Search Results for: corona

Det kom en ny större studie som visade fina resultat av D-vitamin som behandling mot Covid-19. Men, liksom många andra studier nu, så fanns den tillgänglig före den hade granskats (sk peer-review vilket säkerställer kvalitet på studier), så studien är tillfälligt borttagen.

Det detta preprint visade var att calcifediol, en form av D-vitamin (här kan du läsa mer om formerna, vanligen används i tillskott Cholecalciferol https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7352679/), minskade behov av intensivvård och minskade också dödligheten i covid-19 kraftigt.

Av de 551 patienter som behandlades med D-vitamin behövde bara 5,4% intensivvård. Medan 21% av de 379 som inte fått D-vitamin behövde intensivvård. Och D-vitamintillskottsgruppen hade 64% lägre dödlighet i Covid-19.

Studien hade 930 covid-19-patienter som deltagare, och är en större variant av den studie på D-vitamin mot Covid-19 som jag skrivit om tidigare. Alla inlagda patienter fick standardbehandling mot Covid och D-vitamin adderades till denna behandling för en del av patienterna.

Problemen med studierna på D-vitamin

Men det fanns några potentiella problem med studien, förutom att den inte hade granskats. Problemen inkluderade att deltagarna i studien inte hade randomiserats (de hade alltså inte slumpmässigt hamnat i behandlings- eller kontrollgrupp), istället hade man sagt att vissa avdelningar på sjukhuset skulle få D-vitamin och andra inte. Det fanns också olikheter mellan behandlingsgruppen och kontrollgruppen, såsom att kontrollgruppen hade färre kvinnor och lägre D-vitaminnivåer vid studiens start (dock var inte skillnaderna jättestora). Studien var inte heller placebokontrollerad.
Studien låg som sk preprint (och kommer troligen att finnas) här om den blir godkänd: https://papers.ssrn.com/sol3/papers.cfm?abstract_id=3771318

Jag har tidigare skrivit om en den mindre studien här: https://4health.se/studie-d-vitamin-effektiv-behandling-av-covid-19

Jag vill också betona att de flesta övriga studier, förutom dessa två, enbart är observationsstudier som tex visar samband mellan blodstatus av vitamin D och hur man insjuknar i Covid-19. Dessa resultat behöver inte säga någonting alls. Bl.a. för att man måste mäta alla olika former av D-vitamin för att kunna uttala sig om detta. Blodstatus går inte heller att översätta till att tillskott av D-vitamin skulle vara hjälpsamt. Tex kan lägre nivåer av lagringsformen av D-vitamin bero på att mer är omvandlat till aktivt D-vitamin, tex vid pågående inflammation.

Vad jag personligen skulle använda mot Covid-19

Om jag skulle drabbas av Covid-19 så skulle jag använda mig av bl.a. D-vitamintillskott, glutation, NAC, gurkmeja och kurkumin samt C-vitamin (trots att jag INTE rekommenderar tillskott av syntetisk C-vitamin /askorbinsyra/ askorbat i vardagen https://4health.se/askorbinsyra-vs-c-vitamin).

I ett tidigt skede skulle jag även använda mig av diverse antimikrobiella preparat och livsmedel, inklusive vitlök, salvia och KS (kolloidalt silver). Samt jod

Troligen skulle jag även använda mig av allmänt immunhöjande / T-cellshöjande åtgärder, inklusive medicinalsvampar som reishi och sidenticka.

Jag rekommenderar dock inte stora doser D-vitamin förebyggande. Jag instämmer till stor del med det Morley Robbins säger i våra podcasts om D-vitamin. (Lyssna främst på avsnitt 218-221, och då särskilt på  https://4health.se/219-morley-robbins-d-vitamin-mineralerna-i-din-kropp-2 ) D-vitamintillskott kan sätta annat ur balans i kroppen. Bl.a. kan en obalans mellan vitamin D och A, hindra A-vitamin. Vilket i sin tur behövs för koppar / ceruloplasmin, vilket i sin tur behövs för cellenergi, användningen av järn i kroppen mm. Men att ta D-vitamin tillfälligt vid infektion, eller i liten dos någon månad under vintern vid sidan av torskleverolja, kan vara vettigt.

Skilj alltså på vad jag skriver om att använda vid smitta och att använda förebyggande och dagligen för ett bra immunförsvar.

