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Anxiety disorders are the most common mental illnesses, affecting up to 40% of women and 20% of men in the course of their lifetimes. Women and adolescent girls are at particularly high risk for the development of anxiety disorders, due to differences in their brain chemistry, psychosocial contributors such as childhood sexual abuse, as well as the hormonal effects of estrogen and progesterone. Since anxiety disorders are so common among women and girls, could early detection lead to improved outcomes?
In a recent clinical guideline, the Women’s Preventive Service Initiative (WPSI) recommends screening all women and adolescent girls ages 13 and older for anxiety disorders, including pregnant and postpartum women. The WPSI is a national coalition of 21 health professional organizations and patient representatives that researches and disseminates evidence-based recommendations for women’s preventive health care services. Their universal screening recommendations are based on a systematic review that demonstrates moderate to high accuracy of screening tools, but clearly acknowledges that no studies have evaluated the effectiveness or harms of screening. While these new guidelines recommend a wider net for screening, as a practicing psychiatrist I believe we should not recommend further screening until the potential harms have been evaluated.
Although the US Preventive Services Task Force (USPSTF) recommends routine screening for depression in adolescents and adults, no recommendations for the screening of anxiety disorders have previously been made. The WPSI’s recommendations are based on studies demonstrating the accuracy of screening instruments, as well as confirmation of the benefits of treatment of anxiety disorders with cognitive behavioral therapy and medications.
According to the media, it seems that anxiety disorders have been increasing in recent years, attributed to various causes: the COVID-19 pandemic, greater performance stress at school or work, social media use, etc. However, we do not have robust epidemiologic data suggesting that the prevalence rate for anxiety disorders has truly increased, due to the imprecision of data collected before the introduction of psychiatric classification systems. Studies conducted with the same population and same methodology over time, such as the National Comorbidity Survey and data from the European Union, have not demonstrated an increase in anxiety disorders. We do know, however, that more individuals are seeking treatment for anxiety, and that more people are willing to speak about their anxiety. We also know that prevalence rates in different countries and cultures are more likely to be due to differences in how the data were collected, rather than due to cultural differences.
As with all other screening tools in medicine, screening tools for anxiety have limitations in diverse populations. Non-Western populations are not represented in the studies used to build screening tools, which results in decreased accuracy in populations in which their use has not been validated. Among people living within the United States, anxiety symptoms also present differently based on ethnic, racial, and cultural contexts; for example, anxiety may present as physical or spiritual complaints. Among immigrants in particular, the effects of migration, legal status, and experiences of discrimination may result in psychological distress and anxiety that are not accurately reflected in anxiety screening tools. The risks of screening for anxiety in populations in whom the screening tools have not been validated include errors in diagnosis and inappropriate treatment (or lack of treatment).
Even among populations in whom anxiety screening tools have been validated, universal anxiety screening for women and adolescent girls poses the following concerns:
Both the Canadian Task Force on Preventive Health Care and the United Kingdom National Screening Committee do not endorse questionnaire-based screening for mental illnesses, given concerns about potential harms and resource use.
The new WPSI guidelines recommend screening all adolescent girls and women for anxiety disorders. Anxiety disorders are particularly common among women, but they are often unrecognized and undertreated. Universal screening for anxiety in this population may help to identify those suffering from anxiety disorders, resulting in earlier evaluation and treatment. However, future research is needed to evaluate the effectiveness of such screening and to assess for potential harms.
The post Should we screen all adolescent girls and women for anxiety? appeared first on Harvard Health Blog.
It's an unfortunate fact that health officials and pandemic response authorities, by and large, are completely ignoring the role a healthy lifestyle plays in the COVID-19 pandemic, focusing instead, almost exclusively, on the necessity for a vaccine.
According to Reuters,1 the U.S. government is planning to launch an "overwhelming" COVID-19 vaccine campaign come November. An unnamed "senior White House administration official" is quoted saying:2
"The fine line we are walking is getting the American people very excited about vaccines and missing expectations versus having a bunch of vaccines in the warehouse and not as many people want to get it. You may not hear a lot about promoting vaccines over the airwaves in August and September but you'll be overwhelmed by it come November."
But is a vaccine really going to be the answer people are hoping for? For example, many have bought into the mainstream narrative that masks are here to stay until or unless there's a vaccine, and getting vaccinated would mean the end to mask mandates.
