Aug
07
2021

A New Disease, Long Covid

Some of the Covid cases do not resolve; this created a new disease, long Covid. The German news magazine “Der Stern” described this in detail. I summarized this in  English here. The English literature also mentions long Covid. Certainly, physicians learnt from observing the course of many Covid-19 cases. It is important to realize that they did not all heal. Some of them seemed to resolve, but then they reoccurred. Other patients suffer from ongoing exhaustion, shortness of breath, tiredness and pains.

When do physicians diagnose long Covid?

If symptoms of Covid-19 do not resolve within 4 weeks after the beginning, physicians diagnose this condition as long Covid. Different subtypes exist.

  • Persistent symptomatic Covid-19: Covid-19 symptoms persist between 4 and 12 weeks from the beginning of Covid-19.
  • Post Covid-19 syndrome: After more than 12 weeks the patient still has Covid-19 symptoms.
  • Long Covid: when a patient develops new Covid-19 symptoms or still has symptoms beyond 4 weeks after Covid-19 physicians diagnose the patient with long Covid.

Who is getting long Covid?

A longitudinal study showed that about 1 in 10 Covid-19 cases can turn into long Covid. In some cases, this can develop out of relatively benign courses of Covid-19 cases. In other cases, a severe Covid-19 case can develop into long Covid. Notably, a research study identified risk major factors for developing long Covid. They found that increasing age, an increased body mass index and female sex were risk factors for developing long Covid. Persistent symptoms of headaches, fatigue, difficulties to breathe and a loss of smell characterize the presence of long Covid. Another criterion was whether a person had to be treated in an ICU setting during the acute phase of Covid-19. These people are at a higher risk to develop long Covid at a later time.

Long Covid symptoms

The most common symptoms of long Covid are tiredness, headaches, problems breathing, concentrating and circulation problems. But fast heart beats, sleeping disorders, chronic pains and hypersensitivity to light and sound are also part of the symptom complex. Researchers found that in 70% of patients with long Covid one or more organs were damaged by the virus. All the affected organs had ACE2 cell receptors. Many patients with long Covid have lung problems.

Pre-existing lung problems

According to one review it was mainly patients with pre-existing lung problems, older patients or patients who had other pre-existing health problems who developed lung complications. 3-5% of long Covid patients can also develop heart problems. Most patients have reduced pumping capacity, heart muscle inflammation, pericardial inflammation or scarred heart tissue. One symptom is very common: fatigue, which is a state of persistent tiredness, exhaustion and listlessness that cannot be managed with sleep. These are the symptoms of a new disease, long Covid.

Treatment possibilities for long Covid patients

The therapy is based on the symptoms. A guideline on post/long Covid, which was recently published jointly by several professional societies, states that there is still no scientifically reliable evidence for a specific therapy. The guideline lists diagnostic recommendations as well as therapy options for various symptoms such as fatigue, olfactory disorders, cardiological, neurological and psychiatric aspects.

Oxygen therapy

The researchers are currently working on a variety of different treatment approaches. Oxygen therapy is one of them. Hyperbaric oxygen tanks are used for this. Patients breathe pure oxygen in these tanks for about two hours a day for several weeks. The first patients treated with this oxygen therapy have reported positive effects according to Dr. Ullrich Siekmann in Aachen, Germany. Further studies, however, are required to confirm these preliminary investigations.

Blood washing or HELP apheresis

Doctors see another possibility of treatment in blood washing. With the so-called “HELP apheresis“, the blood is freed from harmful substances in a similar way to dialysis in kidney failure patients. Blood washing is already in use for people who have had strokes or heart attacks and where other medicines do not help. Researchers used this procedure also for long Covid patients.

Supplements that may help

According to Dr. Jacob Teitelbaum, a board-certified internist, these supplements may be helpful: N-acetyl cysteine (NAC), glutathione, CuraMed (a curcumin supplement), and omega-3 supplementation. These supplements treat chronic inflammation.

A New Disease, Long Covid

A New Disease, Long Covid

Conclusion

Long Covid is a sub-category of Covid-19 in patients whose symptoms do not resolve. This is subject to intensive research, which I summarized here. These patients have characteristic symptoms. Newer treatment options seem to consist of pressurized oxygen therapy and of blood washing with the name of “HELP apheresis”. Certain supplements that are anti-inflammatory may also be of benefit. Despite these new efforts this leaves many patients with organ damage and continuing chronic symptoms.

Apr
03
2021

Pollen Allergies Make Covid-19 Infection Rates Worse

A recent study showed that pollen allergies make Covid-19 infection rates worse. This was published in the Proceedings of the National Academy of Sciences (PNAS) in March 2021.

The study determined that airborne pollen exposure enhances susceptibility to respiratory viral infections. Specifically, this includes SARS-CoV-2 infections as well. There were 130 test sites in 31 countries across 5 continents where measurements were made. Pollen concentration, air humidity and temperature, population density and lockdown effects on Covid-19 figures were measured. In countries with high pollen counts, high humidity and higher temperatures the Covid-19 rates were up to 44% higher than in countries with low pollen counts and colder climates.

PNAS study in more detail

In the following I am discussing the PNAS study in more detail. The SARS-CoV virus from the SARS epidemic in 2002 and the present SARS-CoV-2 virus are both capable to suppress the body’s interferon response to either virus. Additionally, there are intracellular proteins with the name “inflammasomes”, which the SARS-CoV-2 virus activates. With excessive activation this causes a cytokine storm, where inflammation spreads through the whole body. In the blood this leads to disseminated coagulopathy with multi organ failures. In the lungs severe acute respiratory syndrome occurs with severe viral pneumonia. On average mortality is 3.4%.

Tree and weed pollen can weaken the immune response

A study from South Korea examined what happens with exposure in asthmatic and allergic school-aged children to tree and weed pollen. https://www.sciencedirect.com/science/article/pii/S0091674919311856.

Allergic reactions make allergic children more prone to rhinovirus infections by reducing interferon in the blood. In addition, allergic reactions stimulate inflammasomes. When the SARS-CoV-2 virus affects an allergic child, both interferon depletion and excessive inflammasome activation make Covid-19 much more severe than in a child without allergies.

Warm spell in the Northern Hemisphere

On March 12, 2020 the WHO announced the Covid-19 pandemic when over 33% of the world’s countries were affected by the SARS-CoV-2 virus. However, at the same time there was a large-scale warm spell across the Northern Hemisphere with tree pollens being distributed across the same regions. This resulted in an exponential increase of Covid-19 cases. The researchers determined that the rates of Covid-19 infections were highest in areas where there was a high tree pollen count, crowding of people and high humidity/temperatures. The researchers used data from 248 airborne pollen monitoring sites in 31 countries. The highest exponential growth rates of Covid-19 occurred in the countries with the highest pollen counts. 6 out of 8 countries studied with regard to high pollen counts showed a significant correlation with regard to Covid-19 infections in excess to just person-to person virus transmission.

Population density and lockdown affecting daily SARS-CoV-2 virus rate

Some countries had a complete lockdown when rates of infection were high. This reduced transmission of the SARS-CoV-2 virus by 50%. Those countries with only a partial lockdown still experienced a significant reduction of infection rates. Rural areas had significantly less daily SARS-CoV-2 virus rates compared to very densely populated cities.