Mer via https://4health.se/?s=corona

Jag har tagit upp hur man kan använda bl.a. glutation och NAC om man drabbas av Covid-19. Både för att aktivera immunförsvaret (rätt delar) och för att dämpa de besvär som kan uppstå tex i form av cytokinstormar. En ny vetenskaplig sammanställning betonar just rollen i att dämpa inflammationen i sjukdomens senare skede. Det är just denna överdrivna immunrespons som gör att Covid-19 kan bli farligt.

Saxat ur artikeln:

“The Role of Glutathione in Protecting against the Severe Inflammatory Response Triggered by COVID-19

The novel COVID-19 pandemic is affecting the world’s population differently: mostly in the presence of conditions such as aging, diabetes and hypertension the virus triggers a lethal cytokine storm and patients die from acute respiratory distress syndrome, whereas in many cases the disease has a mild or even asymptomatic progression. A common denominator in all conditions associated with COVID-19 appears to be the impaired redox homeostasis responsible for reactive oxygen species (ROS) accumulation; therefore, levels of glutathione (GSH), the key anti-oxidant guardian in all tissues, could be critical in extinguishing the exacerbated inflammation that triggers organ failure in COVID-19. The present review provides a biochemical investigation of the mechanisms leading to deadly inflammation in severe COVID-19, counterbalanced by GSH. The pathways competing for GSH are described to illustrate the events concurring to cause a depletion of endogenous GSH stocks. Drawing on evidence from literature that demonstrates the reduced levels of GSH in the main conditions clinically associated with severe disease, we highlight the relevance of restoring GSH levels in the attempt to protect the most vulnerable subjects from severe symptoms of COVID-19. Finally, we discuss the current data about the feasibility of increasing GSH levels, which could be used to prevent and subdue the disease.”

“Among the many functions of GSH, some are worthy of mention in relation to their impact on the exacerbated inflammation taking place in COVID-19 and in relation to the symptoms developed in the disease.

1. GSH protects cells by neutralizing (i.e., reducing) ROS, which are key signaling molecules that play an important role in the progression of inflammatory disorders. The relationship between ROS production and proinflammatory cytokine activation is well established [22]. An enhanced ROS generation by polymorphonuclear neutrophils at the site of inflammation causes endothelial dysfunction and tissue injury [23].

2. The conjugation of GSH to xenobiotics is particularly abundant; glutathione S-transferase enzymes catalyze GSH conjugation to lipophilic xenobiotics, facilitating the excretion or further metabolism of many drugs. The conjugation process is illustrated by the metabolism of N-acetyl-p-benzoquinone imine (NAPQI). NAPQI is a reactive metabolite formed by the action of cytochrome P450 on paracetamol (acetaminophen). Glutathione conjugates to NAPQI and the resulting product is excreted [24].

3. Many enzymes use GSH as a cofactor or substrate. For example reactions requiring GSH as a key cofactor are catalyzed by the prostaglandin H synthase, the rate-limiting enzyme in the production of prostaglandins and thromboxane [25], which are essential regulators of vascular function. Moreover, the enzyme leukotriene C(4) synthase conjugates LTA(4) with GSH to form the leukotriene LTC(4), the parent compound of the cysteinyl leukotrienes [26]; these molecules are potent mediators of airway narrowing.

4. GSH is used to synthesize S-nitrosoglutathione (GSNO), an endogenous S-nitrosothiol that plays a critical role in nitric oxide (NO) signaling and is a source of bioavailable NO. The generation of GSNO can serve as a stable NO pool which can properly transduce NO signaling [27]. NO produced by nitric oxide synthase eNOS and nNOS, in the presence of GSH, can effectively modulate vessels and neuronal functions, regulating the blood flow according to the local calcium influx.

As a consequence of the competition between these and many other GSH-consuming pathways, on one hand, the raging inflammation and oxidative stress triggered by the viral infection steals GSH from core functions such as NO-dependent vasodilatation; on the other hand, when other biochemical pathways are consuming GSH, the patient is not protected from an inflammation that can prove fatal.”

“ACE expression and activity are modulated by glutathione; in fact, the oxidized form GSSG shows an activating effect on ACE activity, whereas the reduced GSH provides an inhibitory effect [28]. Finally, the boosted ANGII production can be due to decreased ACE2 expression and activity; this is the case with coronavirus infection, which recognizes ACE2 as its extracellular binding site [29]. Compared to SARS-COV-1, SARS-CoV-2 has about 4-fold higher affinity for ACE2 [30]. Infection of cells by SARS viruses that bind ACE2 results in two effects: inhibition of ACE2 activity and decrease of ACE2 expression in infected cells”

“By reducing ROS production, GSH inhibits NF-kB activation and consequently keeps the cytokine storm under control.”

