Researchers sought to determine whether a comprehensive and personalized program, designed to mitigate risk factors of Alzheimer's disease could improve cognitive and metabolic function in individuals experiencing cognitive decline. Findings provided evidence that this approach can improve risk factor scores and stabilize cognitive function.
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Researchers have for the first time identified stem cells in the region of the optic nerve, which transmits signals from the eye to the brain. The finding presents a new theory on why the most common form of glaucoma may develop and provides potential to treat a leading cause of blindness.
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A new study that followed 400 households after the 2015 Nepal earthquakes provides insight into better understanding the factors that contribute to resilience and change in short-term rural natural disaster recovery.
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Atrial fibrillation (afib) is a common heart rhythm disorder in which the upper chambers of the heart (the atria) beat fast and irregularly. Afib commonly causes recurrent symptoms, usually palpitations and shortness of breath, and can negatively affect quality of life. Afib also substantially increases the risk of stroke, and is also associated with heart failure, high blood pressure, and diabetes. People with afib routinely require lifelong treatment with blood thinners, to prevent blood clots that can lead to strokes.
Doctors are only recently understanding the importance of lifestyle factors in treating afib. Modifiable lifestyle factors are so important and under-recognized that the American Heart Association (AHA) recently released a scientific statement summarizing the latest research on this topic. The AHA wants both doctors and patients to understand the relationship between lifestyle and afib, and to work as a team to put these lifestyle factors into practice. Following is a discussion of important lifestyle factors, how they may impact afib, and what you can do.
Obesity
One of the strongest factors associated with afib is body weight. Obesity (defined as body mass index [BMI] > 30) has been shown in multiple studies to be linked to the development of afib. Obesity is associated with changes to electrical signaling within the atria, as well as structural changes to the heart’s upper chambers. Overeating can also cause inflammation via changes in hormone and cell-signaling pathways in the atria. Several studies have shown that as we gain weight, fat is deposited in the heart (as well as other places throughout the body), and this can trigger arrhythmias, most commonly afib.
Obesity can also be a cause of new or worsening hypertension (high blood pressure), which promotes further structural changes in the heart. Obesity also can cause obstructive sleep apnea and diabetes, both of which independently increase risk of afib.
The good news is that for people who are overweight or obese, just a 10% reduction in weight seems to improve symptoms related to afib.
Exercise
For decades cardiologists have encouraged people to exercise, because exercise reduces the risk of dying from cardiovascular causes. Not only is exercise good, but physical inactivity is actually detrimental; a sedentary lifestyle contributes to afib and may actually be an independent predictor of this condition. The AHA recommends 150 minutes per week of moderate-intensity aerobic exercise, or 75 minutes per week of vigorous-intensity aerobic exercise, to improve cardiovascular health. Regular exercise helps to prevent atrial fibrillation and, if you already have afib, reduces symptoms and improves afib-related quality of life.
If you are not already exercising, talk to your physician about starting a low-intensity exercise program. Brisk walking is a great form of moderate exercise and allows for physical distancing. Start with 20 minutes a day and gradually increase your pace and duration to achieve at least 150 minutes per week of moderate-intensity activity.
Sleep disorders
Obstructive sleep apnea (OSA) is a sleep disorder in which people stop breathing for short periods while they are sleeping. It is the most common form of sleep-disordered breathing and is strongly associated with cardiovascular disease. There is also a very high prevalence of OSA in people with afib, and recurrence of afib symptoms is higher in people with more severe OSA.
Cardiologists now routinely screen people with recurrent afib symptoms for OSA. Treating OSA with continuous positive airway pressure (CPAP) appears to improve afib symptoms.
If you experience afib symptoms, ask your doctors if you should have a sleep study to check for OSA.
Alcohol
Alcohol is a known risk factor for atrial fibrillation, and there is mounting evidence that the old adage “less is more” may be true for drinking if you have afib. A recent study in the New England Journal of Medicine found less afib when patients decreased or abstained from alcohol.
If you have afib, try cutting back on alcohol, or even not drinking at all. Talk to your doctor if you are having trouble reducing your alcohol consumption.
Diabetes
The risk of afib is higher in patients with type 2 diabetes. While the mechanism is not well understood, it’s likely that elevated blood sugars directly damage the heart and promote structural, electrical, and autonomic changes within the heart tissue.
The good news is that better blood sugar control improves both the severity and frequency of afib symptoms. Lifestyle changes that promote exercise and limit inactivity can also help with weight loss and blood sugar control.
Diet
Dietary changes can translate into weight loss, and also help to control blood sugar if you have diabetes. Changing your diet can be challenging, but eating less processed foods and more fresh vegetables and fruit is a good starting place. Target bad habits, like snacking or eating out of boredom. And consider transitioning to a Mediterranean diet, which helps control weight, blood sugar, and blood pressure.
When we say someone has a quick mind, it may be in part thanks to our expanded cerebellum that distinguishes human brains from those of macaque monkeys, for example. High-res imaging shows the cerebellum is 80% of the area of the cortex, indicating it has grown as human behavior and cognition evolved.
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The number of adults in the United States who suffer from major depressive episodes at some point in their life is far higher than previously believed, a new study finds.
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Researchers have been able to dial up and down creatures' lifespans by altering the activity of proteins found in roundworm cells that tell them to convert sugar into energy when their cellular energy is running low. Humans also have these proteins, offering up the intriguing possibilities for developing longevity-promoting drugs.
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The number of adults in the United States who suffer from major depressive episodes at some point in their life is far higher than previously believed, a new study finds.
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Researchers have revealed the multiple, intertwined cell death systems that prevent the spread of the 'intracellular' bacterium Salmonella, an important cause of typhoid fever which kills more than 100,000 people annually.
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For this study, the 3D brain organoid was used to model the effects of oxygen deprivation and inflammation on blood brain barrier function to better understand what is happening in a human brain during an ischemic stroke.
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Compounds tested for their potential as antibiotics have demonstrated promising activity against one of the deadliest infectious diseases - tuberculosis (TB).
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Researchers have discovered another set of pore-like holes, or channels, traversing the membrane-bound sac that encloses the deadliest malaria parasite as it infects red blood cells. The channels enable the transport of lipids -- fat-like molecules -- between the blood cell and parasite, Plasmodium falciparum. The parasite draws lipids from the cell to sustain its growth and may also secrete other types of lipids to hijack cell functions to meet its needs.
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More than 200 genes with novel and known roles in glioblastoma - the most aggressive type of brain cancer - offer promising new drug targets. Researchers engineered a new mouse model to show for the first time how a mutation in the well-known cancer gene, EGFR initiates glioblastoma, and works with a selection from more than 200 other genes to drive the cancer.
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Of the CRISPR-Cas9 tools created to date, base editors have gotten lots of attention because of their seemingly simple editing: they neatly replace one nucleic acid with another, in many cases all that should be needed to fix a genetic disease. Scientists have now determined the structure of the latest base editor as it swaps out nucleic acids, showing why it can go off target but also how it can be improved.
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People who laugh frequently in their everyday lives may be better equipped to deal with stressful events - although this does not seem to apply to the intensity of laughter.
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The debate about the origin of SARS-CoV-2 continues, as does the debate over whether the pandemic could have been quashed had Chinese authorities acted and shared information about the outbreak sooner.
According to a Hong Kong whistleblower scientist who has fled to the U.S., the Chinese government and World Health Organization representatives in Hong Kong covered up the Wuhan outbreak, allowing it to spread unchecked around the world.
In the featured Fox News interview, the whistleblower, Dr. Li-Meng Yan — who worked at the University of Hong Kong School of Public Health, a top coronavirus research lab — claims her early investigation into the SARS-like outbreak in Wuhan could have helped prevent a global pandemic from developing, had her supervisors shared her findings.