The researchers observed the following:

  • There was a lag effect of 4 days between the increase of pollen concentration in the air and infection increase with the SARS-CoV-2 virus
  • Pollens in the air caused infection rates of SARS-CoV-2 to rise by 10 to 30%, but in some high pollen areas even up to 44%.
  • Lockdowns reduced infection rates of SARS-CoV-2 by 50%
  • Higher environmental temperatures and higher humidity of the air also increased infection rates of SARS-CoV-2, although this may have occurred indirectly by increasing the pollen count in the air

Discussion

  1. The authors added a thorough discussion of the multiple factors regarding the increase of the infection rate of Covid-19 in 2020. They pointed out that climatic factors, air pollutants, or pollen, often exert their effects at the same time. They quantitated the contribution of the pollen count in the air easily. In contrast, pollution and climatic factors were not predictable in their effects.
  2. The infection rate of the SARS-CoV-2 virus always lagged behind the increase in pollen count by 4 days. The researchers observed this in all those countries where increasing pollen counts were a significant factor.
  3. The epithelial lining of the nasal cavity is the target of inhaled pollen. The researchers cited several publications regarding reduced interferon production as a result of exposure to pollens in the nasal mucous membranes. This leaves the immune system with a weakness, which the SARS-CoV-2 virus exploits. Recently specialists discussed the use of intravenous interferon to interrupt the cytokine storm caused by the SARS-CoV-2 virus.
Pollen Allergies Make Covid-19 Infection Rates Worse

Pollen Allergies Make Covid-19 Infection Rates Worse

Conclusion

In a recent publication researchers showed that pollen allergies make Covid-19 infection rates worse. The investigators had 130 test sites in 31 countries across 5 continents where they took measurements. They measured pollen concentration, air humidity, temperature, population density and lockdown effects on Covid-19 figures. In March of 2020 there was a warming trend in the Northern Hemisphere. This caused pollen counts to significantly rise in many countries. The result was that the mucous membranes in the nasal cavity weakened. This made it easier for the SARS-CoV-2 virus to multiply and invade. A lag period of 4 days occurred between the rise of the pollen count and the start of SARS-CoV-2 infection. The authors recommend that those who react to pollens in the air should wear pollen filtering masks in the spring season. This minimizes the danger of getting viral infections including SARS-CoV-2 infections following pollen exposure.

Dec
26
2020

Hormones Play an Important Role in Survival from Covid-19

I am describing here that hormones play an important role in survival from Covid-19. There are two publications that illustrate that point.

Estrogens protect women against Covid-19

A study from Dec. 4, 2020 covering 17 countries and involving nearly 70,000 women discovered these principal findings.

  • Women aged 20 to 50 have moderately higher Covid-19 infection rates than men
  • In all of the age groups men have higher mortality rates than women
  • Beyond the age of 50 the fatality rate from Covid-19 is 50% higher in men than that of women
  • Postmenopausal women above the age of 50 and on estradiol supplementation had 50% less mortality from Covid-19 than women without estradiol supplementation

The researchers said about the study: “In a nutshell, it’s likely that the apparently protective effects of 17β-estradiol, a naturally occurring, abundant female hormone, relate to a key property of this molecule: it attenuates the so-called “cytokine storm” that’s thought to underlie much of the cellular-scale and organ/tissue-level damage wrought by a SARS-CoV-2 infection, via dysregulation of a patient’s immune response.”

Men need enough testosterone to fight Covid-19

Another study from September 17, 2020 pointed out that males have much worse outcomes with Covid-19 than females. Men are affected by Covid-19 twice as often as females and they experience a much more severe course with a higher mortality. The authors also point out that there is a direct correlation between lower serum testosterone levels in men and inflammation severity by cytokines and poor clinical outcomes. The decline in total and free testosterone in aging men leads to serious pulmonary complications and the need to treat the patient in the ICU. The Covid-19 coronavirus utilizes Angiotensin-Converting Enzyme II (ACE2) for entry into the host cell. A male requires testosterone for ACE2 expression. Lower testosterone causes higher mortality in men. In contrast, if testosterone in a male is too high, blood clots can form in the circulatory system, which often lead to complications and deaths in patients with Covid-19.

Vitamin D levels and course of Covid-19

There are three major effects that vitamin D has.

  1. A strengthening of the epithelial barrier not allowing the coronavirus to penetrate into the lung tissue as easily.
  2. Release of defensins and cathelicidin, two crucial antiviral polypeptides, that eradicate the SARS-CoV-2 virus in the system.
  3. Interruption of the “cytokine storm”, an overwhelming inflammation which is responsible for viral pneumonia to develop. Without the cytokine storm there is no damage to the lungs, and people do not need treatment in the ICU. This is particularly important for people above the age of 60 and for people with pre-existing diseases.

Similarly, with the stabilizing effect of vitamin D regarding the immune function more severe forms of Covid-19 can turn into less severe forms with a better outcome.

Discussion

Research showed that in women estrogen has a modifying effect on the course of Covid-19. In males it is testosterone that leads to an improved course of Covid-19. Both sexes require adequate doses of vitamin D, which helps to strengthen the epithelial barrier. In addition, enough vitamin D releases defensins and cathelicidin, two crucial antiviral polypeptides that eradicate any virus in the system. Vitamin D also interrupts the “cytokine storm”, an overwhelming inflammation, which is responsible for viral pneumonia to develop. All of these factors together modify the course of Covid-19 and improve the probability of survival from this otherwise serious viral illness.

Hormones Play an Important Role in Survival from Covid-19

Hormones Play an Important Role in Survival from Covid-19

Conclusion

Two lines of research showed that both women and men do better with Covid-19 when their hormone levels are either adequate or are substituted to normal levels. Women in menopause taking estradiol for postmenopausal symptoms had 50% less mortality from Covid-19. Men who were testosterone deficient and were put on testosterone supplementation do better with respect to Covid-19. In aging men total and free testosterone decline and serious pulmonary complications occur with a need to treat the patient in the ICU. On top of hormones both men and women benefit from high doses of vitamin D, which strengthens the epithelial barrier. Vitamin D also releases defensins and cathelicidin, two crucial antiviral polypeptides that fights the SARS-CoV-2 virus directly. In addition, vitamin D interrupts the “cytokine storm”, an overwhelming inflammation which causes the viral pneumonia. Taken together the hormones and vitamin D can improve the outcome of Covid-19 significantly.

This text includes part of this blog.

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Oct
31
2020

Blood Type Has Some Bearing on the Severity of Covid-19 Coronavirus

Two independent research publications concluded that blood type has some bearing on the severity of Covid-19 coronavirus infections. One was published in Denmark, the other one in Canada.

In the US the 4 common blood types occur with this frequency: group O: 45% (O positive 38%, O negative 7%); group A:  40% (A positive 34%, A negative 6%); group B: 11% (B positive 9%, B negative 2%) and group: AB 4% (AB positive 3%, AB negative 1%). Positive and negative stands for the Rh group (the rhesus factor, which is another type of blood group).

Two separate publications

Denmark study

Briefly, the Denmark study showed that when positive and negative tests for the SARS-CoV-2 virus were checked in relationship to blood groups, blood group O had 13% less coronavirus infections, group A had 9% more infections, group B had 6% more infections and group AB had 15% more infections than negative controls. This means that blood group O is relatively protected from the SARS-CoV-2 virus. The investigators were fast to add that this does not give people with a group O blood type a licence to go to the pub and celebrate.

Canadian study

The Canadian study looked at 125 critically ill people with positive SARS-CoV-2 virus tests. Of these 95 had ABO blood types available. All these patients were admitted to the ICU. Here are the significant findings: 32% of blood group A required intubation versus 84% of AB patients, 35% of O group patients and 61% of B patients required intubation. 12% of A patients and 32% of AB patients, but only 5% of blood group O patients and 9% of B patients required kidney support (continuous renal replacement therapy). In addition, group O and group B patients required a median ICU stay of only 9 days. In contrast, group A and AB had to stay in the ICU for 13.5 days.