Considering the fact that neither masks nor vaccines offer significant protection against the virus, chances are such hopes will get dashed. Maria Elena Bottazzi, a COVID-19 vaccine developer at Baylor College of Medicine, recently warned3 that social distancing and face masks will likely still be required even after a vaccine becomes available, as the vaccine will not offer 100% protection against infection.
So, don't be fooled. Vaccines will be in addition to what we are told to do now, not a replacement. Even Moderna's CEO Stephanie Bancel stated4 that if the vaccine reaches 90% effectiveness, which is a beyond overly optimistic projection, people with high-risk health conditions will need to continue wearing masks.
In addition to not necessarily removing the "need" for masks and social distancing mandates in the future, the novel mRNA vaccines being developed against COVID-19 may also be an autoimmune disorder disaster in the making, as explained in "The Well-Known Hazards of Coronavirus Vaccines" and "Gates Tries to Justify Side Effects of Fast-Tracked Vaccine."
The Atlantic succinctly stated the truth of the matter in the August 4, 2020, article, "The Coronavirus Is Never Going Away":5
"If there was ever a time when this coronavirus could be contained, it has probably passed. One outcome is now looking almost certain: This virus is never going away … We will probably be living with this virus for the rest of our lives …
What does the future of COVID-19 look like? That will depend, says Yonatan Grad, on the strength and duration of immunity against the virus. Grad, an infectious-disease researcher at Harvard, and his colleagues have modeled6 a few possible trajectories.
If immunity lasts only a few months, there could be a big pandemic followed by smaller outbreaks every year. If immunity lasts closer to two years, COVID-19 could peak every other year …
In SARS, antibodies … wane after two years. Antibodies to a handful of other coronaviruses that cause common colds fade in just a year. 'The faster protection goes away, the more difficult for any project to try to move toward eradication,' Grad told me."
Many who have steadfastly isolated themselves for months on end and dutifully wear a mask everywhere they go probably do not want to hear this. If the virus isn't going away no matter what we do, then there are only two choices: Continue social distancing and mask-wearing for the remainder of our days, or return to life as it was pre-COVID, when influenza seasons were met with blasé equanimity.
For many, neither of these options is satisfactory. They are, however, reality. COVID-19 is unlikely to be eradicated, and if you haven't contracted it already, you likely will at some point.
At present, it's still unclear whether you can contract it more than once, but if that's the case, then flu season will likely include the possibility of COVID-19 outbreaks as well.
Facing reality head-on is the best way forward, if you ask me, and that means your best bet is to get yourself into good shape through diet and exercise. You simply cannot hide from this virus, for the simple reason that you cannot stop breathing.
At this point, it may be worth reminding yourself that life involves the risk of illness and death. Every day of every year of your life, you face the possibility of illness, be it an infectious disease or chronic illness.
Each year of your life you've faced the possibility of influenza, for example. Maybe a mild case, maybe a really serious one. Regardless, you've probably never considered isolating yourself for months each year and giving up on doing the things you love for fear you might get the flu and die.
Despite the fact that uptake of seasonal influenza vaccines has seen an uptick thanks to various mandates, the flu continues to circulate and affects large numbers of vaccinated individuals every year. Influenza has not been eradicated, and the flu vaccine has consistently been shown to provide very little in terms of protection against it.
In all likelihood, that's where we'll be with COVID-19 as well. The good news is that, much like with influenza, your chances of staying well, or only getting a mild case, are primarily dependent on your immune function, and this is something you can do something about.
We now have a significant amount of data showing that certain comorbidities raise your risk of severe COVID-19 illness and death. Among the top ones is obesity, so addressing excess weight will go a long way toward lowering your risk.
In the U.K., obesity is now being targeted as part of the country's coronavirus prevention strategy.7 In a recent announcement, Prime Minister Boris Johnson said he intends to ban TV junk food advertising before 9 p.m. and limit in-store promotions. Online ads for unhealthy foods may also be banned.8
Johnson's decision was in large part influenced by his own bout with COVID-19, which he believes was made more serious by his excess weight. Several studies support his suspicion. As noted in the July 13, 2020, issue of the Journal of Virology:9
"Over the years, humans have adopted sedentary lifestyles and dietary patterns have shifted to excessive food consumption and poor nutrition. Overnutrition has led to the constellation of metabolic abnormalities that not only contributes to metabolic reprogramming but also limits host innate and adaptive immunity.