Yan claims her supervisor, WHO consultant Leo Poon, asked her to, secretly, investigate reports of a SARS-like illness spreading in Wuhan, China, in late December 2019. The Chinese government had refused overseas experts from getting involved, and Poon wanted her to figure out what was really going on.
Human-to-Human Spread Was Recognized From the Start
Yan, who has many professional colleagues in China, turned to a friend who works in the Chinese Center for Disease Control and Prevention and had first-hand information about the outbreak. Yan was told there was likely human-to-human transmission occurring, as they had found family clusters of cases.
The WHO, meanwhile, did not confirm the human-to-human spread potential for several weeks. On the contrary, an official WHO statement said the virus "does not transmit readily between people." In a Tweet, WHO also stated that preliminary investigations by Chinese authorities "found no clear evidence of human-to-human transmission."
January 16, 2020, Yan was again asked to reach out to her contacts in China to see if she could learn more. Her CDC contacts were fearful, but it became clear that patients and front-line doctors were not being properly protected, and that Chinese authorities were trying to keep a lid on the flow of information.
When she updated Poon, he told her to stay silent and not cross the Chinese government, or else they'd both be "disappeared." Yan felt it was crucial to inform the public, but Poon took no action. The co-director of the University of Hong Kong School of Public Health laboratory, professor Malik Peiris, also stayed quiet.
Yan believes WHO colluded with the China Communist Party (CCP) government to prevent information about the virus from coming out. The WHO quite predictably denies her claims.
Yan describes how, since her escape, the CCP has been trying to smear her name and ruin her professional reputation, saying she's been kidnapped by Americans, and even that she has a mental disorder. Her professional webpages and affiliations have been deleted and removed.
Yan Doesn't Provide Any Shocking Revelations
On the whole, though, Yan doesn't really tell us anything we didn't already know. It's been clear that China delayed telling the public about the Wuhan outbreak. She doesn't indicate having any information about the virus' origin, and she certainly does not provide any useful recommendations for how to protect ourselves.
In fact, she parrots the recommendations of most governments — staying 6 feet apart, using alcohol-based disinfectants and wearing surgical masks. Aside from disinfectants, which may be useful for killing viruses on hands and surfaces, social distancing and mask wearing have no basis in actual science.
Of course, the Chinese have been known to wear face masks in public for some time, but they've primarily been worn to protect the wearer against air pollution1,2 — not infectious disease. Just because masks prevent inhalation of dangerous air pollution does not mean they work against viruses.
All of that said, she's certainly correct when saying that the CCP's attempts to keep details of the Wuhan outbreak from the public allowed the virus to spread, not only through China but also across the world.
SARS-CoV-2 Did Not Evolve Naturally, Scientists Say
With regard to the origin of SARS-CoV-2, scientists keep finding more clues indicating it's not a naturally-evolved virus. Among them are two recent papers by Norwegian and British researchers Sørensen, Susrud and Dalgleish.
In the first paper,3 "A Candidate Vaccine for Covid-19 (SARS-CoV-2) Developed from Analysis of its General Method of Action for Infectivity," published in the journal Quarterly Review of Biophysics Discovery, they claim to have identified inserted sections in the spike surface that allows it to bind to and enter human cells.
According to the authors, "The SARS-CoV-2 spike is significantly different from any other SARS that we have studied."
The second paper,4 "The Evidence Which Suggests That This Is No Naturally Evolved Virus: A Reconstructed Historical Aetiology of the SARS-CoV-2 Spike," published by the Norwegian periodical Minerva,5,6 July 13, 2020, presents several arguments for why SARS-CoV-2 is likely to have been manipulated in the lab.
As in the first paper, the researchers stress anomalies in the spike protein of the virus. The abstract reads, in part:7
"… SARS-CoV-2 is possessed of dual action capability … The likelihood of this being the result of natural processes is very small. The spike has six inserts which are unique fingerprints with five salient features indicative of purposive manipulation.
We then add to the bio-chemistry a diachronic dimension by analysing a sequence of four linked published research projects which, we suggest, show by deduction how, where, when and by whom the SARS-CoV-2 Spike acquired its special characteristics. This reconstructed historical aetiology meets the criteria of means, timing, agent and place to produce sufficient confidence to reverse the burden of proof.
Henceforth, those who would maintain that the COVID-19 pandemic arose from zoonotic transfer need to explain precisely why this more parsimonious account is wrong before asserting that their evidence is persuasive, most especially when, as we also show, there are puzzling errors in their use of evidence."
US-China Collaborated on Coronavirus Research
Sørensen also highlights open source studies describing the creation of new chimeraviruses that have SARS-coronavirus as a base. For example, researchers have exchanged properties between bat coronaviruses and human SARS viruses. So, there can be no doubt that the technology and know-how exists. Minerva reporter Aksel Fridstrom writes:8
"Furthermore, Sørensen's article points to the fact that Wuhan's Virology Institute again in 2010 took part in gain-of-function experiments with international collaborators, where SARS-coronavirus was provided with additional properties that increase the virus's ability to infect humans."
In that research, an HIV pseudovirus was used to express seven bat ACE2 receptors. The binding properties of these bat ACE2 receptors were compared to human ACE2 receptors in order to determine which one would have the greatest ability to bind to and infect human cells.
The international collaborators in this case included researchers at the University of North Carolina. Five years later, in 2015, the University of North Carolina again collaborated with the Wuhan Institute of Virology, performing gain-of-function research in which bat viruses were manipulated to create a chimeric virus capable of binding to human upper airway cells. That particular virus was called SHC014-MA15.
"Sørensen and his co-authors write that this work created 'a chimeric virus with very high infectivity potential targeted to the human upper respiratory tract' and that what is being described is 'in fact, precisely SARS-CoV-2 properties,'" Fridstrom writes.9
Virus Origin Papers Are Being Shunned by Scientific Journals
One of the reasons Sørensen, Susrud and Dalgleish chose to publish their science paper in a magazine rather than a scientific journal is because of the difficulty getting papers about the virus' origin published. There's tremendous stigma attached to this topic.
The journal Nature was recently caught blocking accounts of people questioning the natural origin of SARS-CoV-2 on Twitter, and several papers discussing the lab origin theory or proposing genetic engineering are languishing on preprint servers, seemingly unable to get accepted for formal publication. Several such papers are mentioned in a July 16, 2020, GM Watch article.10
Sørensen, Susrud and Dalgleish had also already gotten the runaround on their first paper. Both the Journal of Virology and Nature rejected it, stating it was "unsuitable for publication." It was eventually accepted by Quarterly Review of Biophysics Discovery, a journal chaired by Stanford University and University of Dundee scientists.
Why COVID-19 Vaccines Are Likely to Fail
Importantly, in "A Candidate Vaccine for COVID-19 (SARS-CoV-2) Developed from Analysis of its General Method of Action for Infectivity,"11 Sorensen et.al. warn that current efforts to develop a COVID-19 vaccine are likely to fail since the etiology of the virus has been misunderstood:12
"These data reveal the biological structure of SARS-CoV-2 Spike and confirm that accumulated charge from inserts and salt bridges are in surface positions capable of binding with cell membrane components other than the ACE2 receptor.
We have also looked at the naked coronavirus spike protein as a concept for the basis of a vaccine, which we have rejected because of high risk of contamination with human-like epitopes.
Analysis of the Spike protein of SARS-CoV-2 shows 78.4% similarity with human-like (HL) epitopes. For the avoidance of confusion, a standard protein blast searches for functionalities and homologies to other proteins.
However, antibodies can only recognize 5-6 amino acids and therefore a 6 amino acid rolling window search for antibody epitopes was performed.
A search so tailored to match against all human known proteins will give a 78.4% human similarity to the SARS-CoV-2 Spike protein, i.e if all epitopes on the 1255 amino acid long SARS-CoV-2 Spike protein can be used by antibodies then there will be 983 antibody binding sites which also could bind to epitopes on human proteins.