Tidigare om glutation bl.a. i podcastavsnitt om Covid-19 https://4health.se/259-dr-cecilia-furst-covid-19 och här https://4health.se/sa-kan-glutation-boosta-ditt-immunforsvar och här https://4health.se/?s=glutation och här https://4health.se/?s=corona

https://www.mdpi.com/2076-3921/9/7/624

Det är välkänt att diabetes är en riskfaktor för Covid-19, men det omvända verkar också gälla.

I UK är ungefär 25% av de som behöver sjukhusvård för Covid-19 diabetiker. Men det verkar också vara så att Covid-19 kan skada de insulinproducerande cellerna, så att man kan utveckla diabetes av virusinfektionen.

Många som anländer till sjukhus med svår Covid-19 har skyhöga blodsockernivåer. En antydan om att insulinmekanismen inte fungerar som den ska. För en del av dessa blir tillståndet kroniskt.

Forskning har visat att ACE-2, proteinet/ receptorn som Sars-Cov-2 binder till när det kommer in i den mänskliga cellen, inte bara finns i lungorna. ACE2 finns också i organ och vävnader som är involverade i glukosmetabolismen – såsom bukspottkörteln, tunntarmen, fettvävnaden, levern och njurarna. Experter tror att viruset kan orsaka flera olika och komplexa dysfunktioner av glukosmetabolism genom att komma in i dessa vävnader. Och därmed leda till diabetes.

Men det behövs betydligt mer forskning för att nå ett avgörande svar kring detta. En global databas, CoviDiab Registry-projektet, inrättades i början av juni för att samla information om Covid-19-patienter med höga blodsockernivåer.

Mer via https://4health.se/?s=corona

Not only may diabetes make a coronavirus infection worse, but Covid-19 may also trigger the onset of the chronic condition in some people, emerging evidence suggests. 

It is well known that underlying health issues increase the likelihood of severe illness or death after contracting the coronavirus. 

In the first two months of the UK’s outbreak, roughly 25 per cent of people hospitalised with Covid-19 with already had diabetes, suggesting that the risk of severe illness among diabetics was four times higher than for the general population. 

But Paul Zimmet, a professor of diabetes at Monash University in Melbourne, told Nature that “two pandemics could be clashing”, with Covid-19 also damaging the cells responsible for producing the hormone insulin. 

He said that dozens of patients suffering from severe Covid-19 have arrived at hospital with very high blood sugar levels – a sign that the body is not producing enough of the hormone. 

A handful of these patients have gone on to rapidly develop the chronic condition, where the body produces either no insulin at all, or not enough to work effectively. 

The theory has some precedent as other viruses are known to precipitate autoimmune diseases, including type 1 diabetes. A paper published in Acta Diabetologica journal in 2009 found that damage to the body caused by Sars, a close cousin of the virus that causes Covid-19, triggered the onset of diabetes in some patients.

More recently, an experimental study in miniature lab-grown pancreases published in the Lancet last week concluded that a Covid-19 infection “could induce new onset diabetes” by damaging the cells responsible for control blood sugar levels. 

The findings have not been confirmed in humans and it is unclear whether Covid-19 plays a direct role in the reduced production of insulin.

But on June 12, a group of 17 leading diabetes experts wrote a letter published in the New England Journal of Medicine warning that new-onset diabetes is being observed in some patients who have tested positive for the Covid-19. 

Research has shown that ACE-2, the protein that Sars-Cov-2 binds to as it enters the human cell, is not only located in the lungs. It is also in organs and tissues that are involved in glucose metabolism – such as the pancreas, the small intestine, the fat tissue, the liver and the kidney.

Experts believe that by entering these tissues, the virus may cause multiple and complex dysfunctions of glucose metabolism, triggering diabetes. 

But there are warnings that considerably more research is needed to reach a conclusive answer. Experts hope for clarity in the coming months after a global database, dubbed the CoviDiab Registry project was established in early June to collect information on Covid-19 patients with high blood-sugar levels. 