Gene study to determine susceptibility for severe Covid-19 disease

In a European genetic study from Italy and Spain 835 patients and 1255 control participants had genetic studies done. It turned out that the genetic loci that determined the severity of Covid-19 followed the blood groups. Blood group A patients had a 45% higher risk of developing severe Covid-19 disease, while group O patients had a 35% lesser risk compared to other blood groups of developing severe Covid-19.

Discussion

Dr. Mypinder Sekhon, an intensive care physician at Vancouver General Hospital stated that people with a blood group O make less of a key clotting factor, which makes them less prone to clotting problems in the blood. Clotting is a major driver in complications of Covid-19. Other possible explanations are the blood group antigens and how they interact with antibodies from the infection with Covid-19 coronavirus. Finally, it could be related to the genes of the blood groups and how they interact with receptors of the immune system. It is interesting to also note that there are genetically different risks that go along the line of the blood groups with group A having much higher risk than group O to develop severe Covid-19 disease.

Blood Type Has Some Bearing on the Severity of Covid-19 Coronavirus

Blood Type Has Some Bearing on the Severity of Covid-19 Coronavirus

Conclusion

Both research in Denmark and in Canada confirmed that blood group O had less coronavirus infections. In the Denmark study there were 13% less severe Covid-19 cases in people with the blood group O than in negative controls. In the Canadian study of 95 patients with severe Covid-19 physicians had to admit them into the ICU. They noted that 84% of blood group AB patients in the ICU required intubation. In contrast, only 35% of O group patients required intubation. With regard to kidney support, 32% of AB patients, but only 5% of O patients required this during their ICU stay.

More research required to understand these findings

The researchers added that it is not clear why there are such differences among patients with different blood groups. They mentioned that more research is necessary. This will reveal why group O has a milder course. It will also show why group O patients require less intubation and shorter ICU stays. Separate genetic studies showed that severe Covid-19 disease develops with blood group A patients (45% higher risk). In contrast group O blood group patients have milder Covid-19 disease (35% less risk). It is with these investigations that we can now understand some of the peculiarities regarding the Covid-19 disease.  It explains why some people develop severe Covid-19 disease while others develop only mild symptoms.

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Sep
26
2020

A New Antibiotic Against Methicillin Resistant Staphylococcus aureus

A US study describes a new antibiotic against methicillin resistant Staphylococcus aureus. It is a lysin-based antibacterial agent.

Physicians have been looking for years for a solution regarding the increasing antibiotic resistance problem. But several attempts in the past have failed.

Staphylococcus infections are the most common bacterial infections of human skin, of soft tissue, joints, bones, and pneumonia. In addition, it can cause endocarditis (=infection of heart valves) and lead to blood poisoning (septicemia).

Staphylococcus aureus is the underlying bacterium behind staph infections. With the introduction of new antibiotics  it takes only 1 to 2 years before this bacterium learns to become resistant. Researchers noticed that the bacteria start to produce lysins and suddenly they are resistant to the latest antibiotic. Further research zeroed in on lysostaphin, which was active against resistant Staphylococcus bacterial strains.

Deimmunized lysostaphin

Lysostaphin is an antibacterial peptide described here in detail. But there still was some interference with immunologically active surface antigens that scientists were later able to overcome. Researchers succeeded lately in removing some of the surface antigens and develop deimmunized lysostaphin. This is what this publication is all about.

It describes how T cells cannot detect the surface antigen properties of deimmunized lysostaphin. This way none of the strength of deimmunized lysostaphin gets lost in the fight against resistant staphylococcus that normally form anti-drug antibodies. Researchers pointed out the importance of the deimmunization process to make deimmunized lysostaphin invisible to the T cells of the immune system.

Vigorous testing of deimmunized lysostaphin

The researchers who investigated the efficiency and safety of deimmunized lysostaphin did the following tests.

  • Although lysostaphin was deimmunized, it retained potent in vitro and in vivo anti-staphylococcal activity. In vitro studies involving Petri dishes with methicillin resistant Staphylococcus aureus showed the effectiveness of deimmunized lysostaphin. In vivo testing in a mouse and rabbit model also showed effectiveness.
  • Deimmunized lysostaphin showed reduced immunogenicity in vivo. Researchers tested this in mice and compared the results to regular lysostaphin, where there was a swift immunological response.

More points regarding deimmunized lysostaphin

  • Immune evasion allows for repeated efficient dosing of deimmunized lysostaphin. This means that the physician can administer the antibiotic (the deimmunized lysostaphin) to fight the methicillin resistant Staphylococcus aureus with several daily doses.
  • The deimmunization process allows deimmunized lysostaphin to evade the immune response that occurs to regular lysostaphin. This prevents future resistance development. It also prevents that the immune responses weaken the anti-methicillin resistant Staphylococcus aureus response.
  • Researchers showed in a difficult rabbit endocarditis model that deimmunized lysostaphin treats MRSA infection successfully. Endocarditis is an infectious disease, which is both difficult to treat in rabbits, but also in humans. For this reason, rabbits are often used as a model when new antibiotics are developed. If they are successful in the rabbit model they often get approval later for human treatments.

Deimmunized lysostaphin in humans

Unfortunately, we are still a few years away from using deimmunized lysostaphin in humans. After successful use of lysostaphin in mice and rabbits the next logical application is to launch human clinical trials. I am convinced that this will be the next step and very likely will be successful.

A New Antibiotic Against Methicillin Resistant Staphylococcus aureus

A New Antibiotic Against Methicillin Resistant Staphylococcus aureus

Conclusion

Researchers found a new antibiotic against methicillin resistant Staphylococcus aureus in a lysin-based antibacterial agent. This peptide has surface antigens that scientists had to removed to make it more effective. The end result was a deimmunized lysostaphin. Researchers tested this new antibiotic that is effective against many antibiotic resistant strains of bacteria successfully in mice and rabbits. The next step is testing in humans. This involves several phases of clinical trials. These clinical trials have to show that there is a lack of toxicity. In addition, they have to show that the new antibiotic is effective against resistant bacteria. I estimate that this process can still take about 5 years from now before the clinician can use this antibiotic routinely. As the new antibiotic is a polypeptide, it the patient cannot take it orally, as the gut is digesting it. The patient has to take it by injection.

Sep
05
2020

How to Manage Clot Formation with Covid-19

A publication in the Canadian Medical Association Journal describes how to manage clot formation with Covid-19. A significant amount of cases among Covid-19 patients come down with clotting problems. This means that an infection with SARS-CoV-2 (or Covid-19 coronavirus) may initially present with a fever and cough. But a few days later it can suddenly turn into a dangerous disease with severe clots, multiple organ failures and death.

Clot occurrence with Covid-19

It is important to realize that most patients with SARS-CoV-2 do not need hospitalization. But physicians admit 10 to 15% of patients to the hospital. Of these 20% end up with treatment in the Intensive Care Unit (ICU). Of all the hospitalized patients between 5% and 30% develop some form of thrombotic event. Notably, complications of clot formation can be a stroke, a heart attack, a pulmonary embolism or a deep vein thrombosis in the leg. In a recent study from the US 400 random hospitalized patients with Covid-19 144 patients were admitted to the ICU. 4.8% had radiologically confirmed deep vein thrombosis. Overall there were 9.5% with thrombotic events that developed during the hospital stay.

How does a coagulopathy develop with Covid-19?