This is what we did and found … [I]n the present context, any vaccine design based on the whole Spike protein of SARS-CoV-2 may not be immunogenic due its high human similarity compared to a vaccine with specifically selected NHL epitopes, such as Biovacc-19 does — and is.
COVID-19 candidate vaccines designed without appreciating these problems may run similar risks to those experienced with HIV vaccines that failed to show protection.
The possibility of inducing autoimmune responses or antibody-dependent enhancements, needs to be carefully guarded against because there is published evidence that an HIV candidate vaccine has actually enhanced infectivity:
'Vaccinations were halted; participants were unblinded. In post hoc analyses, more HIV infections occurred in vaccinees vs placebo recipients in men who had Ad5-neutralizing antibodies and/or were uncircumcised. Follow-up was extended to assess relative risk of HIV acquisition in vaccinees vs placebo recipients over time.'
Such antibody-dependent enhancement (ADE) has been observed for coronaviruses in animal models, allowing them to enter cells expressing Fc𝛾R. ADE is not fully understood: however, it is suggested that antibody-dependent enhancements may come as a result of amino acid variability and antigenic drift."
They also point out that choosing an adjuvant after the primary vaccine design work has been completed, which is how vaccine development is typically done, may be yet another serious mistake that could make a COVID-19 vaccine really dangerous.
Many Different Lab Origin Hypotheses Have Been Presented
Another scientist who questions the natural evolution theory is Jonathan Latham, Ph.D., a molecular biologist and virologist. In a June 2, 2020, Independent Science News article,13 Latham and Allison Wilson, Ph.D., a geneticist, dissect the zoonotic origin theory, showing the research simply does not support this claim.
While they do not dispute the idea that SARS-CoV-2 started out as a bat coronavirus at some point, they dispute the mechanism by which it supposedly gained the ability to infect humans. In his article, Latham lays out several different lab origin hypotheses, which are also reviewed in my interview with him, featured in "Cover-Up of SARS-CoV-2 Origin?"
Is SARS-CoV-2 Really a Novel Virus?
Latham and Wilson continue their search for the truth in a July 15, 2020, Independent Science News article.14
"… enormous scientific attention has been paid to the molecular character of the SARS-CoV-2 virus, including its novel genome sequence in comparison with its near relatives," Latham writes.
"In stark contrast, virtually no attention has been paid to the physical provenance of those nearest genetic relatives, its presumptive ancestors, which are two viral sequences named BtCoV/4991 and RaTG13."
According to Latham, SARS-CoV-2 may not be an entirely novel virus after all. A highly conserved close ancestor, BtCoV/4991, has been listed in the database for seven years and has been featured in the published literature. When the Wuhan lab later resequenced this sample, they simply renamed it, thereby obscuring its history.
As Latham explains in his article15 — which I encourage you to read in its entirety — BtCoV/4991 was found in samples collected in a mineshaft in Yunnan province, China in 2012-2013.
The samples were collected after six miners contracted a strange respiratory illness that sound remarkably similar if not identical to COVID-19. Three of them died. While the disease had only been described in a Chinese thesis written by the doctor who treated the miners, Latham had the thesis translated into English.
"The evidence it contains has led us to reconsider everything we thought we knew about the origins of the COVID-19 pandemic," Latham writes.16"It has also led us to theorize a plausible route by which an apparently isolated disease outbreak in a mine in 2012 led to a global pandemic in 2019.
The origin of SARS-CoV-2 that we propose below is based on the case histories of these miners and their hospital treatment. This simple theory accounts for all the key features of the novel SARS-CoV-2 virus …"
Key features Latham and Wilson believe can be explained by their theory include:
The origin of the novel furin cleavage site on the virus' spike protein that enhances its spread in the human body
The "exceptional affinity of the virus spike protein for human receptors"
The virus' lack of evolution since the pandemic began
The reason SARS-CoV-2 targets the lungs
While they do not claim SARS-CoV-2 was genetically engineered, they believe gain-of-function research performed at the Wuhan Institute of Virology played "an essential causative role in the pandemic."
The Mojiang Miners Passage Hypothesis
Latham and Wilson go on to explain their hypothesis, which they've dubbed the Mojiang miners passage (MMP) hypothesis. Again, I recommend reading the original article, but for your edification, I've chosen to quote a larger than usual section to summarize it for you:
"We suggest, first, that inside the miners RaTG13 (or a very similar virus) evolved into SARS-CoV-2, an unusually pathogenic coronavirus highly adapted to humans. Second, that the Shi lab used medical samples taken from the miners and sent to them by Kunming University Hospital for their research. It was this human-adapted virus, now known as SARS-CoV-2, that escaped from the WIV in 2019 …
Passaging is a standard virological technique for adapting viruses to new species, tissues, or cell types. It is normally done by deliberately infecting a new host species or a new host cell type with a high dose of virus. This initial viral infection would ordinarily die out because the host's immune system vanquishes the ill-adapted virus.
But, in passaging, before it does die out a sample is extracted and transferred to a new identical tissue, where viral infection restarts. Done iteratively, this technique … intensively selects for viruses adapted to the new host or cell type …
We agree that ordinary rates of evolution would not allow RaTG13 to evolve into SARS-CoV-2 but we also believe that conditions inside the lungs of the miners were far from ordinary. Five major factors specific to the hospitalized miners favored a very high rate of evolution inside them.
The lungs of the miners, we suggest, supported a very high viral load leading to proportionately rapid viral evolution. Furthermore, according to the Master's thesis, the immune systems of the miners were compromised and remained so even for those discharged. This weakness on the part of the miners may also have encouraged evolution of the virus …
In support of the MMP theory we also know something about the samples taken from the miners. According to the Master's thesis, samples were taken from patients for 'scientific research' and blood samples (at least) were sent to the WIV …
The logical course of such research would be to sequence viral RNA extracted directly from unfrozen tissue or blood samples and/or to generate live infectious clones for which it would be useful (if not imperative) to amplify the virus by placing it in human cell culture. Either technique could have led to accidental infection of a lab researcher …
We propose that, when frozen samples derived from the miners were eventually opened in the Wuhan lab they were already highly adapted to humans to an extent possibly not anticipated by the researchers. One small mistake or mechanical breakdown could have led directly to the first human infection in late 2019.
Thus, one of the miners, most likely patient 3, or patient 4 (whose thymus was removed), was effectively patient zero of the COVID-19 epidemic. In this scenario, COVID-19 is not an engineered virus; but, equally, if it had not been taken to Wuhan and no further molecular research had been performed or planned for it then the virus would have died out from natural causes, rather than escaped to initiate the COVID-19 pandemic."
As discussed in "Bioweapon Labs Must Be Shut Down and Scientists Prosecuted," the COVID-19 pandemic should be a wake-up call for the world to reconsider the wisdom of gain-of-function research. Lab escapes are guaranteed to occur, sooner or later. We got lucky this time, in the sense that SARS-CoV-2 is far less deadly than initially feared. But the government response to the pandemic has been devastating.
Global shut-downs have taken a massive toll on mental and financial health, not to mention the global economy as a whole. Could we survive as a species if something with a really high lethality were to get out? These are crucial questions that deserve public discussion and close scrutiny by lawmakers.
The benefits of vitamin D have been well-documented over the years. I believe that getting your vitamin D status optimized to between 60 ng/mL and 80 ng/mL is one of the best things you can do to help protect yourself against the fall infectious disease season, which is expected to include both flu and COVID-19.
Health authorities are warning of a second wave of COVID-19, which means the time to start addressing your vitamin D level is now. But, as important as it is to get your level optimized by fall, it's just as important to keep it there throughout the year.