“As has been stated, we’ve not encountered a virus like Sars-CoV2 before for the breadth of disease it causes,” Prof James Hildreth, president of Meharry Medical College, said. “Now evidence [is] accumulating that Covid-19 virus may cause diabetes. Clearly suggests that people who are pre-diabetic or diabetic should definitely avoid Covid-19 infection.”

https://www.nature.com/articles/d41586-020-01891-8

https://www.sciencedirect.com/science/article/abs/pii/S2213858720301522

https://www.telegraph.co.uk/global-health/science-and-disease/covid-19-may-trigger-diabetes-growing-body-evidence-suggests/

Även om man kan debattera dödstalen och huruvida Covid-19 är en pandemi eller ej, så är det för många en obehaglig sjukdom.

Brittiska The Telegraph meddelar bl.a. hur nästan en tredjedel av Covid-patienter kommer tillbaka till sjukhusvård inom fem månader och att en åttondel dör, enligt ny statistik från ONS (Office for National Statistics).
En tidigare studie visade att hela 87 % av de som vårdats på sjukhus för allvarlig covid-19 har långvariga symtom som kvarstår minst två månader – trots att de testar negativt för coronaviruset. Värk i leder eller bröst, andningssvårigheter och utmattning är de vanligaste symtomen.
Allt ovan gäller ju dem som insjuknar så pass svårt att det krävs sjukhusvård. Många gör ju inte det, ska tilläggas.

De som drabbas illa av det nya coronaviruset utvecklar hjärtproblem, diabetes och problem med levern och njurarna.

Dessutom upptäcker man förvånansvärt många nya diabetiker efter Covid-19. Man vet fortfarande inte om det handlar om typ 1 eller typ 2 i huvudsak “We don’t know if it’s because Covid destroyed the beta cells which make insulin and you get Type 1 diabetes, or whether it causes insulin resistance, and you develop Type 2, but we are seeing these surprising new diagnoses of diabetes” Mer om kopplingen mellan Covid-19 och diabetes imorgon.

Forskare uppmanar nu till brådskande tilltag gällande övervakning och kontroller av personer som skrivits ut från sjukhus efter Covid-19.

Mer via https://4health.se/?s=corona och tidigare angående långtids-covid: https://4health.se/?s=lång+covid

The Telegraph skriver:

Almost a third of recovered Covid patients will end up back in hospital within five months and one in eight will die, alarming new figures have shown.

Research by Leicester University and the Office for National Statistics (ONS) found there is a devastating long-term toll on survivors of severe coronavirus, with many people developing heart problems, diabetes and chronic liver and kidney conditions.

Out of 47,780 people who were discharged from hospital in the first wave, 29.4 per cent were readmitted to hospital within 140 days, and 12.3 per cent of the total died.

The current cut-off point for recording Covid deaths is 28 days after a positive test, so it may mean thousands more people should be included in the coronavirus death statistics.

Researchers have called for urgent monitoring of people who have been discharged from hospital.

Study author Kamlesh Khunti, professor of primary care diabetes and vascular medicine at Leicester University, said: “This is the largest study of people discharged from hospital after being admitted with Covid.

“People seem to be going home, getting long-term effects, coming back in and dying. We see nearly 30 per cent have been readmitted, and that’s a lot of people. The numbers are so large.

“The message here is we really need to prepare for long Covid. It’s a mammoth task to follow up with these patients and the NHS is really pushed at the moment, but some sort of monitoring needs to be arranged.”

The study found that Covid survivors were nearly three and a half times more likely to be readmitted to hospital, and die, in the 140 days timeframe than other hospital outpatients.

Prof Khunti said the team had been surprised to find that many people were going back in with a new diagnosis, and many had developed heart, kidney and liver problems, as well as diabetes.

He said it was important to make sure people were placed on protective therapies, such as statins and aspirin.

“We don’t know if it’s because Covid destroyed the beta cells which make insulin and you get Type 1 diabetes, or whether it causes insulin resistance, and you develop Type 2, but we are seeing these surprising new diagnoses of diabetes,” he added.

“We’ve seen studies where survivors have had MRS scans and they’ve cardiac problems and liver problems.

“These people urgently require follow up and the need to be on things like aspirin and statins.”

The new study was published on a pre-print server and is yet to be peer reviewed. However experts described the paper as “important”.

Commenting on the study on Twitter, Christina Pagel, director of the clinical operational research unit at University College London said: “This is such important work. Covid is about so much more than death. A significant burden of long-term illness after hospitalisation for Covid.”