Truly, SARS-CoV-2 enters the body cells through an interaction of its viral spike protein with the angiotensin-converting enzyme 2 (ACE2) receptor. To explain, numerous organs and tissues express this receptor. This includes lung alveolar type 2 epithelial cells, endothelium, the brain, heart and kidneys. To emphasize, ACE2 leads to angiotensin II degradation. With the SARS-CoV-2 stimulation of the ACE2 receptor there may be an accumulation of angiotensin II, which causes a procoagulant state. Injury of the endothelium explains inflammation in the lining of the blood vessels in multiple organs. Commonly affected organs are lungs, heart, kidneys and intestines. The inflammatory reaction is what can lead to clot formation. When part of an organ has died off because of mini clots that destroyed part of the organ, this process can eventually lead to organ failure. Lung failure, heart failure and kidney failure can develop in these sick patients.

Adequate vitamin D blood levels are important for the immune system

By all means, vitamin D is very important for the integrity of the immune system. With vitamin D blood levels below 15 to 20 ng/mL (37.5–50 nmol/L) the immune system is paralyzed, and any viral or bacterial infection tends to overwhelm the body. Of course, this is the reason why the mortality due to Covid-19 coronavirus is highest in patients with these low vitamin D blood levels. People with secondary illnesses (diabetes, arthritis, autoimmune diseases, cancer) and patients above the age of 60 have the lowest vitamin D blood levels and have the highest mortality rates. This publication describes this in more detail.

Best vitamin D blood level is in the upper normal range (50-80 ng/mL)

Above a vitamin D blood level of 30 ng/mL (=75 nmol/L) a patient’s immune system is functioning normally. However, the immune system is strongest at a vitamin D blood level of 50–80 ng/mL (125–200 nmol/L), which is the upper range of the normal level for vitamin D in the blood.

Keep in mind that vitamin D toxicity occurs only above 150 ng/mL (375 nmol/L).

Specific effects of vitamin D on Covid-19

There are three major effects that vitamin D has.

  1. A strengthening of the epithelial barrier not allowing the coronavirus to penetrate into the lung tissue as easily.
  2. Release of defensins and cathelicidin, two crucial antiviral polypeptides that eradicate any virus in the system.
  3. Interruption of the “cytokine storm”, an overwhelming inflammation which is responsible for viral pneumonia to develop. Without the cytokine storm there is no damage to the lungs and people do not need treatment in the ICU. This is particularly important for people above the age of 60 and for people with pre-existing diseases.

In like manner, with the stabilizing effect of vitamin D regarding the immune function more severe forms of Covid-19 can turn into less severe forms with a better outcome.

Treatment of patients with Covid-19 who have clotting problems

Patients need to be assessed with respect to their risk of developing clots. This publication describes that high risk patients have elevated D-dimer levels. When blood clots dissolve the body produces D-dimer, a protein fragment. Normally the D-dimer test is negative in a person that does not produce clots. But in sick patients with Covid-19 who form clots this blood test typically shows D-dimer >2500 ng/mL. In addition the tests show high platelet counts (more than 450 × 109/L), C-reactive protein (CRP) >100 mg/L and an erythrocyte sedimentation rate (ESR) >40 mm/h.

Indeed, with this constellation of blood tests in a severe Covid-19 case in the ICU setting, the physician uses heparin intravenously or subcutaneously to counter clot formation. However, this needs to be balanced against the risk of causing severe internal bleeding.

Separate from the anticoagulant effect, heparin seems to also suppress inflammatory cytokine levels. In addition, heparin suppresses neutrophil chemotaxis and migration. Physicians rescued many patients from death using heparin therapy.

Risk versus benefit clinical trials of heparin therapy are required

At this point there are only retrospective clinical trials available to describe risk versus benefit of heparin therapy. Some show no difference, others do. There are two international clinical trials on their way to shed more light on this situation. Until the results of these clinical trials are available, physicians need to treat patients to the best of their knowledge.

How to Manage Clot Formation with Covid-19

How to Manage Clot Formation with Covid-19

Conclusion

Clot formation in sick Covid-19 patients is responsible for many deaths in Covid-19 patients. The SARS-CoV-2 (or Covid-19 coronavirus) causes a cytokine storm with injury to the lining of the arteries. This can affect multiple vital organs and the condition may lead to organ failure. This activates the clotting system and causes clots all over the body. When this process occurs, patients get very sick and the death rate climbs. Physicians were able to rescue some patients with heparin therapy. Two international clinical trials are on the way. Hopefully  these trials answer questions about this newer treatment method. The downside of heparin therapy is the complication of massive bleeding, which causes deaths as well. When it comes to Covid-19, don’t rely on curative medicine. Strengthen your immune system by preventative therapy like vitamin D3 that can interrupt the cytokine storm.

And even with a “well-prepared” immune system it is extremely important to follow all the guidelines of distancing, disinfecting and wearing face masks. We need all the help we can get!

Jul
25
2020

The Immune System Changes With Age

When we are young, we do not think about our immune system, but the immune system changes with age. When we are older than age 60, we notice that we may be taking longer to recover from a flu.

How does the immune system work?

There are two parts to the immune system, the innate immune system and the adaptive immune system. The innate immune system works to protect us from bacteria, viruses, toxins and fungi from the time we are born. The adaptive immune system uses B lymphocytes from the bone marrow to produce antibodies against viruses. This provides often lifelong immunity against this specific virus, but takes 3 to 5 days to kick in. Vaccinations can also trigger antibody production to protect us from viruses in the future. Both the adaptive and the innate immune system work together closely.

What are the ingredients for a fully functioning immune system?

The immune system consists of various immune organs that are distributed throughout the body. The bone marrow produces lymphocytes, granulocytes, macrophages, eosinophils and basophils. The adenoids in the back of the nasal passages and the tonsils in the back of the throat contain a lot of lymphocytes that are ready to protect us from colds and flus. We have lymph nodes throughout the body and they are connected with lymphatic vessels. The lymph nodes filter the lymph fluid that travels in the lymphatic vessels.

Other sites of lymphocyte production

The small intestine contains the Peyer’s patches, a collection of lymphocytes that protect our gut from invading bacteria or viruses. The spleen is located in the left abdominal cavity under the diaphragm. It removes old red blood cells and provides lymphocytes for the immune system. The thymus gland is located between the breast bone and the trachea. It changes bone marrow derived lymphocytes (B cells) into T lymphocytes that can process antigens from viruses and pass them on to the adaptive immune system for a full antibody response.

Cellular interactions between various players of the immune system

Back in the 1970’s it was already known that there were bone marrow derived B lymphocytes and thymus processed T lymphocytes. We knew then that B cells were involved in antibody production (adaptive immunity). T lymphocytes were thought to turn into killer T lymphocytes to kill cancer cells. But some T cells were T helper cells to process antigen and present it to B lymphocytes for antibody production.

More research since then refined what we know about the cells of the immune system.

Natural killer cells (NK cells)

Natural killer cells (NK cells) are part of the innate immune system. They attack cancer cells and cells that are infected by viruses. It takes about 3 days for their full action to develop. NK cells utilize the cell surface histocompatibility complex to decide whether to destroy a cell or not. T cell lymphocytes do not have the ability to do that. In the Covid-19 coronavirus situation NK cells play an important role to combat the disease right away.

Monocytes

They are large white blood cells that can differentiate further into macrophages and dendritic cells. Monocytes are part of the innate immunity, but they have an antigen presenting capability, which makes them also part of the adaptive immunity.

Memory T cells

The immune system learns to adapt to viruses and bacteria that we have come in contact with. The reason for the memory of the immune cells are the memory T cells. They replicate like stem cells, which keeps a clone of T lymphocytes, T helper cells and cytotoxic T killer cells in the background. They circulate through the body including the lymph glands and the spleen.