Ideally, your body makes vitamin D when your skin is exposed to sunlight. This is why it's also called the sunshine vitamin.1 The best indicator of your vitamin D level is a blood test measuring the concentration of 25-hydroxy vitamin D, also called 25-OH vitamin D.2
In addition to the crucial role it plays in your immune system, researchers have also found that it's integral to optimizing leptin levels, which in turn are linked to obesity.3 In one study, researchers measured vitamin D and metabolic markers in two age- and gender-matched groups.4
They learned that individuals with deficient or insufficient vitamin D had a higher risk of metabolic syndrome. The results from several studies have also revealed a link between low levels of vitamin D and nonalcoholic fatty liver disease, although the results have not been consistent.
Foot Pain Associated With Knee or Hip Osteoarthritis
Recently, insufficient levels of vitamin D have been associated with foot pain linked to knee osteoarthritis (OA). Before delving into the results of the research, it's important to understand the relationship between low back pain and foot pain associated with severe knee OA.
In a study from 2010, researchers found that those who had OA in the knee and had pain in other joints in the body, were more likely to experience more intense knee pain.5,6 More specifically, the researchers found that when pain was present in the lower back, foot and elbow on the same side as the affected knee, the individual rated their knee pain as more severe than those who did not have pain in other joints.
The study was led by a physician from Harvard Medical School and involved the use of data from the Osteoarthritis Initiative, a study of knee OA involving people from several locations in the northeastern area of North America. The researchers included 1,389 participants who were between 45 and 79 years of age. The results showed that 57.4% had pain in their lower back, and those same individuals had a higher pain score in their knee.
Another group of participants from the same initiative and in the same age range were gathered for a second study.7 Researchers evaluated 1,255 individuals who had symptoms of knee pain related to OA. They noted that 25% of them had foot pain and the majority of those had pain in both feet.
After adjusting for confounding variables, they discovered that people who had foot pain also had lower scores on other health measures compared to those who did not have pain. Those who had bilateral or ipsilateral pain had lower health scores. This suggested that the side of the body where the foot pain occurred was important.
In a third study published in the Journal of the American Podiatric Medical Association, scientists also evaluated the side of the body where foot pain occurred and compared it to the presence of knee OA.8 One author commented about the importance of this identification:9
"The study shows that a physician evaluating a patient for foot pain should also ask about possible hip or knee pain, and vice versa, so we can address all of a patient's issues. In medicine, many times it comes down to 'what does your MRI look like or what does your x-ray look like?'
But it's really important to conduct a thorough medical history and physical exam. A comprehensive orthopedic evaluation may prompt a broader treatment strategy and possibly a referral to another specialist."
Vitamin D May Reduce Pain Level
People with knee OA may experience mild, moderate or severe pain.10 The Arthritis Foundation compares pain medications used for osteoarthritis listing nonsteroidal anti-inflammatories (NSAIDS), acetaminophen and injections of steroids or hyaluronic acid as treatments.11
In some cases, antidepressants are used to treat chronic pain, such as Duloxetine (Cymbalta).12 In all cases, the medications have a long list of side effects. In one study, comparisons were made between NSAIDs and opioids, a drug with known addictive properties, to relieve OA pain. Researchers found that both types of medication reduced pain and the effects were nearly identical.13
When the use of opioids use has been measured across counties, researchers have found that where there is a higher prevalence of disability and arthritis, there is also a higher rate of opioid prescriptions.14
In a recently published study, researchers sought to determine whether sufficient levels of vitamin D could lower foot pain in those with knee OA.15 Using data from a randomized, double-blind placebo-controlled study they undertook a post-hoc data analysis.16
Members of the group were randomly assigned to receive either a monthly dose of vitamin D3 or a placebo for two years. The participants had a mean age of 63.2 years. Of the 413 who were enrolled, 340 completed the study. The researchers used the Manchester Foot Pain and Disability Index (MFPDI) to rate the patients' perceived pain. At the start of the study 23.7% had disabling foot pain.
The data showed greater improvement in people receiving vitamin D and in those who maintained a sufficient level of vitamin D. They concluded that "supplementation and maintenance of sufficient vitamin D levels may improve foot pain in those with knee OA."17 In an article published in Rheumatology Advisor, it was noted that the study had several limitations, one of which may have significantly underestimated the results:18
"The study had several limitations, including those secondary to a post-hoc analysis, lack of data on the clinical importance of the differences in MFPDI scores, and potential underestimation of the benefits of vitamin D, as >60% of patients in placebo group had sufficient vitamin D levels at the end of follow-up."
Slow Osteoarthritis Progression With Omega-3 Fats
A second nutrient the body uses to prevent or slow the progression of OA is omega-3 fat. Dietary fat is essential to good health. While eating too much or not enough is damaging, without healthy fat your body does not work properly.19
Polyunsaturated fats (PUFA) are one type of essential fat, which means you must eat them since the body doesn't make them. The two main types of PUFAs are omega-3 and omega-6.
Both must be consumed in the right amounts or you may develop chronic inflammation. You'll find high concentrations of omega-6 in processed food, and corn, safflower and sunflower oils. While the ideal ratio is 1-to-1, most who eat a Western diet are getting 16 times more omega-6 than is considered healthy.20
As I've written recently, one of the problems with chronic inflammation may be that it promotes the damaging and dangerous cytokine storm found in those with severe COVID-19. The omega-3 index is a measure of omega-3 fat in the blood, or specifically in the red blood cell membranes. It is given as a percentage, with 8% or higher being ideal, putting you in the lowest risk zone.21
In a global meta-analysis of past studies measuring omega-3 levels, the researchers found areas with "very low blood levels (less than or equal to 4%)" included North, Central and South Americas, Europe and Africa.22
This is important since the balance of omega-3 and omega-6 can help regulate inflammation23 and slow the progression of OA after an injury,24 as demonstrated in animal studies. In naturally occurring OA, animals fed a diet rich in omega-3 reduced OA by 50% over those fed a standard diet.25
In a human trial, researchers found that supplementing with fish oil did not change the cartilage volume in knee osteoarthritis, but it did reduce the participants' pain scores over two years.26 Additionally, researchers have discovered a link between OA and metabolic syndrome.27
While metabolic syndrome increases the risk for OA, balancing your omega-3-to-omega-6 ratio can help reduce the potential risk of metabolic syndrome. The authors of one recent meta-analysis concluded:28
"The present meta-analysis indicates that higher intakes of omega-3 PUFAs, but not omega-6 PUFAs, was associated with lower MetS risk; adding to the current body of evidence on the metabolic health effects of circulating/dietary omega-3 PUFAs."
In a second paper, the authors wrote:29
"Lately, an inverse relationship between omega-3 fatty acids, inflammation, obesity and CVDs has been demonstrated … Omega-3 PUFAs have been shown to decrease the production of inflammatory mediators, having a positive effect in obesity and diabetes mellitus type-2. Moreover, they significantly decrease the appearance of CVD risk factors."
Based on these studies, it's apparent that omega-3 has an impact on OA pain and that it can slow the progression of OA as well as help prevent metabolic syndrome, which also raises the risk of OA.
Number of People With Osteoarthritis Has Doubled
The authors of a study published by Harvard University found that people currently living in America were more than two times more likely to have knee osteoarthritis than those who lived there before World War II. They looked at more than 2,000 skeletons with the goal of determining the age of the disease.30
Interestingly, there was a rise in disease after confounding factors were accounted for, such as longer life and the meteoric rise in rates of obesity since 1940.31 The researchers controlled for age and body mass index and still found a significant rise in people with OA. One author was quoted in the Harvard Gazette, saying:32
"We were able to show, for the first time, that this pervasive cause of pain is actually twice as common today than even in the recent past. But the even bigger surprise is that it's not just because people are living longer or getting fatter, but for other reasons likely related to our modern environments. Knee osteoarthritis is not a necessary consequence of old age. We should think of this as a partly preventable disease."