Last year, researchers at North Bristol NHS Trust found that three quarters of virus patients treated at Bristol’s Southmead Hospital were still experiencing problems three months later.

Symptoms included breathlessness, excessive fatigue and muscle aches, leaving people struggling to wash, dress and return to work.

Some patients say they have been left needing a wheelchair since contracting the virus, while others claim they can no longer walk up the stairs without experiencing chest pain.

In December, the ONS estimated that one in 10 people who catch coronavirus go on to suffer long Covid with symptoms lasting three months or more.

Overall, roughly 186,000 people in private households in England in the week beginning November 22 were living with Covid-19 symptoms that had persisted for between five and 12 weeks, the most up-to-date ONS data shows.

https://news.yahoo.com/almost-third-recovered-covid-patients-180255388.html

https://www.telegraph.co.uk/global-health/science-and-disease/nine-10-people-have-persistent-symptoms-months-recovering-severe/

https://www.telegraph.co.uk/global-health/science-and-disease/covid-19-may-trigger-diabetes-growing-body-evidence-suggests/

Det är vid det här laget väl känt att män generellt drabbas mer och hårdare än kvinnor av det nya coronaviruset. Fler män blir svårt sjuka, fler män vårdas på IVA och fler män dör med covid-19. I Sverige har 800 fler män dött i covid-19 än kvinnor, trots att fler kvinnor testat positivt för sjukdomen. Om man tittar globalt så är risken för att dö med covid-19 ungefär 1,7 gånger högre för män än för kvinnor. I en ny artikel i Science sammanfattar forskare den kunskap och de teorier som finns hittills om vad det här kan bero på – och många teorier handlar om att det är skillnader i kvinnors och mäns immunförsvar som ligger bakom.

Jag har skrivit om det i tidigare inlägg, bl.a. en del här https://4health.se/hur-hart-vi-drabbas-av-corona-beror-pa-genetiska-skillnader-i-olika-varldsdelar-befolkningar och här https://4health.se/?s=män+drabbas . Läs gärna också om skillnaderna mellan kvinnors och mäns immunsystem: https://4health.se/skillnader-mellan-det-manliga-och-det-kvinnliga-immunsystemet-forklarar-skillnader-i-sjukdomar

Det finns flera skillnader mellan mäns och kvinnors immunförsvar. En sak är att de åldras olika. Hos båda könen försvagas immunförsvaret med åldern, framförallt efter 60 år. Men den försvagningen är kraftigare hos män och sker normalt 5-6 år tidigare än hos kvinnor. Det gör att män, särskilt då äldre män, har svårare att kontrollera virusinfektioner.

Men män har också generellt ett sämre immunförsvar än kvinnor och i alla åldersgrupper över 30 år ser man att män drabbas hårdare och är överrepresenterade när det gäller döda med covid-19. Till och med mer än vid många andra infektioner.

Dessutom finns viktiga immunrelaterade gener på X-kromosomen.

I möss har man sett att receptorn som SARS-Cov2-viruset binder till (ACE2) kan regleras av könshormonet östrogen. Det skulle kunna förklara ytterligare en skillnad i hur man reagerar på infektionen.

Forskarna reflekterar också kring andra kända skillnader mellan män och kvinnors immunsystem, såsom “females generally mount a more robust immune response to vaccines, such as influenza vaccines. However, the heightened immune responses in females can also lead to detrimental immunopathology in infections” Jag reflekterar här över kvinnor som utvecklar långtidssymtom efter covid, samt utvecklar autoimmuna sjukdomar efter infektion generellt.

Läs mer om skillnaderna i immunsystemet i nedan text ur artikeln.

Mer via https://4health.se/?s=corona

Ur artikeln:

“the risk of death in males is ∼1.7 times higher than in females (1). Aging is strongly associated with higher risk of death in both sexes, but at all ages above 30 years, males have a significantly higher mortality risk, rendering older males the most vulnerable group (1). Sex differences are intertwined with differences in gender roles socially and with behavioral factors, which also influence COVID-19 incidence and outcomes. However, there are also possible biological mechanisms of male sex bias that affect the severity of COVID-19, particularly with respect to immune responses.”