Immunosenescence as we age

There are several factors that come together, which age our immune system. The term for this is “immunosenescence“. There are genetic differences and differences due to the sex hormones. Estrogens increase the response of the immune system. In contrast, progesterone and androgens (including testosterone) decrease the immune response. This may be the reason why women tend to live longer than men.

As we age there are more and more memory T cells (both cytotoxic T cells and T helper cells). This weakens the formation of the natural killer cells (NK cells) of the innate immune system. Even the initiation of the adaptive immune system can be slower when we age and also the response to the flu vaccine. In addition, this can pave the way to autoimmune diseases.

The immune system changes with age: Evidence of immunosenescence

The following 3 factors show whether a person has immunosenescence:

  • The immune system has difficulties to respond to new viruses/bacteria or to vaccines
  • Accumulation of memory T cells crowding out cells of the rest of the immune system
  • Low-grade inflammation that is chronic and persists (“inflamm-aging”)

The process of immunosenescence starts with the involution of the thymus gland around the time of puberty. At that time the sex hormone secretion is highest. At the same time a growth factor from the bone marrow and the thymus gland decreases. It has the name interleukin-7 (IL-7). The end result is a slow decrease of the innate immune system with age and a more substantial weakening of the adaptive immune system due to a lack of naïve T and B cells. 

Chronic viruses can weaken the immune system further

The varicella herpes zoster virus causes chickenpox. In some people the chickenpox virus can persist, but the immune system actively keeps it controlled. In the 60’s or 70’s when the immune system is weakened from aging, there can be a flare-up as shingles, a localized form of the chickenpox virus.

Another virus, the human cytomegalovirus can cause a chronic infection that often persists lifelong. In this case the immune system is chronically weakened because of a massive accumulation of T memory cells, which keeps the human cytomegalovirus infection at bay.

What we need when the immune system changes with age 

Vitamin A

Both the innate and adaptive immunity depend on vitamin A and its metabolites. The skin cells and mucosal cells function as a barrier, which is important for the innate immunity. The skin/mucosal lining of the eye, the respiratory tract, the gastrointestinal and genitourinary tracts help the innate immunity to keep viruses and bacteria out of the body. Vitamin A is important to support macrophages, neutrophils and natural killer (NK) cells. In addition, vitamin A supports the adaptive immune system, namely T and B lymphocytes, so that the body can produce specific antibodies against viruses.

I do not take vitamin A supplements as I eat diversified foods like spinach, vegetables, poultry, Brussels sprout, fish and dairy products that contain vitamin A and carotenoids.

Vitamin C

This vitamin is a powerful antioxidant. It can neutralize reactive oxygen species, which are produced when the immune cells fight viruses and bacteria. Neutrophils, lymphocytes and phagocytes are all supported by vitamin C. Vitamin C and E co-operate in their antioxidant functions. Vitamin C is essential for a strong antibody response with bacterial or viral infections. I take 1000 mg of vitamin C once daily.

Vitamin D

The immune system is very dependent on vitamin D as the immune cells all contain vitamin D receptors. People who have less than 10 ng/mL of vitamin D in the blood are vitamin D deficient. They have much higher death rates when they get infected with the Covid-19 coronavirus.

Vitamin D regulates the expression of target genes. At the center is the vitamin D receptor, which is a nuclear transcription factor. Together with the retinoic X receptor (from vitamin A) the vitamin D receptor binds small sequences of DNA. They have the name “vitamin D response elements” and are capable of initiating a cascade of molecular interactions. The result is a modulation of specific genes. Researchers identified thousands of vitamin D response elements that regulate between 100 and 1250 genes.

You need enough vitamin D for your immune system

When enough vitamin D is present in the blood (more than 30 ng/mL) the immune system releases the peptides cathelicidins and defensins, which effectively destroy bacteria and viruses.

Vitamin D has mainly an inhibitory function regarding adaptive immunity. It inhibits antibody production from B cells and also dampens the effect of T cells. Researchers reported that vitamin D3 is useful in the treatment of autoimmune diseases.

I am a slow absorber of vitamin D3 as repeat blood vitamin D levels showed. I need 10,000 IU of vitamin D3 daily to get a blood level of 50-80 ng/mL (=125-200 nmol/L). This is the higher range of normal. Everybody is different. Ask your physician to check your blood level of vitamin D. Toxic vitamin D blood levels are only starting above 150 ng/mL (= 375 nmol/L).

Vitamin E

This is a vitamin that is fat soluble and helps the body to maintain its cell membranes. But researchers found that vitamin E also stimulates the T cell-mediated immune response. This is particularly important for the aging person to prevent respiratory tract infections. I take 125 mg of Annatto tocotrienols per day (this is the most potent form of vitamin E).

Vitamin B6

This vitamin is important for antibody production by B cells. Vitamin B6 regulates the metabolism of amino acids, which in turn form proteins. Antibodies and cytokines require vitamin B6. The T helper immune cells that initiate an adaptive immune response depend on vitamin B6 as well. I take a multi B complex vitamin (Mega B 50) twice per day, so I supplement with a total of 100 mg of vitamin B6 daily.

Folate

Folic acid is a coenzyme for the metabolism of nucleic acids and amino acids. Studies in humans and animals have shown that folate deficiency leads to increased susceptibility to infections. People with folate deficiency develop a megaloblastic anemia with immune weakness that leads to chronic infections. With my B complex supplement I get 2 mg of folic acid daily.

Vitamin B12

Methylation pathways depend on vitamin B12 as a coenzyme. Vitamin B12 is also involved as a coenzyme in the production of energy from fats and proteins. In addition, hemoglobin synthesis depends on vitamin B12. Patients with vitamin B12 deficiency develop pernicious anemia. These patients also have a weak immune system due to natural killer cell activity suppression and because circulating lymphocyte numbers are significantly decreased.

Treatment with cyanocobalamin reverses the immune weakness rapidly and treats pernicious anemia at the same time. I take 50 micrograms twice per day as part of the Mega-B50 multivitamin tablet. But I also inject 1000 micrograms of vitamin B12 every 6 months subcutaneously to be sure it is absorbed into the body. In older age the intrinsic factor from the stomach lining, which is required for absorption of vitamin B12 in the small intestine, can be missing, leading to vitamin B12 deficiency despite swallowing supplements.

Minerals required for a good immune response

Researchers identified five minerals that are essential for a strong immune system. They are zinc, iron, selenium, copper and magnesium.

Zinc

Zinc is important for a normal function of the innate and adaptive immune system. As zinc cannot be stored in the body, taking regular zinc supplements (30 to 50 mg daily) is important. I take 50 mg of amino acid chelated zinc daily.

Iron

Iron is important for cell oxygen transport and storage, DNA synthesis and for mounting an effective immune response. In particular it is the T cell differentiation and proliferation where iron is needed. Iron deficient people get a lot of infections because the immune system is paralyzed. I eat one spinach salad or steamed spinach daily, which gives me enough iron supply per day.

Selenium

Selenium is a trace mineral that is important for a normal immune response and for cancer prevention. When selenium is missing, both the adaptive and innate immune system are suffering. In this case viruses are more virulent. With selenium supplementation cell-mediated immunity is improved and the immune response to viruses is more potent. I take 200 micrograms of selenium per day.

Copper

Deficiency in copper results in a very low neutrophil blood count and causes susceptibility to infections. Copper is a trace mineral that participates in several enzymatic reactions. It is important for the innate immune response to bacterial infections. A well-balanced Mediterranean diet contains enough copper, which is why I do not supplement with extra copper.

Magnesium

An important cofactor for vitamin D in the body is magnesium. Magnesium participates in many enzymatic reactions. Between vitamin D and magnesium, the immune system is strengthened. I take 150 mg of magnesium citrate twice per day. By the way, magnesium also helps us to get a restful sleep, if we take it at bedtime.