In the skeletons of people over the age of 50, the data showed knee osteoarthritis was 2.6 times more common in those who were born in the post-industrial age, as compared to those born in the late 1800s.33 The researchers also found the rate of OA in both knees in the post-industrial era was 1.4 times higher.
If you are among those who have OA, consider using vitamin D3 supplements to raise your serum levels. It is important to include vitamin K2 MK-7 for reasons I discuss in "What Are the Health Benefits of Vitamin K2?", including reducing your risk of atherosclerosis.
Steady progress in reducing the rates of premature cardiac death in the US began slowing in 2011, largely due to rising rates of out-of-hospital premature cardiac deaths, especially among younger adults. County-level disparities in premature cardiac death rates across the US have widened over the past two decades.
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In a pilot study of people living with HIV or high levels of cholesterol, researchers found that a six-week course of a cholesterol-lowering medication improved the function of the coronary arteries that provide oxygen to the heart.
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Even short, single antibiotic courses given to young animals can predispose them to inflammatory bowel disease (IBD) when they are older, according to new researchers. The study provides further evidence supporting the idea that the use of antibiotics in children under 1 year old disrupts the intestinal microbiota - the trillions of beneficial microorganisms that live in and on our bodies - that play a crucial role in the healthy maturation of the immune system and the prevention of diseases.
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As the summer warmth lures us outside, parents may be struggling to get their teenagers to follow sun protection guidelines. It can be challenging to catch the attention of younger people, for whom health concerns such as skin cancer feel like a lifetime away. One promising strategy for educating teens about sun-protective behavior is to appeal to their vanity and meet them where they are — on their smartphones.
Mobile app reveals possible effects of UV exposure
A recent study in JAMA Dermatology looked at the impact of using a face-aging mobile application on sun-protective behaviors in a group of Brazilian high school students. The face-aging mobile app used in the study, called Sunface, allows the user to take a selfie and shows what they might look like in five, 10, 15, 20, and 25 years, based on three levels of exposure the user selects: sun protection, no sun protection, and weekly tanning.
The face-aging mobile app modifies selfies by adding skin changes from chronic ultraviolet (UV) radiation exposure, such as from the sun or tanning beds. Signs of photoaging (premature aging of the skin from chronic sun exposure) include brown spots, increased facial wrinkles, uneven skin pigmentation, enlarged or broken blood vessels, and actinic keratoses (gritty rough spots that are precursors to skin cancer). While the accuracy of the face-aging app algorithm is unclear, it creates a reasonable facsimile of the effects of chronic sun exposure.
Study finds teens may be motivated by vanity
The JAMA Dermatology study authors divided the high school students into two categories. One group of students was shown the effects that UV exposure could have on their future faces via the app. The app also provided information about sun protection. The control group did not receive any intervention or sun protection education. At the start of the study, the researchers collected information from all study participants about their sunscreen application, tanning bed use, and performance of skin self-examinations. They then followed the students over six months to re-assess for changes in baseline behaviors. The study was led by the app developer.
In the face-aging app group, the percentage of students using sunscreen every day increased from 15% at the start of the study to 22.9% at the six-month follow up. There was no increase in sunscreen use in the control group. There was also an increase in the proportion of students in the face-aging app group who performed at least one skin self-examination during the six months of follow-up. There was no corresponding increase in the control group. Finally, while use of tanning beds had decreased in the mobile app group at the three-month follow up, tanning bed use returned to nearly baseline six months after students used the face-aging app. This is troubling, because indoor tanning increases the risk of skin cancers, including the deadliest form, melanoma.
The face-aging app had greater impact on high school girls, meaning boys were less likely to be motivated by appearance-based educational efforts. Over a lifetime, men are more likely than women to develop and die from melanoma, so other methods are needed to promote sun-safe behaviors in teenage boys.
One limitation of the study is that because students in the control group did not receive any basic sun protection education, it is not 100% clear whether the app’s face-aging simulation, the UV protection information provided by the app, or some combination of the two was responsible for the study findings.
Early sun-protective behaviors can have a lasting impact
Early sun-protective behaviors can have a lasting impact on the development and appearance of photoaging, and can reduce the risk of developing skin cancer. Beginning in infancy, children should be kept out of direct sunlight and covered with sun-protective clothing with an ultraviolet protective factor of 50+. Sunscreens are safe for infants starting at 6 months.
During adolescence and beyond, a tanned appearance is often associated with youthfulness and health. Instead of using a tanning bed, opt for a sunless tanning cream to achieve a similar effect — but be sure to apply a sunscreen, since tanning creams generally don’t contain sun-protective factor unless explicitly stated on the label. Another option is to apply a tinted sunscreen.
The following tips can help reduce photoaging and risk for skin cancer.
Avoid peak hours of the sun’s intensity (generally between 10am and 2pm) and seek shade when outdoors.
Wear sunscreen, even when it’s cloudy, raining, or snowing:
broad-spectrum UVA/UVB coverage
SPF 30+, which blocks 97% of the sun’s rays (no sunscreen blocks 100% of the rays)
water-resistant (be sure to reapply every two hours when outside or after getting wet or toweling off)
Wear sun-protective clothing (UPF 50+) like broad-brimmed hats, long-sleeved shirts, and pants.
Researchers have discovered that children younger than 5 years with mild to moderate COVID-19 have much higher levels of genetic material for the virus in the nose compared to older children and adults. The findings point to the possibility that the youngest children transmit the virus as much as other age groups.
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Researchers have reported a new form of electronics known as 'drawn-on-skin electronics,' allowing multifunctional sensors and circuits to be drawn on the skin with an ink pen.
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A leading COVID-19 vaccine candidate raised neutralizing antibodies and robustly protected non-human primates (NHPs) against SARS-CoV-2, the virus that causes COVID-19.
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Wealthier communities went from being the most mobile before the COVID-19 pandemic to the least mobile, while poorer areas have gone from the least mobile to the most mobile, according to a new study.
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Researchers conducted the world's first data-driven study of parenting classes based on the Respectful Approach intervention. The Respectful Approach, modeled on Resources for Infant Educators (RIE)TM, guides parents to treat young children as capable and independent humans who can flourish if given safe space and freedom from too much adult direction.
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New research shows that children only learn to do jigsaw puzzles once they have reached a certain stage of development. Three-year-olds use trial and error, but four-year-olds are able to use information in the picture to complete the puzzles. The research team say this understanding is the foundation of learning to draw and paint.
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Music training does not have a positive impact on children's cognitive skills, such as memory, and academic achievement, such as maths, reading or writing, according to a study published in Memory & Cognition.
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Children in low-income neighborhoods in Baltimore tended to have more asthma symptoms when levels of the synthetic chemical BPA (Bisphenol A) in their urine were elevated, according to a new study.
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Research shows that insecticide-treated mosquito nets, the mainstay in the global battle against malaria, are not providing the protection they once did - and scientists say that's a cause for serious concern in tropical and subtropical countries around the globe.
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Right now, there are three types of COVID-19 tests:1
Molecular — Also known as a PCR (polymerase chain reaction) test, this test detects whether genetic material of the virus is present in the sample collected from your throat or sputum (the back of your sinuses)
Antigen — This test, sometimes referred to as "rapid test," detects viral proteins
Antibody — Also known as a serology test, it detects the presence of antibodies in your blood
The first two, molecular and antigen, are so-called "viral tests" that detect active infections, whereas the antibody test will tell you if you've developed antibodies in response to a previous coronavirus infection. It typically takes your body one to three weeks after an infection clears to start making antibodies against the virus in question.