“male sex is more often associated with lower immune responses and higher susceptibility and/or vulnerability to infections in animals. This is generally also the case in humans (2): Male patients have higher viral loads for hepatitis B virus (HBV) and HIV (2). Conversely, females generally mount a more robust immune response to vaccines, such as influenza vaccines. However, the heightened immune responses in females can also lead to detrimental immunopathology in infections”

“The physiological response to virus infection is initiated when virus replication is detected by pattern recognition receptors. This leads to two antiviral programs by the infected cells: (i) cellular antiviral defense programs mediated by type I and type III interferons (IFNs) to limit viral replication and spread, and (ii) cytokine and chemokine production to recruit and coordinate immune cells, such as monocytes and neutrophils that can phagocytose and eliminate infected cells. Notably, COVID-19 is characterized by strong innate immune cytokine and chemokine responses despite the disproportionately low antiviral defense signature mediated by IFNs (3). Patients with severe COVID-19 exhibit high serum concentrations of proinflammatory cytokines and chemokines, with particularly high concentrations of interleukin-6 (IL-6) and the inflammasome-associated cytokines IL-1β and IL-18 (4). Exacerbated systemic inflammation is associated with extensive pulmonary pathology, including massive infiltration of monocytes and neutrophils. Increased neutrophil count is associated with poor clinical outcome (5). The robust induction of these inflammatory cytokines and cells may be a compensatory response to the ability of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) to evade IFN responses, which necessitates the engagement of IFN-independent defense mechanisms (6).

The plasma concentrations of several key innate immune cytokines and chemokines, such as IL-8 and IL-18, are increased in male patients compared with female patients in the early phase of COVID-19. Conversely, female patients have higher plasma concentrations of type I IFN (IFNα) over the disease course (7). Notably, autoantibodies that inhibit type I IFN signaling have been reported in a subset of severely ill patients, the majority (94%) of whom were older males (8). By contrast, T cell activation at the early phase of SARS-CoV-2 infection is robust even in older female patients, whereas male patients have a significant decline with age. Male patients with poor T cell activation at the early phase of disease onset have worse COVID-19 outcomes, whereas no such difference is observed in female patients (7).

What could be the potential underlying mechanism of this sex dimorphism in immune response? One culprit is the sex chromosomes: A substantial number of important immune-related genes are encoded on the X chromosome. Although one of the two copies of the X chromosome in females is usually epigenetically silenced [X chromosome inactivation (XCI)], some critical immune-related genes, including Toll-like receptor 7 [TLR7, whose viral RNA sensing elicits strong type I IFN production in its major producer, plasmacytoid dendritic cells (pDCs)], can escape from XCI in some proportion of cells. This makes the population “mosaic” for biallelic expression, which leads to higher gross expression of some immune-related genes in females (9). Human pDCs have also been reported to have higher expression of interferon regulatory factor 5 (IRF5) in females. Higher expression of these genes leads to more robust type I IFN responses in females, and this is one of the potential mechanisms involved in females’ enhanced protection against viral infections, including COVID-19 (1, 2).

Sex has a major impact on immune cell transcriptomes; immune cells or even the immune system are differentially affected by aging, depending on sex. Aging induces a decline in the proportion of naïve T cells that is more prominent in males, and B cells decline after age 65 only in males (10). Males have abrupt and drastic changes in the epigenetic landscape of their immune cells between ages 62 and 64, and subsequently males exhibit an accelerated immunosenescence phenotype that is characterized by enhanced innate proinflammatory gene expression and lower gene expression related to adaptive immunity, which could potentially predispose older males to hyperinflammation and poor adaptive immune responses.

By contrast, major changes in the epigenetic landscape of immune cells occur in females 5 to 6 years later than in males, with this gap largely corresponding to the life span differences between sexes (10). It is notable that females generally mount more pronounced cytokine responses in viral infections, although this is not the case with COVID-19. Instead, males have higher plasma concentrations of innate proinflammatory cytokines such as IL-8 and IL-18 (7). This could be because patients who have severe disease are generally of older age, and the background transcriptomic and epigenetic sex differences in immune cells in these older individuals are possibly amplified and more explicitly manifested in the context of SARS-CoV-2 infection (see the figure).

The other important biological factors are sex hormones. In a mouse model of SARS-CoV infection, higher mortality in male mice was observed and was attributed to the protective roles of the female sex hormone estrogen (1). Studies using various cell types and animal models have shown that the expression of angiotensin-converting enzyme 2 (ACE2), the host cell entry receptor for SARS-CoV-2, is modulated by estrogen (1). This likely occurs through transcriptional regulation by estrogen receptor signaling, although the detailed molecular mechanisms are yet to be identified and the consequences of the type of ACE2 modulation (up- or down-regulation) could be cell type– and context-dependent. Estrogen receptors are widely expressed by many cell types, including immune cells, and estrogen is a critical regulator of gene expression and functions in innate immune cells, including monocytes, macrophages, and dendritic cells, as well as in lymphocytes such as T helper 1/2 (T_H1/2) cells, regulatory T cells (T_regs), and B cells. One of the major forms of estrogen, estradiol, has been shown to dampen the production of excessive innate inflammatory cytokines by monocytes and macrophages (1). Menopause is an independent risk factor for female patients, and concentrations of estradiol and anti-Müllerian hormone, which is produced by cells in developing follicles and is an endocrine marker for oocytes remaining in the ovaries (ovarian reserve), are inversely correlated with COVID-19 severity (11). Conversely, androgen-deprivation therapies for prostate cancer have been reported to reduce the risk for SARS-CoV-2 infection (12). Like estrogen receptors, androgen receptors are expressed widely among immune cells, regulating the transcription of various genes, and the outcome of their signaling has been shown to be generally immunosuppressive (1).

Despite the emerging understanding of sex differences of immune responses in COVID-19, many questions remain. Sex is not binary, and little is known regarding immune responses to viral infections, including COVID-19, in individuals with disorders of sex development (DSD) or transgender individuals. DSD describes congenital conditions in which the development of chromosomal, gonadal, and anatomical sex is atypical. For example, Klinefelter syndrome (also known as 47, XXY) results in phenotypes such as gynecomastia (enlarged breast tissue in males) and small testes with hypogonadism. This condition accompanies a series of comorbidities, in particular a high frequency of autoimmune diseases, such as systemic lupus erythematosus (SLE). The prevalence of SLE among Klinefelter syndrome patients is higher by a factor of 14 than among 46, XY males; this is comparable to its prevalence among 46, XX females, which suggests a gene dosage effect of the X chromosome (13). Additionally, transgender is a collective term encompassing those whose gender identities or gender roles differ from those typically associated with the sex they were assigned at birth. Little is known about the immune responses in these individuals, some of whom are undergoing gender reassignment hormone therapies. It is possible that DSD and transgender individuals mount distinct immune responses to viral infection in general and also in COVID-19.

Sex differences in immunity also have implications for responses to SARS-CoV-2 vaccination or reinfection. Analysis of convalescent plasma showed that male sex, older age, and hospitalization for COVID-19 were associated with greater SARS-CoV-2 antibody titers (14). This could be related to increased disease severity in this demographic of patients, with increased viral load driving more B cell activation and antibody production. Alternatively, higher amounts of antiviral antibodies could be due to compensatory increases in antibody production due to suboptimal qualities of antibodies generated in older males, which are unable to neutralize the virus effectively. Antibodies with suboptimal neutralizing ability have the capacity to promote viral invasion into host cells such as macrophages [called antibody-dependent enhancement (ADE)]. However, there has been no clear evidence of ADE in COVID-19. With other viral infections, fatal diseases in dengue virus infection (dengue hemorrhagic fever and dengue shock syndrome) have been associated with ADE. Upon secondary infection with a virus of a serotype different from that of the primary infection, the fatalities from these severe diseases were primarily seen in adult females despite the male dominance in dengue hemorrhagic fever prevalence (15). The mechanism remains unknown but may be due to heightened inflammation in females, leading to capillary permeability.

It is important that studies of COVID-19 patients report results in a sex-disaggregated manner, not only to elucidate differential disease pathogenesis, but also to enable a deeper understanding of this disease and the eventual development of better treatment and preventive strategies. It should be standard practice to collect and report sex-disaggregated data for this and for all infectious disease and vaccine studies in the future.”

https://science.sciencemag.org/content/371/6527/347

https://www.dn.se/vetenskap/forskare-nya-teorier-om-varfor-man-drabbas-hardare-av-covid-19/

https://sverigesradio.se/artikel/7652493

I en ny studie av effekterna av riktlinjerna under Covid-19 ser man hur reglerna om att stanna hemma och inte träffa andra har lett till ökat stillasittande, viktuppgång och sämre psykiskt mående. Dessutom har en stor andel försämrat sina matvanor bl.a. genom att äta mer ohälsosamma snacks/ mellanmål. Och många hade också försämrade sömnvanor genom att de somnar senare.