Other dietary factors that strengthen the immune system

Polyunsaturated omega-3 fatty acids

It is important to note that polyunsaturated omega-3 fatty acids are essential for the body and help to modulate the immune system. I take 1800 mg of omega-3 (EPA/DHA) twice per day. I also like to eat fish and seafood at least 3 times per week.

Probiotics

Prebiotics benefit both the innate and the adaptive immune system. They strengthen the epithelial gut barrier, which is an important innate immune defence. Probiotics also lower the risk for Clostridium difficile gut infections. I take one probiotic every morning.

The Immune System Changes With Age

The Immune System Changes With Age

Conclusion

The immune system consists of different organs like the bone marrow, the spleen, lymph glands, Peyer’s patches in the gut, the thymus gland and more. There is the innate immune system, which responds immediately to a virus like the Covid-19 coronavirus. The adaptive immune response involves antibody production against, for instance, the measle virus or the mumps virus. With the aging process the immune system slows down (immunosenescence). This involves an accumulation of memory T cells and a depletion of natural killer cells (NK cells). This means that the innate immunity is getting weaker as we age and chronic inflammation occurs more often. This is the reason why people above the age of 65 get more severe symptoms from the Covid-19 coronavirus. They are also more affected by influenza-type illnesses.

Take supplements to strengthen the immune system

I reviewed the cofactors of a healthy immune system in some detail. It is important that you pay attention to these, particularly the vitamin D3 intake. With a strong immune system, we can survive viral infections better, including the current Covid-19 coronavirus. Future research will likely detect how to reactivate a sluggish immune system in older people. This way vaccination responses following flu injections will become more reliable in seniors.

Jul
11
2020

Fat Deposits Mean Higher Covid-19 Risk

A new study showed that fat deposits mean higher Covid-19 risk. This study was reviewed here.

The article is based on the June 10, 2020 publication of the British Medical Journal.

They did large population studies showing that obesity is an independent risk factor for severe disease and death from Covid-19. One study with 428,225 participants had 340 admitted to hospital with confirmed Covid-19 coronavirus. 44% of them were overweight and 34% were obese. Another study, the OpenSAFELY study used linked electronic health records. 17,425, 445 participants were included and 5,683 Covid-19 deaths occurred. In this study there were 29% overweight and 33% obese persons. The researchers noted a dose-response relationship between excess weight and severity of Covid-19. The researchers removed confounding factors like age, sex, ethnicity, and social deprivation.

Critical illness and death rates in overweight and obese people

They realized that critical illness caused by Covid-19 was increased compared to normal-weight people as follows.

  • Covid-19 risk 44% higher in overweight people
  • Covid-19 risk 97% higher in people with obesity

This means that the risk for serious illness from Covid-19 was 1.44-fold for overweight persons and 1.97-fold for obese persons compared to normal-weight controls. The OpenSAFELY study also looked at the death rates from Covid-19 for people with obesity. Two obesity categories were investigated: obesity with a BMI of 30-34.9 and BMI of greater than 40 compared to normal-weight controls. Here are the death rates.

  • BMI of 30-34.9: 1.27-fold increased risk
  • BMI of greater than 40: 2.27-fold risk

Possible mechanisms explaining fat deposits mean higher Covid-19 risk

The researchers mentioned three possible mechanisms why overweight and obese people may have higher Covid-19 disease and death rates than normal-weight controls.

First, angiotensin converting enzyme-2 is found with higher frequency in fat cells of overweight and obese persons. Researchers are aware of the fact that the Covid-19 coronavirus uses this enzyme to enter body cells. It may also be the reason that fat cells become reservoirs that can shed virus for much longer than in normal-weight people with less fat cells. They pointed out that others have seen this also and found it with other viruses. In the case of influenza A, obesity prolonged viral shedding by 42% compared to normal-weight controls. And with H1N1 influenza obesity was an independent risk factor for hospitalization and death.

Weaker immune system, more lung resistance

Secondly, any virus can weaken the host’s defence of the immune system. Researchers showed this previously with the influenza virus. But now with Covid-19 coronavirus the cytokine storm due to a weak immune system is a major factor in making the viral infection worse. A lack of vitamin D is another factor in promoting the cytokine storm.

Third, obesity decreases lung function and it is difficult to improve this. There is greater lung resistance in the airways and it is difficult to expand the lungs in obese patients. When the doctor transfers patients with obesity to the intensive care unit, it is more difficult to increase their oxygen saturation with artificial ventilation.

Unhealthy environment, so fat deposits mean higher Covid-19 risk

The researchers point out that we live in a very unhealthy environment. In 2016 there were 1.9 billion people worldwide who were overweight or obese. These figures are rapidly rising. Presently about 65% to 70% are overweight or obese in the UK or the US. Obesity causes high blood pressure, heart disease, strokes, type 2 diabetes and cancer. We are all surrounded by processed food with extra salt, sugar, wheat and other unhealthy ingredients. The high mortality and deaths rates of Covid-19 in overweight and obese people point to the problem that society has.

Reduce salt, sugar and saturated fats in food

The culprits are salt, sugar and saturated fats. Merchants and food producers must reduce them in processed food. In the UK new government regulations have already resulted in lower salt content in foods. As a result, there is less high blood pressure and cardiovascular disease is in decline. All nations need to reduce salt, sugar, and saturated fat. When the weight comes down, we all are less prone to catching dangerous viruses.

Fat Deposits Mean Higher Covid-19 Risk

Fat Deposits Mean Higher Covid-19 Risk

Conclusion

The pandemic has taught us a new lesson, namely that overweight and obese people are at higher risk of contracting Covid-19 coronavirus. In a research paper of the British Medical Journal concrete figures showed that the Covid-19 risk is 44% higher in overweight people and that it is 97% higher in people with obesity. The OpenSAFELY study also showed that obese people with a BMI of 30-34.9 have a 1.27-fold increased risk of catching Covid-19. But morbidly obese people with a BMI of greater than 40 have a 2.27-fold risk of catching Covid-19. There is a clear linear dose-response curve between the amount of fat a person accumulates and the risk for Covid-19.

Cut out junk food and decrease your risk for Covid-19

Covid-19 is directly related to the amount of junk food we eat. As a result we can say that eating junk food increases the Covid-19 risk. The opposite is true also: sensible eating and cutting out junk food makes you lose some pounds, and your risk for Covid-19 decreases.

Jun
27
2020

A New Antibiotic, Teixobactin Can Overcome Antibiotic-Resistant Superbugs

A new antibiotic, teixobactin can overcome antibiotic-resistant superbugs. The discovery of teixobactin took place in 2015. It is a peptide with 11 amino acid units. Teixobactin is derived from a gram-negative bacterium, Eleftheria terrae. It is the first of a new class of antibiotics that can kill superbugs. Two examples, for instance are methicillin-resistant Staphylococcus aureus and resistant Mycobacterium tuberculosis. Researchers have been battling with difficult solubility of teixobactin and problems synthesizing this peptide in the laboratory. Teixobactin binds to the membranes of the bacteria it fights. This is a new mechanism for this new class of antibiotics, different from conventional antibiotics.

Mechanisms of fighting bacteria resistant to conventional antibiotics

But it is exactly this quality that is necessary to fight the antibiotic-resistant bacteria. The researchers showed that teixobactin binds weakly to a component of the bacterial cell wall, called “Lipid II”. But they found a second mechanism, namely blocking precursors of cell membrane synthesis in the bacteria they fight. Because of these unique mechanisms it is possible for them to fight a multitude of bacteria resistant to conventional antibiotics. Teixobactin has a unique molecular structure, which makes it difficult for resistant bacteria to develop resistance to it.

