in patients from 23–94 years old; however, cerebrovascular events predominated in older patients²². Additional neurological complications reported in other coronaviruses infections may also be applicable for SARS-CoV-2 and further research is needed.

Fixating on issues such as locating the source or natural reservoir for the original point of infection for the SARS-CoV2 virus is, at this stage, premature and a waste of precious resources. It may be worthwhile pointing out that we have still not located the origins of the Ebola virus and for both viruses, never may. Clearly, our attention needs to be focused on developing a deeper and clearer understanding of covid’s mechanisms to fully address the pathological consequences for our bodies, some of which are only now becoming apparent, and no doubt, more will emerge over time.

Unless we want covid’s lasting legacy to be one of chronic illness affecting millions, we know where we need to be focusing our attention, and that focus needs to be immediate.

Acknowledgements

The following paper, entitled ‘Infection Mechanism of SARS-COV-2 and Its Implication on the Nervous System’ was broadly referenced in this article. To view the original, please follow the link.

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