Jag känner verkligen av det där med det mentala måendet själv. Som ensamstående då jag varannan vecka inte har min son och träffar mindre människor än normalt. Det är som om min kropp har cravings efter fysisk närhet och att umgås med andra. Jag har aldrig upplevt detta så här tidigare. Och då träffar jag ändå ett fåtal väl valda vänner, som får agera familjesubstitut. Jag känner hur bristen på närhet och att umgås som vanligt med vänner och familj påverkar det mentala måendet. För vissa kanske det mer handlar om oro över pandemin som sådan, för mig handlar det om att jag känner att vi är flockdjur och att detta inte är normalt. Oavsett så påverkas vårt mående.

Positiv beröring är livsviktigt för hälsan. Hudkontakt utsöndrar en cocktail av må bra-hormoner som oxytocin, men även dopamin och serotonin. Dessutom minskar beröring stresshormonet kortisol. 

Det finns en evolutionär förklaring. Beröring var ett sätt att hålla ihop gruppen. Att röra varandra är ett sätt att visa att man är vänner och är nära varandra. Har man inte fått beröring på lång tid då betyder det att man hamnat utanför.

Social distansering under pandemin gör nu att många saknar hudkontakt. Men en annan ny studie visar att husdjur kan kompensera för det till stor del. 

Har du märkt några negativa eller positiva effekter på din hälsa under detta coronaår?

Observera att detta inte är jag som lägger någon värdering i vad som är rätt och fel mht corona. Bara forskning och en reflektion av vad som händer i oss. Jag tror att vi bör begränsa smittspridningen på olika sätt, men jag tror bl.a. baserat på detta att den svenska modellen är bättre än lockdown. Och jag tror mer på frihet och ansvar, istället för frihetsberövande av friska människor så som vissa länder gjort.

Undersökningens deltagare är främst från engelskspråkiga länder, och inte minst USA. Den svenska modellen har ju varit annorlunda, så detta är ju främst applicerbart på andra länder. Samtidigt har Sverige flest ensamhushåll i världen, så det kanske drabbar oss hårdare av den anledningen.

Ur studien:

Objective: Stay-at-home orders in response to the COVID-19 pandemic have forced abrupt changes to daily routines. This study assessed lifestyle changes across different BMI classifications in response to the global pandemic.

Methods: The online survey targeting adults was distributed in April 2020 and collected information on dietary behaviors, physical activity, and mental health. All questions were presented as “before” and “since” the COVID-19 pandemic.

Results: In total, 7,753 participants were included. The sample included 32.2% of individuals with normal weight, 32.1% overweight, and 34.0% had obesity. During the pandemic, overall scores for healthy eating increased (p<0.001), due to less eating out and increased cooking (p<0.001). Sedentary leisure behaviors increased while time spent in physical activity (absolute time and intensity-adjusted) declined (p<0.001). Anxiety scores increased 8.78±0.21 during the pandemic and the magnitude of increase was significantly greater in people with obesity (p≤0.01). Weight gain was reported in 27.5% of the total sample compared to 33.4% in participants with obesity.

Conclusions: The COVID-19 pandemic produced significant health effects, well beyond the virus itself. Government mandates together with fear of contracting the virus have significantly impacted lifestyle behaviors alongside declines in mental health. These deleterious impacts have disproportionally affected individuals with obesity.

….43.5% reported an increase in unhealthy snacking. Overall, 20.7% perceived they were eating healthier and 35.6% reported eating less healthy. A perceived shift towards unhealthy eating was accompanied by increases in sedentary behaviors, declines in physical activity, a later sleep onset time, and nearly twice the increase in reported anxiety compared to those eating healthier. ..

..Sleep onset and wake time significantly changed (onset: 42.41±1.61 and wake: 59.33±2.15 minutes later, both p<0.001). Changes to sleep quality varied, 43.8% reported worsened sleep quality while 10.2% reported improved sleep quality…

https://pubmed.ncbi.nlm.nih.gov/33043562/

(fulltext: https://europepmc.org/backend/ptpmcrender.fcgi?accid=PMC7675243&blobtype=pdf)

https://www.svt.se/nyheter/vetenskap/husdjur-spelar-viktig-roll-under-pandemin