Antibiotic resistance

Resistance to antibiotics is a worldwide problem. There are several factors that worked together to make antibiotic resistance such a big issue. For instance, in the past many doctors prescribed antibiotics for any viral cold, even knowing that antibiotics only work against bacteria. Aside from this, the agricultural practice of using antibiotics as a growth stimulator is also an important factor for antibiotic resistance to develop. It is the bacteria that become resistant, not the human body. Several clinical entities involving resistant bacteria exist that show the magnitude of the problem.

Flesh-eating disease

Necrotizing fasciitis (or flesh-eating disease) can develop when you swim in contaminated waters and the bacterium, Vibrio vulnificus enters through skin sores or wounds. The CDC warns that you should stay out of salt water or brackish water, if you have a skin wound. The flesh-eating bacteria, Vibrio vulnificus can become very aggressive, once it has entered the body. Right now, 1 out of 5 people who get infected will die and many people require ICU treatment. Others need limb amputations. All of this can happen within only 1 or 2 days of becoming ill. The hope is that with the development of teixobactin as an injectable medication or as an oral pill there will no longer be deaths, amputations and scarring due to this bacterium, as the antibiotic will very quickly eradicate Vibrio vulnificus. I have previously written about what hospitals can do to fight superbugs.

The most common antibiotic-resistant bacteria

Here is a brief review of the most common antibiotic-resistant bacteria.

Mycobacterium tuberculosis

Since the 1950’s and 1960’s tuberculosis was treatable with a combination of two antibiotics over a period of six months to two years. But in the last 10 years more and more resistant strains of tuberculosis have developed. This is called multi-drug-resistant TB. In 2013 statistics showed that 3.7% of newly diagnosed tuberculosis cases were multi-drug-resistant TB. Many of these cases can be traced back to prisons and homeless shelters.

Methicillin-resistant Staphylococcus aureus (MRSA)

MRSA has become a common resistant bacterium that can present with difficult to treat boils in the skin, but also as a fulminant infection as necrotizing fasciitis (or “flesh-eating disease”). About 1/3 of the cases of flesh-eating disease are caused by MRSA.

Clostridium difficile (C. difficile)

This gut bacterium is naturally resistant to many antibiotics. The rest of the gut bacteria usually suppress the growth of C. difficile. But many patients can get overgrowth of C. difficile in their gut following treatment with antibiotics. Recolonization with probiotics can help to reintroduce a balanced bowel flora. In the US about 500,000 individuals come down every year with diarrhea due to C. difficile. This leads to approximately 15,000 deaths yearly.

Vancomycin-resistant Enterococci (VRE)

Physicians find enterococci in the gut and the female genital tract of patients. They can become resistant when the patient is treated with vancomycin for another infection. The VRE can then become a problem of its own with difficult to treat infections in the genital tract of females, the gut or in wounds from surgery. It has become a problem in immunocompromised patients.

The gonorrhea causing bacteria

In the last 70 to 80 years Neisseria gonorrhoea, the cause of gonorrhea, has been treated with only one antibiotic, but gradually the bacterium developed antibiotic-resistance. Lately, with more and more resistant strains of Neisseria gonorrhoea, the CDC has recommended to treat gonorrhea with two overlapping antibiotics.

Carbapenem-resistant Enterobacteriaceae (CRE)

There are two problem bugs among this category of enterobacteria, Klebsiella species and Escherichia coli (E. coli). These bacteria reside in hospitals where they can accumulate and are present in patients with immune system compromise. Medical devices like catheters and ventilators transmit these bacteria. Once a patient is sick with CRE, there is a danger of blood poisoning (septicemia), which has a high death rate.

How do regular antibiotics kill bacteria and how can they become resistant?

Normally, when antibiotics are not resistant, they interfere with the cell membrane production of the bacteria. Specifically, conventional antibiotics prevent bacteria from synthesizing a molecule, called peptidoglycan. Without peptidoglycan bacteria are not stable enough to survive in humans. But there are other mechanisms as explained in this link how antibiotics manage to kill bacteria.

Now I like to address the question how bacteria can become resistant to conventional antibiotics. This happens with overuse of antibiotics, i.e. prescribing antibiotics when a person suffers from a viral illness where antibiotics do not work. Other overuse comes from agriculture where cattle in feed lots get antibiotics as growth promoters. The FDA is strongly criticizing this practice, because residuals of antibiotics in beef can alter the bowel flora in man. The antibiotics kill all the sensitive bacteria. But the resistant bacteria, that have undergone mutations and adapted to the antibiotics, will survive.

Why teixobactin and analogues can avoid resistance

Since the detection of teixobactin many analogues have been synthesized. A new antibiotic, teixobactin can overcome antibiotic-resistant superbugs. The teixobactin analogues need more fine tuning, but they will be a breakthrough in the treatment of resistant bacteria. As this peptide attacks two targets on bacteria, it is not easy for bacteria to develop resistance against these new antibiotics.

A New Antibiotic, Teixobactin Can Overcome Antibiotic-Resistant Superbugs

A New Antibiotic, Teixobactin Can Overcome Antibiotic-Resistant Superbugs

Conclusion

Resistant bacteria have become a serious health concern in the last decade. Physicians overprescribing antibiotics and farmers feeding antibiotics to cattle in feedlots as growth promoters were the driving forces. In 2015 came the breakthrough and discovery of teixobactin. This is a peptide with 11 amino acid units. Teixobactin is a derivative of a gram-negative bacterium, Eleftheria terrae. A new antibiotic, teixobactin can overcome antibiotic-resistant superbugs. In the meantime, researchers have been able to improve solubility by developing teixobactin analogues. More research is necessary. But all of the researchers who work in this field claim that this will very soon be extremely useful for patients with super bugs. This super-antibiotic will be a weapon fighting super bugs. Before the release of this medication clinical trials will be the next step.

Jun
06
2020

Adequate Vitamin D Level Strengthens the Immune System

The Covid-19 coronavirus crisis is teaching us that an adequate vitamin D level strengthens the immune system.

When we age, our resistance to infections weakens, but this may be because our immune system needs more vitamin D3. I have reviewed the super powers of vitamin D3 before in 2014. In the past the thought was that the human body would need only 400 IU of vitamin D3 every day to cure rickets. And these were the daily vitamin D3 recommendations from medical authorities for several decades. Gradually it became known that for cancer prevention, infection prevention, cardiovascular illness prevention and for diabetes prevention much higher doses of vitamin D3 were necessary. As pointed out in the previous link, almost 50% of the world population is deficient in vitamin D. This is due to a lack of exposure to sunlight and due to inadequate supplementation with vitamin D3.

History of vitamin D

Dr. Adolf Windaus received the Nobel prize for chemistry in 1928. It was to acknowledge “… his studies on the constitution of the sterols and their connection with vitamins”. His work involved the metabolism of vitamin D and the precursors of vitamin D.

Rickets

As the above link shows, rachitic children were treated since the mid 1800’s with cod liver oil and since the early 1900’s also with ultraviolet light. But we know now that 400 IU of vitamin D3 per day is just enough to cure rachitic children, but it is not enough to strengthen the immune system to fight influenza viruses or the Covid-19 coronavirus. I will discuss further below what vitamin D blood levels are important to achieve a healthy state of the immune system.

Adequate vitamin D level strengthens the immune system

The immune system is very complicated and consists of many cell types that interact with each other and the rest of the body. It is important to recognize that the innate immune system immediately inactivates intruding viruses. But the vitamin D blood concentration has to be high enough. The acquired immunity consists of antibodies that are produced by B cells. The antibodies were produced during prior infections that you have survived and you are now immune to. However, other antibodies that circulate in your blood may have originated from vaccines you received in the past (whooping cough, measles, tetanus, diphtheria etc.). With the Covid-19 coronavirus it is the innate immunity that plays the biggest role until a vaccine will be found in the future.