Impaired immune responses and chronic inflammation in metabolically diseased microenvironments provide the ideal conditions for viral exploitation of host cells and enhanced viral pathogenesis."
In the U.S., few officials have addressed the proverbial elephant in the room. The town of Huntington in New York stands out as a rare exception. As reported by Bill Maher in the featured video, Huntington officials have urged all 200,000 residents to "go on a diet because [with] COVID-19, you're twice as likely to have a poor outcome if you're obese."
As noted by Maher, obesity has always killed us, albeit slowly. "Mixed with COVID, it kills you fast," he says, adding:
"Why not an all-out campaign to educate the public on the dangers of a diet of sugary, chemical-laden crap? … Why not campaign to get decent food into poorer neighborhoods? Why not for every PSA for masks, a PSA for a recipe of a healthy meal?
I think so many lives could have been saved if at the very beginning of this crisis the medical establishment had made a more concerted effort to tell Americans, 'While you're in lockdown, getting free money for not working, you need to do something too.' Even the poorest person could switch out soda at meals for water …
A national campaign to improve health could have improved our chances against this disease [and] made us feel better about ourselves to boot. But it was never even mentioned … We cannot have body positivity be a third rail anymore … This issue is too fundamental to who lives and who dies."
Hopefully, the U.S. will eventually follow in the U.K.'s footsteps and take action against junk food advertisements. Clearly, advertising works, and it's not helping anyone make the right choices for their health. In the meantime, you'd be wise to take matters into your own hands.
There's little doubt that processed foods, junky snacks and soft drinks are key culprits in the rise of obesity and chronic diseases that also inflate the risk of death from COVID-19. As such, they should be the first to be eliminated from your diet moving forward.
If anything good is to come of this pandemic, it would be the widespread recognition of the impact obesity has not just on chronic diseases, but also on viral contagions such as SARS-CoV-2. A recent editorial published in the BMJ highlights the importance of diet and the significant yet hidden influence the processed food industry has had in the COVID-19 pandemic:10
"It is now clear that the food industry shares the blame not only for the obesity pandemic but also for the severity of COVID-19 disease and its devastating consequences.
During the COVID-19 pandemic an increase in food poverty, disruptions to supply chains, and panic buying may have limited access to fresh foods, thus tilting the balance towards a greater consumption of highly processed foods and those with long shelf lives that are usually high in salt, sugar, and saturated fat.
Moreover, since the start of the COVID-19 pandemic the food industry has launched campaigns and corporate social responsibility initiatives, often with thinly veiled tactics using the outbreak as a marketing opportunity (for example, by offering half a million 'smiles' in the form of doughnuts to NHS staff)."
They not only call on the food industry to immediately stop promoting unhealthy food and drinks, but also call on governments to force reformulation of junk foods to better support health. With research showing that being obese doubles the risk of being hospitalized for COVID-19,11,12 the authors noted:13
"These findings suggest that modification of lifestyle may help to reduce the risk of COVID-19 and could be a useful adjunct to other interventions, such as social distancing and shielding of high risk."
Johns Hopkins University researchers have also suggested obesity might eventually shift the burden of COVID-19 onto younger patients, as a dataset of 265 COVID-19 patients showed younger individuals admitted to the hospital were more likely to be obese.14
According to recent research, even mild obesity can influence COVID-19 severity. Researchers from the Alma Mater Studiorum University of Bologna in Italy analyzed 482 COVID-19 patients hospitalized between March 1 and April 20, 2020,15 concluding "Obesity is a strong, independent risk factor for respiratory failure, admission to the ICU and death among COVID-19 patients."
Using body mass index (BMI) to define obesity, the researchers found an increased risk for more severe COVID-19 infection started at a BMI of 30, which is considered "mild" obesity (a BMI between 25 and 29.9 is considered overweight). Lead study author Dr. Matteo Rottoli said in a news release:16
"Health care practitioners should be aware that people with any grade of obesity, not just the severely obese, are a population at risk. Extra caution should be used for hospitalized COVID-19 patients with obesity, as they are likely to experience a quick deterioration towards respiratory failure, and to require intensive care admission."
Specifically, patients with mild obesity had a 2.5 times greater risk of respiratory failure and a five times greater risk of being admitted to an ICU compared to nonobese patients. But get this, those with a BMI of over 35 were 12 times more likely to die from COVID-19.17
"Whereas a BMI ≥ 30 kg/m2 identifies a population of patients at high risk for severe illness, a BMI ≥ 35 kg/m2 dramatically increases the risk of death," the researchers explained.18
A July 2020 report19 by Public Health England also reviews research demonstrating how excess weight affects COVID-19 outcomes. For example, one systematic review found that, compared to healthy weight patients, patients with a BMI above 25 were:
The report also highlights data showing the risk of hospitalization, intensive care treatment and death progressively increase as your BMI goes up. As for how obesity raises risks during viral infections, the chronic, low-grade inflammation it causes is a likely factor.
Inflammation triggered by obesity is also thought to be responsible for the threefold greater risk of pulmonary embolism (blood clots in the lungs) seen in obese COVID-19 patients.20,21 Obesity-related dysregulation of lipid synthesis can also aggravate lung inflammation, thereby contributing to increased disease severity in viral respiratory infections specifically.22
In addition to that, excess body weight and fat deposition around the internal organs put pressure on your diaphragm, which makes it more difficult to breathe when you have a respiratory infection.23 Other mechanisms by which obesity may increase COVID-19 severity, include:24
The take-home message here is that if you are obese, even if only mildly so, focusing on getting down to a healthy weight may help you ward off viral illnesses, including COVID-19. Losing weight will also help you avoid other obesity-related health problems such as diabetes, high blood pressure and heart disease — all of which, by the way, raise your risk of COVID-19 complications and death.
According to a study by The Istituto Superiore di Sanità, Italy's national health authority,25 more than 99% of fatalities from COVID-19 occurred among people who had underlying medical conditions. Among that 99%, 76.1% had high blood pressure, 35.5% had diabetes and 33% had heart disease either alone or as comorbidities.26
One of the most powerful strategies to optimize your weight is to restrict your eating window to six to eight hours each day, making sure to eat your last meal at least three hours before bedtime. This is known as time-restricted eating or intermittent fasting, and is a powerful intervention to reduce insulin resistance and restore metabolic flexibility.
With respect to diet recommendations, my experience is consistent with a cyclical ketogenic diet being highly effective to restore metabolic flexibility and reduce insulin resistance.
This involves radically limiting carbs (replacing them with healthy fats and moderate amounts of protein) until you're close to or at your ideal weight, as this will allow your body to start burning fat as its primary fuel and to increase the sensitivity of your insulin receptors.
Most people use carbs as their primary fuel source (thanks to excessive and frequent carb intake). They have lost the ability to effectively burn fat for fuel, which in turn leads to metabolic dysfunction, insulin resistance and weight gain. Once you have regained your ideal body weight, then you can cycle carbs back in a few times a week.
One of the best books written on this subject is my classic "Fat for Fuel." If you haven't read it, then you are in for a treat, as COVID-19 is the catalyst that will motivate you to not only read the book but apply its radical metabolic benefits.
Additionally, get regular exercise each week and increase physical movement throughout your waking hours, with the goal of sitting less than three hours a day. Making sure you're getting sufficient sleep (typically eight hours for most adults) and tending to your emotional health are also important factors that can influence your weight, general health and immune function.
Chronic stress, for instance, may increase your risk for visceral fat gain over time,27 which means addressing your stress levels is imperative for maintaining your ideal weight. Taking steps to lead a healthy lifestyle overall will have a snowball effect, helping you to reach a healthy weight while also bolstering your resilience against infection and disease.
Coronaviruses were identified in the mid-1960s and so named for the crown-like spikes on the surface of the cell. Until the first SARS-CoV arrived in 2003, there were four common coronaviruses.1 The CDC’s list of symptoms for these viruses shows that they are the same as those of the common cold.2 They include a runny nose, sore throat, headache, fever and cough.
However, from what scientists have discovered since the start of the global pandemic, the symptoms and long-term effects are far different for SARS-CoV-2. Initial symptoms include fever, cough, shortness of breath, fatigue and loss of taste or smell.3 However, unlike a natural coronavirus, the additional complications can affect the cardiovascular system, kidney, liver and lungs.4
One of the identified underlying dysfunctions that trigger shortness of breath and severe lung complications is hypercoagulability. In one study, patients who were admitted to Padova University Hospital in Italy for acute respiratory failure showed "markedly hypercoagulable thromboelastometry profiles." The researchers said:5
"In conclusion, COVID-19 patients with acute respiratory failure present a severe hypercoagulability rather than consumptive coagulopathy. Fibrin formation and polymerization may predispose to thrombosis and correlate with a worse outcome."
Clot formations throughout the body may be associated with other complications arising after the illness has resolved. It appears that the difference between people who have a mild or severe illness may be related to the body’s ability to reduce the hypercoagulability and the hyperimmune response that leads to a cytokine storm.
An antioxidant is a molecule that keeps other molecules from oxidizing. Glutathione is a powerful antioxidant that may play a significant role in the COVID-19 illness process. There are 20 amino acids that can bind together in different formations to create a protein molecule.6
However, glutathione is a tripeptide, which means there are only three amino acids that line up to form a glutathione molecule. These are cystine, glycine and glutamate. Together they help use and recycle other antioxidants, such as vitamin C and CoQ10.7,8
This means your body uses glutathione to increase the effectiveness of these antioxidants and it helps to recycle the molecules. Without glutathione, the antioxidant capacity is significantly reduced. This function may be what earned glutathione the nickname “master antioxidant.”9
N-acetylcysteine (NAC) plays a role as a precursor to glutathione.10 Clinical evidence has also demonstrated the effects NAC has, independent of its role with glutathione, including a thrombolytic effect. It also improves oxidative stress and the inflammatory response.11,12,13,14
In late March 2020, one medical student put this theory to the test when his mother, 48-year-old Josephine Bruzzese, was diagnosed with pneumonia at NYU Langone Hospital-Brooklyn. Without an available COVID-19 test, they sent her home as a suspected case. She was prescribed hydroxychloroquine and azithromycin, which helped improve some symptoms, but not her breathing.
When she was unable to stand, and had severe respiratory problems,15 her son contacted Dr. Richard Horowitz, a specialist who was treating his sister for Lyme disease, who suggested using glutathione to help reduce the inflammation and protect Bruzzese's lung tissue. The results were dramatic.
Within one hour after receiving a 2,000 mg dose of glutathione, her breathing was better, and she could stand. She continued to take glutathione for five days and has not had a relapse. Speaking to a reporter from the New York Post, Horowitz shared that he is working to design an extensive clinical trial to prove the effectiveness of what he calls "an easy treatment that is not expensive."
May 5, 2020, Memorial Sloan Kettering Cancer Center posted a trial to Clinicaltrials.gov announcing a study involving the use of NAC in patients with COVID-19. In this first-of-its-kind research, the study team plans to enroll patients with severe disease: One group in the study will receive 6 grams of NAC intravenously each day in addition to other treatments.16
About the same time the study was announced by Memorial Sloan Kettering, a Russian scientist published papers proposing that glutathione plays a crucial role in a person's ability to respond to a COVID-19 infection and the resulting severity of disease.17,18,19 In this short video, Dr. Roger Seheult explains the science.
Additionally, Dr. Alexey Polonikov, from Kursk State Medical University, theorizes glutathione can be used as a preventive against, and treatment of, the illness. Polonikov studies human molecular genetics and oxidative stress.20
Based on the exhaustive literature analysis he conducted, he later said he believes glutathione deficiency is a plausible reason for serious illness with COVID-19:21
“(1) oxidative stress contributes to hyper-inflammation of the lung leading to adverse disease outcomes such as acute respiratory distress syndrome, multiorgan failure and death;
(2) poor antioxidant defense due to endogenous glutathione deficiency as a result of decreased biosynthesis and/or increased depletion of GSH is the most probable cause of increased oxidative damage of the lung, regardless which of the factors aging, chronic disease comorbidity, smoking or some others were responsible for this deficit.”
As Polonikov writes22 and Seheult describes in the video, oxidative damage from reactive oxygen species (ROS) plays a significant role in severe disease with COVID-19. In another video, Seheult explains how COVID-19 sets the stage for significantly increasing oxidative stress by increasing superoxide, a damaging ROS.23
Importantly, this raises superoxide in people who start with high levels due to chronic diseases such as heart disease, diabetes and high blood pressure. As the virus uses the ACE2 enzyme, it generates angiotensin II, which in turn generates more superoxide.
The virus also attracts a type of neutrophil (polymorphonuclear leukocytes) that can also raise the production of superoxide. The superoxide then produces other hydroxyl radicals, including hydrogen peroxide (H2O2).
These ROSs, which cause cellular damage, can be reduced with glutathione peroxidase as it oxidizes glutathione in the process of reducing H2O2 to water. As you can see, a deficiency of glutathione would create a build-up for ROS as Polonikov describes.
Antioxidant defense against ROS damage is crucial for whole body homeostasis. Polonikov believes a higher rate of severe illness from the virus in older adults and those with comorbidities suggests there are related biological processes that make these specific individuals more sensitive. He writes:24
“Specifically, impaired redox homeostasis and associated oxidative stress appear to be important biological processes that may account for increased individual susceptibility to diverse environmental insults.”
In one evaluation of COVID-19 patients from six hospitals in Atlanta, researchers found independent factors that raised the risk of hospitalization. These included smoking, having Type 2 diabetes, being male, being Black, being of advanced age and being obese.25 Polonikov found evidence that a glutathione deficiency may be implicated in these comorbidities.
In his paper he identifies the progressive reduction in endogenous glutathione with aging. This, he believes, makes “the elderly more susceptible to oxidative damage caused by different environmental factors compared to younger individuals.”26 He points out that deficiencies in endogenous glutathione are also found in people who have other comorbid conditions.
He proposes these decreased levels with chronic disease could begin a shift toward oxidative stress and exacerbate pulmonary inflammation, ultimately leading “to acute respiratory distress syndrome (ARDS), multiorgan failure and death.”27 Some men and some smokers also have lower levels of glutathione, which increases their risk.
In another ongoing study on the genetics of redox homeostasis and Type 2 diabetes, four patients from the control group contracted COVID-19. Blood samples were collected and used to measure ROS and glutathione levels.28
All four were female nonsmokers without chronic disease who had a confirmed positive PCR test. In cases of individuals who recovered quickly, the ROS-to-glutathione ratio was 2.075-to-0.712 or less.
In patients with more significant disease, the ratio was 3.677-to-0.531 in one patient and as high as 2.73-to-0.079 in the second. In the first patient with significant disease the ratio was more than double that in patients who recovered quickly. In the second patient the ratio was more than 11 times greater.
In terms of vitamin D, Polonikov proposes the relationship between vitamin D and severe disease may have more to do with a glutathione deficiency. He points to several studies that correlate glutathione levels with vitamin D29,30 and another in which scientists found that lower levels of l-cysteine, a glutathione precursor, correlated with lower vitamin D levels in people with Type 2 diabetes.31
In a recent animal study researchers also looked at whether glutathione deficiency could induce changes that impaired the metabolism of vitamin D.32 They found the deficiency could alter the biosynthesis and explained the mechanism for vitamin D deficiency that occurs with a glutathione deficiency.
The researchers suggest there's a potential benefit to supplementing with glutathione in order to reduce vitamin D deficiency. Polonikov writes that this study supplies information on the importance glutathione plays in the control of endogenous vitamin D biosynthesis and demonstrates the benefits of treatment in reducing vitamin D deficiency.
I believe both nutrients are vital for protection against severe disease. While a glutathione deficiency may impact your ability to synthesize vitamin D, this is applicable only when you have enough sun exposure or supplements to raise your vitamin D level.
However, we know it is difficult to get enough sun in the Northern Hemisphere, especially during the winter months. Additionally, most people use copious amounts of sunscreen or avoid the sun altogether, which can make the deficiency problem worse.
Your glutathione levels can be optimized using food, supplements and exercise. Polonikov believes that NAC taken orally may be a preventive strategy to help support your levels. In his paper he concluded:33
“Therefore, oral administration of N-acetylcysteine as a preventive measure against viral infections, as well as intravenous injection of NAC or reduced glutathione (GSH is highly bioavailable) in patients with serious illness may be effective options against novel coronavirus SARS-CoV-2 infection."
As he discusses in the video, Seheult believes there is more to the damage by COVID-19 than oxidative stress.34 He points out that the clots removed from patients with confirmed COVID are rich with platelets, indicating another mechanism involving disulfide bonds. He goes on to explain:35
“And, as we've already talked about N-acetylcysteine and reduced glutathione will break these disulfide bonds and cause them to lyse and potentially relieve the obstruction and the hypoxemia with COVID-19. Again, this is all a hypothesis, but it looks as though it's fitting together."
Foods that have had a positive impact on glutathione production include cruciferous vegetables such as broccoli, green tea, curcumin, rosemary and milk thistle.36 Getting quality sleep may also help.37,38
Different types of exercise can influence your levels. In one study researchers enrolled 80 healthy but sedentary volunteers to measure the type of exercise that may have the greatest effect.39 They found that aerobic training in combination with circuit weight training showed the greatest benefit.