Common Cold Can Trigger Positive COVID-19 Antibody Test
Each of these COVID-19 tests have their issues and controversies. The problem with antibody testing is that there are seven different coronaviruses known to cause respiratory illness in humans.2 Four of them cause symptoms associated with the common cold:
229E
NL63
OC43
HKU1
In addition to the common cold, OC43 and HKU1 — two of the most commonly encountered betacoronaviruses3 — are also known to cause bronchitis, acute exacerbation of chronic obstructive pulmonary disease and pneumonia in all age groups.4 The other three human coronaviruses — which are capable of causing more serious respiratory illness — are:
SARS-CoV
MERS-CoV
SARS-CoV-2
The tricky part is that the antibodies created by these different coronaviruses appear very similar, and the U.S. Centers for Disease Control and Prevention admits recovering from the common cold can trigger a positive antibody test for COVID-19, even if you were never infected with SARS-CoV-2 specifically. As explained on the CDC's "Test for Past Infection" web page:5
"Antibody tests check your blood by looking for antibodies, which may tell you if you had a past infection with the virus that causes COVID-19. Antibodies are proteins that help fight off infections and can provide protection against getting that disease again (immunity). Antibodies are disease specific …
A positive test result shows you may have antibodies from an infection with the virus that causes COVID-19. However, there is a chance a positive result means that you have antibodies from an infection with a virus from the same family of viruses (called coronaviruses), such as the one that causes the common cold."
Unclear if Cross-Reactive Antibody Tests Are Still Being Used
In a July 10, 2020, interview with KTTC news, Mayo Clinic chair of clinical microbiology, Dr. Bobbi Pritt, said:6
"Early on we had labs using tests that have not received that [U.S. Food and Drug Administration] review and some of those tests … may have given you a false positive and detected the normal coronavirus that circulates and causes the common cold.I would say the vast majority have been extensively tested to show that they do not cross react and give you false positives due to the common cold [anymore]."
While experts at the Mayo Clinic claim these cross-reactive antibody tests were an early problem that has since been corrected and eliminated, the CDC does not confirm or deny the accuracy of this statement on its "Test for Past Infection" web page.7
So, it's unclear whether the antibody tests manufactured and used today are still capable of delivering a positive result if you were recently exposed and recovered from the common cold virus.
Back on April 29, 2020, infectious disease specialist and CNN medical analyst Dr. Kent Sepkowitz noted that "deciphering between the common cold antibody and the COVID-19 antibody is a real challenge scientifically,"8 but that doesn't mean it cannot or hasn't been done.
On a side note, labs are now reporting a shortage of chemicals and disposable pipette tips required to perform COVID-19 tests, which means longer wait times — again. As Scott Shone, director of the North Carolina State Laboratory of Public Health, told The New York Times,9,10 July 23, 2020, “It’s like Groundhog Day. I feel like I lived this day four or five months ago,” referring back to the early days of the pandemic when test supplies were in short supply.
Some Coronaviruses May Impart Resilience Against COVID-19
While the CDC warns it's still uncertain whether COVID-19 antibodies prevents reinfection, or if it does, for how long, researchers in Singapore have presented evidence11,12,13 suggesting the immunity is likely to be long-lasting.
They discovered common colds caused by the betacoronaviruses OC43 and HKU1 appear to make you more resistant to SARS-CoV-2 infection, and that the resulting immunity might last as long as 17 years.
The authors suggest that if you've beat a common cold caused by a OC43 or HKU1 betacoronavirus in the past, you may have a 50/50 chance of having defensive T-cells that can recognize and help defend against SARS-CoV-2. As reported by the Daily Mail:14
"Scientists have found evidence that some immunity may be present for many years due to the body's 'memory' T-cells from attacks by previous viruses with a similar genetic make-up — even among people who have had no known exposure to Covid-19 or SARS …
Blood was taken from 24 patients who had recovered from COVID-19, 23 who had become ill from SARS and 18 who had never been exposed to either SARS or COVID-19 …
Half of patients in the group with no exposure to either Covid-19 or SARS possessed T-cells which showed immune response to the animal betacoronaviruses, COVID-19 and SARS. This suggested patients' immunity developed after exposure to common colds caused by betacoronavirus or possibly from other as yet unknown pathogens."
According to the researchers, their findings demonstrate that:15
"Virus-specific memory T-cells induced by betacoronavirus infection are long-lasting, which supports the notion that COVID-19 patients would develop long-term T-cell immunity. Our findings also raise the intriguing possibility that infection with related viruses can also protect from or modify the pathology caused by SARS-Cov-2."
Added support for these conclusions were published May 14, 2020, in the journal Cell. This study16 found that not only did 70% of samples obtained from recovered COVID-19 patients have resistance to SARS-CoV-2 on the T-cell level but so did 40% to 60% of people who had not been exposed to the virus. According to the authors, this suggests there's "cross-reactive T cell recognition between circulating 'common cold' coronaviruses and SARS-CoV-2."
Other Researchers Report Low Immunity Post-Recovery
The immunity issue isn't entirely cut and dry, though. Other research, which looked at antibody levels in recovered COVID-19 patients in Germany, found they lost their antibodies after two to three months.
"Clemens Wendtner, a chief physician at the hospital, tested COVID-19 patients for immunity after they had been treated for the disease at the end of January 2020. The tests showed a significant decrease in the number of antibodies," DW reported in a July 14, 2020, article.17
"Wendtner says 'neutralizing' antibodies, which stop a viral attack, fell in four out of nine of the patients who were tested, within two to three months. Those findings coincide with a similar investigation done in China.
That study also found that antibodies in COVID-19 patients do not persist in the blood. Further research is still required. But these initial findings suggest that a second infection is possible …"
However, it is important to realize that loss of the ability to determine antibody levels may not necessarily reflect lack of immune protection, as there may be innate cell mediated immunity that provides protection that is not being measured by the humoral antibody production.
Will COVID-19 Behave Like the Common Cold?
If reinfection is possible, then COVID-19 would behave much like the common cold and seasonal influenza, which can strike more than once — if not in a single season, then certainly in any given year. If that's the case, then "immunity passports" and most other COVID-19 interventions, such as school closings and business shutdowns, become even more questionable than they already are.
If SARS-CoV-2 ends up behaving like other human coronaviruses that cause the common cold, immunity may only last six to 12 months, a European study18 says. Here, they did not look at SARS-CoV-2 antibodies but, rather, antibodies against the other four coronaviruses that cause the common cold, none of which were long-lasting. According to BGR, which reported the findings:19
"'Frequent reinfections at 12 months post-infection and substantial reduction in antibody levels as soon as 6 months post-infection' were observed for those viruses.
If the novel coronavirus behaves the same way, then talk of 'immunity passports' and herd immunization is pointless. A person who recovered from COVID-19 could get it again in six to 12 months without another vaccine shot …
The researchers note that the human coronaviruses are 'biologically dissimilar' and 'have little in common, apart from causing the common cold.' But SARS-CoV-2 doesn't have to be similar to any of them to follow the same immunity pattern."
Is Herd Immunity Against COVID-19 Possible?
The issue of reinfection also raises questions about whether herd immunity is ever going to be possible. Studies cited by The Daily Mail20 claim herd immunity against COVID-19 could be achieved if just 10% to 43% of people develop lasting immunity.
This is a far cry from the percentages typically required for vaccine-induced "herd immunity" (which is really a misnomer, as vaccine-induced immunity doesn't work like natural immunity, and herd immunity is really only achieved when enough people recover from the illness in question). According to The Daily Mail:21
"The concept of herd immunity hinges on people only being affected once, so that when a certain number of people have been infected with the virus already it can't spread any more.
It remains a mystery as to whether this is the case for COVID-19 but, if it is, then herd immunity could offer some protection during a second wave of the disease …
Researchers now say it could work to some extent if only one or two out of 10 people have been infected naturally and become immune to the disease … Another study has taken a similar line and suggested herd immunity could develop at around 43 percent of the population getting infected … Immunity among the most socially active people, scientists say, could protect those who come into contact with fewer others."
Optimizing Vitamin D May Be Your Best Bet
Considering the many questions surrounding the possibility of reinfection and herd immunity, I believe one of your best bets is to address an underlying weakness that can have a significant impact on your COVID-19 risk, namely vitamin D insufficiency.
As for testing, I do not recommend getting a viral test (which checks for active infection) unless you have COVID-19 symptoms and need it to guide your treatment. Swabbing the back of your nasal cavity has its risks, and can actually introduce an infection or, some speculate, even some more nefarious agents.
Getting tested just for the heck of it doesn't really make sense. Even if you test negative, you can get infected at any point after leaving the test site. If you have to get tested in order to travel or return to work, an antibody test may be more appropriate. Even if your antibodies wane with time, you're still going to be immune for a while.
The best test are your clinical symptoms. If you have symptoms suggestive of coronavirus infection, then my best recommendation is to start nebulizing food grade hydrogen peroxide at 0.1% as suggested in the video below and discussed in my article on the topic.
I would also make sure that your vitamin D levels are adequate, as discussed in my paper on the topic. If you don't know your vitamin D level and have not been in the sun or taken over 5,000 units of vitamin D a day, it would likely help to take one bolus dose of 100,000 units, and make sure you are taking plenty of magnesium, which helps convert the vitamin D to its active immune modulating form.
Another great option that is less expensive, easier to get and likely more effective than hydroxychloroquine, would be quercetin with zinc as discussed in my recent article on the subject.
The body of evidence demonstrating the medicinal value of cannabis is growing and becoming more compelling, yet there continues to be resistance to using cannabidiol (CBD). Even as the legal arguments are settling, many are resistant to using cannabis sativa (hemp) or cannabis indica (marijuana).
Cannabis has been a popular botanical medicine for thousands of years, valued for its healing properties. Through at least the 19th century it could be found in U.S. pharmacies.1 Then, in 1970, the herb was declared a Schedule 1 controlled substance.2 This is a classification reserved for drugs with a “high potential for abuse” and “no accepted medicinal use.”3
Three years later, the Drug Enforcement Agency was formed and they began their fight against marijuana.4 It may be hard for many to shake the idea that a plant once associated with hippies, rebellion and counterculture has medicinal value and may be important to optimal health.
CBD May Use Three Pathways in the Fight Against COVID-19
Although there is nothing in the chemical makeup of CBD to suggest it specifically attacks COVID-19, some experts believe the anti-inflammatory properties could present a potential treatment for pulmonary inflammation that ultimately can lead to death.
In the severe form of the disease, damage leads to acute respiratory distress syndrome (ARDS), raising the mortality rate of those with ARDS to nearly 50%.5 Hyperactivity of the immune system has been dubbed a “cytokine storm” and is characterized by a release of inflammatory mediators including interleukins and chemokines.
However, Emily Earlenbaugh, co-founder of a cannabis consulting company and a contributor to Forbes, points out that as the body recognizes pathogens, immune cells trigger an early cytokine response that helps control the infection.6,7 This means the body requires cytokines at the start of an infection, but a hyperactive immune response later on can lead to lung damage and severe pneumonia.
Among the different cannabinoids that have been extracted from the cannabis plant, it is CBD that has shown strong anti-inflammatory properties.8 It makes sense, then, to investigate whether CBD can treat ARDS.
Earlenbaugh writes in Forbes that researchers have studied CBD for three ways it may help in the treatment of COVID-19. These include the ability to reduce inflammation, act as a potential antiviral and affect ACE2 expression.9
CBD May Calm the COVID-19 Cytokine Storm
In an interview with CBS News, Earlenbaugh spoke of past research in which CBD demonstrated the ability to act as an interleukin-6 inhibitor, and thus affect the hyperactive immune response.10,11
A more recent study by scholars from Augusta University in Georgia concluded that CBD had a potential protective role during ARDS, which may make it a valuable part of treatment for COVID-19 “by reducing the cytokine storm, protecting pulmonary tissues, and re-establishing inflammatory homeostasis.”12
While more clinical trials are needed to determine dosage and timing before CBD can be part of mainstream treatment, researchers believe they have evidence it can help patients avoid mechanical ventilation and death from ARDS. Babak Baban, immunologist and corresponding author of the study, commented:13
"ARDS is a major killer in severe cases of some respiratory viral infections, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and we have an urgent need for better intervention and treatment strategies. The natural instinct of the virus is to make more of itself. It weaves with our DNA to make the cell produce food and everything it needs."
In their animal study, a synthetic analog was used to mimic the activity of SARS-CoV-2.14 CBD was administered in a pattern that would be like the human experience with the virus and treatment. The animals showed quick clinical improvement, and in a subsequent examination it was found that their lung damage had totally or partially healed.
Terpenes Have Antiviral Activity
Terpenes, also found in the cannabis plant, have been another focus of study for the antiviral properties as scientists search for natural remedies in the treatment of some viruses,15 inflammatory diseases16 and SARS.17
Terpenes are phytochemicals and the oils that give the plant a distinctive flavor and odor.18 Some have antiviral activity, which may help fight COVID-19. A team from the Israel Institute of Technology led by Dedi Meiri, Ph.D., spoke with a reporter from Health Europa about a formulation having been extracted from cannabis and being tested against SARS CoV-2.19
In the initial study, the team is trying to identify the molecules capable of reducing the hyperactive immune response without completely suppressing the system. In the second phase they plan to look at how the plant may affect the viral process through ACE2 receptors.
The hope is that terpenes found in cannabis can help modulate the overreaction of the immune system, which causes organ system failure leading to death.20
Your Body Has an Endocannabinoid System
Endocannabinoids were discovered in the 1990s, which in turn led to the realization that the human body makes endogenous cannabinoids to influence those receptors.21 Endocannabinoids are similar in structure to the cannabinoids found in cannabis.
Board certified nutritionist Carl Germano is an expert on phytocannabinoids and the importance of the endocannabinoid system (ECS) in the human body. He likens the ECS system to the conductor of an orchestra, in which the orchestra is your organ system.22
He goes on to explain how this important system may not be fully appreciated and understood, as there continues to be a stigma — even in medical schools — where students and researchers are testing the boundaries of human biology and physiology:23
"The ECS has been the subject of many scholarly textbooks … Quite frankly, this is something that should be taught from high school to college to medical school. Unfortunately, because of the stigma attached to cannabinoids … less than 13 percent [of medical schools in the U.S.] are teaching the ECS.
I say, 'Are you insane? This is like saying that for the next 70 years we will not teach the cardiovascular system, as if it never existed.' We now have to dismantle this medical travesty … The whole thing is about education. This is critical and crucial to our health and well-being.
We have to dismantle the stigma, and we have to start educating ourselves to understand that the ECS is probably one of the most important medical discoveries in quite some time … understanding the enormity of this system and what it does and what it influences throughout the entire human body."
Documented Health Benefits Associated With CBD
CBD is only one of more than 100 compounds that are classified as cannabinoids and found in the cannabis plant. Since cannabinoid receptors are part of our physiology, it should come as no surprise that CBD has so many health benefits. There are myriad medical uses that have been attributed to CBD, many of them scientifically documented. However, as Germano warns:24
“We must get off this single magic bullet bandwagon. We must appreciate the full gamut of all of these phytocannabinoids as a whole and that they complement each other because CBD is not the answer to support the endocannabinoid system as a whole.”
You’ll find more information about cannabis production, quality and medicinal benefits at “The Many Medicinal Benefits of Cannabis and Cannabidiol (CBD).” Here are just a few of benefits associated with health conditions that raise the risk for severe COVID-19:
Allergic asthma — "CBD treatment decreased the inflammatory and remodeling processes in the model of allergic asthma," according to the European Journal of Pharmacology25
Anxiety and sleep — "Cannabidiol may hold benefit for anxiety-related disorders," The Permanente Journal26
Blood pressure — "This data shows that acute administration of CBD reduces resting BP and the BP increase to stress in humans," JCI Insight27
Diabetes — "These results suggest that the neuroprotective effects of CBD in middle-aged diabetic rats ... are related to a reduction in neuroinflammation," Neurotoxicity Research28
Feed Your Body’s Endocannabinoid System
In my interview with Germano, he talked about the conditions that may result when endogenous cannabinoids are not produced. This can produce a number of symptoms such as inflammation, stress, anxiety and depression.29 Others include poor eye health, insomnia, neurological problems and poor bone health.
Before reaching for a supplement, consider taking steps to raise your endogenous production of cannabinoid compounds. A paper published in PLOS|One explains how nutrients, such as omega-3 fatty acids, exercise, chiropractic care, massage and acupuncture influence the function of your ECS.30
If you choose to use a supplement, then I strongly recommend buying from a reputable company. As I’ve written in the past, Amazon has misled consumers because they allow vendors to tag their items at will, despite their policy of forbidding the sale of any controlled substance.31
Products containing CBD oil fall into this category, based on a technicality of the law.32 Yet, you can still find hemp extract and other products containing CBD on the website.33 One healthy option is using hemp, which was legalized in 2018 with the Farm Bill.34 As Germano has said, CBD alone is not enough to support the body’s endocannabinoid system. Hemp oil has 100 other phytocannabinoids to help meet many of those needs, including CBD.35
The former Olympic swimming champion has reminded us exactly why we need to stop obsessing over the scales and start show our bodies the appreciation it deserves.
The largest and most complex CRISPR system has been visualized by researchers in a new study. The system may have potential applications in biomedicine and biotechnology, the researchers believe.
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A spice that has been used by ancient cultures for eons, turmeric has hit the mainstream - and for good reason. Nutritionist Kriben Govender shares his family recipe for a soothing turmeric milk that's perfect for when you're feeling under the weather.
When couples argue, mediation improves the outcome of the confrontation. But that's not all: mediation is also linked to heightened activity in key regions of the brain belonging to the reward circuit. This is the first time that a controlled, randomized study has succeeded in demonstrating the advantages of mediation for couple conflicts and identifying a related biological signature.
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A new technique that can spot a potential preterm birth in asymptomatic high-risk women, with up to 73% accuracy months before delivery, has been developed by scientists.
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The differing immune system responses of patients with COVID-19 can help predict who will experience moderate and severe consequences of disease, according to a new study.
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Two doses of an experimental vaccine to prevent COVID-19 induced robust immune responses and rapidly controlled the coronavirus in the upper and lower airways of rhesus macaques exposed to SARS-CoV-2, scientists report.
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Continuous positive airway pressure, or CPAP, is the most common treatment prescribed for obstructive sleep apnea (OSA). CPAP involves wearing a mask that fits into the nostrils, underneath or over the nose, or over the nose and mouth, through which pressurized air is delivered via tubing from a machine to keep the upper airway open during sleep. CPAP is recommended by the American Academy of Sleep Medicine (AASM) as the initial treatment for moderate or severe OSA, and in mild cases of OSA when associated with insomnia, disrupted sleep, or excessive daytime sleepiness. When used consistently, and when treatment is effective, CPAP improves daytime sleepiness, quality of life, and it can have positive impacts on cardiac and metabolic health.
The effectiveness of CPAP depends on using the device correctly and consistently, since OSA is a chronic disease that requires long-term treatment. Most sleep doctors, myself included, recommend that patients with sleep apnea use their treatment whenever they sleep, in order to derive optimal benefit. While there are many patients who love their CPAP machines and report the treatment to be life-changing, and are unable to sleep without CPAP, there are others who learn to accept and tolerate CPAP because they appreciate either the functional benefits (such as better mood and less daytime sleepiness) or medical improvements they get from using the device. However, many patients struggle with CPAP.
CPAP is not easy and there are common complaints
Despite the many potential benefits, CPAP adherence estimates from clinical data and insurance groups suggest that about 50% of CPAP users either do not reach minimum adherence criteria or discontinue the treatment. Each patient is unique and may have individual struggles with CPAP; however, there tend to be similar themes among users. Some of the common complaints I hear from patients who have trouble tolerating CPAP include
mask issues, including mask discomfort, skin irritation or marks, feelings of claustrophobia, or discomfort with the appearance of wearing a mask
dryness, especially waking with a dry mouth
removing the mask during sleep
pressure intolerance, from either too much pressure or not enough pressure; trouble exhaling against the CPAP pressure; or swallowing air (aerophagia)
breathing that feels out of sync
noise from the machine bothering the patient or their bed partner.
Troubleshooting issues with CPAP tolerance
First and foremost, patients should partner with their doctor and healthcare team. OSA is a serious disease that warrants treatment. Before starting treatment, patients should be educated about OSA, learn about all treatment options and new technologies, and know what to expect with CPAP. Patients benefit from close clinical follow-up, including a review of data from their CPAP device (which may also be important for continued insurance coverage). Family and/or partner support is also important, as friends or family can help encourage and support CPAP use.
Other tips to improve adherence:
Behavioral and medication interventions. Cognitive behavioral therapy or short-term use of sleep medications can help people adjust to CPAP.
The right mask. If the mask does not fit, the treatment may not work well. There are many mask sizes and types, including nasal masks that fit over or under the nose, nasal pillows that fit in the nostrils, full face masks that cover the mouth and nose, hybrid masks that sit under the nose and cover the mouth, and even helmet masks that cover the face. A mask fitting is advised when patients start treatment, and several fittings may be needed.
Mouth breathing is another mask-related factor to consider. When a patient sleeps with their mouth open, the pressure from the CPAP leaks out the mouth. This causes dryness, and also prevents CPAP from keeping the upper airway open. Mask leak can also result in noise and mask removals during sleep. A mask that covers the mouth will probably be needed, though sometimes adding a chinstrap can keep the jaw closed and prevent mouth breathing.
The right pressure. Some people require vastly different pressure when on their back vs. on their side, or in one sleep stage vs. another. While a pressure range can be helpful, if the range is too wide, the machine cannot adjust rapidly enough to meet the pressure requirements. Weight changes may also impact pressure requirements. Following device data and/or evaluating with a treatment sleep study in a sleep lab can help identify the best pressure.
Address coexisting conditions. Some people use CPAP consistently, tolerate it, but are still sleepy. CPAP is not a substitute for inadequate sleep. Sleep apnea can coexist with other sleep problems that might contribute to daytime sleepiness. Sometimes CPAP is not tolerated because sleep is poor, or fragmented due to other issues such as anxiety, PTSD, insomnia, poor sleep habits, or circadian disorders. These other problems need to be addressed.
Consider alternative treatments. CPAP is the first-line treatment, but not the only treatment for OSA. Consider combining treatments or pursuing an alternative treatment if CPAP is not tolerated or is not desired.
New CPAP innovations can help
A variety of technological advances may improve CPAP comfort and adherence. Some of these include
heated humidification, a comfort intervention that can help with nasal congestion and dryness
ramp-up features that allow the machine to start off at a low or minimal pressure as the patient adjusts and falls asleep
expiratory pressure relief, where the pressure from the machine decreases slightly during exhalation, which is especially helpful when a higher pressure setting is needed to keep the airway open
auto-titrating CPAP machines, which allow for a range of pressures to be set; the machine self-adjusts the pressure when it senses that more or less pressure is needed to keep the airway open. This is helpful for those who require higher pressures in one body position (back vs. side) or sleep stage (dream/REM sleep vs. nondream/NREM).
modems that allow the machine to transmit data (either cellular or by wi-fi), so both the patient and their doctor can determine the effectiveness of the treatment.
The bottom line
CPAP is an effective treatment for OSA. If you are struggling with CPAP tolerance, do not give up, but rather talk to your clinician. Proper education, support, personalized troubleshooting, new technologies, and close clinical follow-up can improve adherence and optimize treatment outcomes.