Vitamin D is a hormone

This 2013 paper explains that vitamin D is a hormone that stimulates its own vitamin D receptor. This is a nuclear receptor that has close relations to the cell DNA and can stimulate more than 900 polypeptides. They are messenger molecules that are involved in a variety of physiological functions. One of the key functions is the immune system. This link explains that T cells that have vitamin D receptors can develop into cytotoxic T cells (also known as “killer T cells”). They are important in fighting cancer, but also parasites.

The key is that the hormone vitamin D can release more than 100 polypeptides that have the power to fight virus attacks including the Covid-19 coronavirus.

Three mechanisms how vitamin D works against the virus

The researchers outlined 3 mechanisms of how vitamin D works:

  • Maintaining tight epithelial junctions making it more difficult for the Covid-19 coronavirus to penetrate.
  • “Killing enveloped viruses through induction of cathelicidin and defensins.” These powerful antiviral polypeptides can kill viruses that have invaded the blood stream within 1 to 2 days.
  • “…And reducing production of proinflammatory cytokines by the innate immune system, thereby reducing the risk of a cytokine storm leading to pneumonia.” It is people who get the viral pneumonia that are at a high risk of death. By bringing the blood level up to the higher range of normal, between 50 and 80 ng/mL, patients that have encountered Covid-19 coronavirus are more likely to survive.

Two polypeptides, cathelicidin and defensins

Again, I like to emphasize that it is not vitamin D that has a direct effect on the virus. It is two polypeptides, cathelicidin and defensins, which are powerful antiviral polypeptides, that are released by vitamin D.

They can kill viruses that have invaded the blood stream and can eliminate the cytokine storm. This all happens very fast, within only 1 to 2 days. But you have to have an adequate vitamin blood level for this to occur (about 50-80 ng/mL).

Sources of vitamin D

First of all, vitamin D is readily absorbed from food. But there are not many foods that contain enough vitamin D for the immune system. The ones that contain vitamin D are as follows:

  • “Fatty fish, like tuna, mackerel, and salmon.
  • Foods fortified with vitamin D, like some dairy products, orange juice, soy milk, and cereals.
  • Beef liver.
  • Cheese
  • Egg yolks. “

Sun induced amount of vitamin D

Secondly, vitamin D can be synthesized in the skin from exposure to sunlight. But for this to happen all the necessary enzymes need to be present.  This link explains that many older people above the age of 65 have low vitamin D blood levels because of a lack of sun exposure and a lack of cutaneous synthesis because of enzyme issues.

Vitamin D supplements

The most reliable source of vitamin D are vitamin D3 supplements. When people supplement with the same dose of vitamin D3 there will be people who get higher vitamin D blood levels than others, as absorption in the gut is different for different people.  The ones who have relatively low vitamin D blood levels are often called “slow vitamin D absorbers”. But when the vitamin D3 dosage is increased even those people will reach the recommended high normal range (50-80 ng/mL).

Vitamin D blood level

The vitamin D blood test has the scientific name “25-hydroxy vitamin D level”. This is now the recognized gold standard for determining who is deficient or has normal levels with respect to vitamin D. The following 2013 publication has studied the vitamin D level of 1,470 healthy Swiss men and women, 60 years or older. Vitamin D levels were classified as severely deficient when the level was below 10 ng/mL. The vitamin D level was deficient between 10 and 20 ng/mL. The level was insufficient when between 21 and 29 ng/mL. A level above 30 ng/mL is normal.

8 % of the subjects were severely insufficient and 66% had insufficient vitamin D levels. Only 26.1% of the subjects had normal levels. Over 50% of healthy older Swiss (above the age of 70) had insufficient vitamin D levels.

Which vitamin D level is safe and which is not?

A peer-reviewed publication of the effects of vitamin D in health and disease contains 269 references.

What vitamin D level is optimal? This question was reviewed in this paper.

  • Below 15 ng/mL the immune system is paralyzed
  • With a level above 30 ng/mL the immune system is working
  • A level of 50-80 ng/mL has the immune system working optimally
  • Above 150 ng/mL toxic vitamin D levels start
  • With 300 ng/mL severe toxicity begins

Vitamin D toxicity

It is only with high levels of vitamin D (more than 150 ng/mL) that you have to worry about high calcium levels in the blood or kidney stones (toxic levels). But the key is to not exceed 80 ng/mL regarding the vitamin D blood level. This gives you a lot of flexibility before you reach toxic levels (above 150 ng/mL). For those who want more information, here is a thorough, peer reviewed publication about vitamin D toxicity with 59 references.

Vitamin D supplement compliance

The question is why not more people take adequate vitamin D3 supplements.  We know that vitamin D can prevent so many chronic diseases including serious viral infections. The answer is complex, but it includes a fear of the population of vitamin toxicity (kidney stone and high calcium levels). However, as pointed out before, this occurs only above a vitamin D level of 150 ng/mL. With proper vitamin D blood level monitoring you never reach toxic levels of vitamin D.

Denial

Denial likely is another major factor. People feel that if they have a balanced diet, they would be protected from vitamin D insufficiency. As pointed out before this is a grave error to think as our food does not contain sufficient vitamin D to strengthen our immune system.

False security with low doses of vitamin D

Finally, there are people who think that low doses of vitamin D, like 1000 IU of vitamin D daily, would be enough. But it is not enough. This is why testing vitamin D blood levels is so important. It is a reality check. The blood level must be in the high normal range (50-80 ng/mL). At this level the immune system functions optimally.

Compliance issues

In this context there was an interesting study done by LifeExtension, a company that publishes monthly health magazines. In this study the company examined the vitamin D blood levels of LifeExtension members. They are the ones who should be knowledgeable in how important it is to have good, preventative vitamin D blood levels. The study showed that 38% of the vitamin D test results were less than 30 ng/mL. In addition, 69% of the vitamin D tests were less than 40 ng/mL. Finally, 85% of the vitamin D test results were less than 50 ng/mL. What this means is that LifeExtension members were non-compliant when it came to taking regular adequate vitamin D3 doses. This resulted in levels that were too low for the majority to protect them from the Covid-19 coronavirus.

Covid-19 coronavirus infections and vitamin D blood level

There is a tight relationship between vitamin D blood levels and the strength of the immune system. Essentially, coronavirus mortality measures who is vitamin D deficient. Without enough vitamin D on board the virus penetrates into the blood stream and penetrates the lining of the respiratory tract. Next the cytokine storm develops, which leads to viral pneumonia. Higher doses of vitamin D3 will mitigate the course of Covid-19 coronavirus.

Adequate Vitamin D Level Strengthens the Immune System

Adequate Vitamin D Level Strengthens the Immune System

Conclusion

The Covid-19 coronavirus pandemic has taught us how important an intact immune system is to survive the virus when you get it. We do know for some time how closely related a good vitamin D level is with the functioning of the immune system. I have reviewed here what a desirable vitamin D level is and how we can achieve this with oral vitamin D3 supplements. The goal is to achieve a vitamin D level in the upper range of normal (50-80 ng/mL). With a level like this the virus cannot penetrate the mucous membranes of the respiratory tract and even if it did, it cannot produce a cytokine storm in the blood that would lead to the deadly viral pneumonia or to blood clots. When the virus invades the bloodstream, vitamin D releases powerful antiviral polypeptides that can kill viruses within 1 to 2 days.

Literature

Here are some peer-reviewed publications on vitamin D: