There’s no shortage of controversies surrounding the COVID-19 pandemic, but the controversy over hydroxychloroquine is perhaps one of the most perplexing and frustrating. Doctors and health experts around the world have spoken out both for and against the use of the drug, some reporting spectacular benefits1 while others warn of mortal dangers.2
In one international poll3 of 6,227 doctors in 30 countries, 37% rated the antimalaria drug hydroxychloroquine as “the most effective therapy” for COVID-19. The poll was done by Sermo, the world’s largest health care data collection company and social platform for physicians.
In Spain, where the drug was used by 72% of doctors, it was rated “the most effective therapy” by 75% of them. The typical dose used by a majority of doctors was 400 milligrams per day.
French science-prize winning microbiologist and infectious disease expert Didier Raoult, founder and director of the research hospital Institut Hospitalo-Universitaire Méditerranée Infection,4 reported5,6 that a combination of hydroxychloroquine and azithromycin, administered immediately upon diagnosis, led to recovery and “virological cure” — nondetection of SARS-CoV-27 in nasal swabs — in 91.7% of patients.
According to Raoult, the drug combination “avoids worsening and clears virus persistence and contagiosness in most cases.” No cardiac toxicity was observed using a dose of 200 mg three times a day for 10 days, along with 500 mg of azithromycin on Day 1 followed by 250 mg daily for the next four days. The risk of cardiac toxicity was ameliorated by carefully screening patients and performing serial EKGs.
As reported by The Highwire (see video above), July 2, 2020, Raoult is quoted as saying failure to prescribe hydroxychloroquine to a COVID-19 patient “should be grounds for malpractice.” Meanwhile, University of Oxford investigators claim the drug is useless and shouldn’t be prescribed at all in hospitalized patients.8
An interesting website tracking hydroxychloroquine trials is c19study.com.9 It lists more than 40 studies and meta-analyses showing positive results of the drug, compared to nine that have reached a negative conclusion.
Dr. Vladimir Zelenko, a primary care physician in Monroe, New York, has also reported excellent results using the drug. He told radio host Sean Hannity he’d had a near-100% success rate using hydroxychloroquine, azithromycin and zinc sulfate for five days. “I’ve seen remarkable results; it really prevents progression of disease, and patients get better,” he told Hannity.
In the video above, Del Bigtree interviews Zelenko about the criticism levied against him for promoting use of the drug. According to Zelenko, hydroxychloroquine deniers “are guilty of mass murder.”
He points out hydroxychloroquine has been used for decades and is safe even for pregnant and nursing women, so he felt very comfortable prescribing it off-label. He prescribed 200 mg of hydroxychloroquine twice a day, 500 mg of azithromycin once a day and 220 mg of zinc once a day, for five days.
The treatment was initiated within the first five days of clinical symptoms of COVID-19, based on “clinical suspicion” of SARS-CoV-2 infection (not lab confirmed testing, as test results took three days and viral load typically explodes by Day 6).
June 30, 2020, Zelenko and two co-authors published a study,10 currently in preprint, which found treating COVID-19 patients who had confirmed positive test results “as early as possible after symptom onset” with zinc, low-dose hydroxychloroquine and azithromycin “was associated with significantly less hospitalizations and five times less all-cause deaths.”
As noted by Zelenko in Bigtree’s interview, the real virus killer in this combination is actually the zinc. The hydroxychloroquine merely acts as a zinc transporter, allowing it to get into the cell. The antibiotic, meanwhile, helps prevent secondary infections.
According to Dr. Meryl Nass, the wildly divergent views on hydroxychloroquine appear to have little to do with its safety and effectiveness against COVID-19, and more to do with a concerted and coordinated effort to prevent its use. In the video11 above, Chris Martensen Ph.D., also reviews the “profound lack of integrity” we’re currently seeing when it comes to hydroxychloroquine.
Indeed, there are several reasons for why certain individuals and companies might not want an inexpensive generic drug to work against this pandemic illness. (A 14-day supply costs just $2 to manufacture12 and can retail for as little as $20.13)
One of the most obvious reasons is because it might eliminate the need for a vaccine or other antiviral medication currently under development.14 Hundreds of millions of dollars have already been invested, and vaccine makers are hoping for a payday in the billions if not trillions of dollars. In a June 27, 2020, blog post, Nass points out:15
“It is remarkable that a series of events taking place over the past three months produced a unified message about hydroxychloroquine, and produced similar policies about the drug in the U.S., Canada, Australia, NZ and western Europe.16
The message is that generic, inexpensive hydroxychloroquine is dangerous and should not be used to treat a potentially fatal disease, COVID-19, for which there are no (other) reliable treatments.
Hydroxychloroquine has been used safely for 65 years in many millions of patients. And so the message was crafted that the drug is safe for its other uses, but dangerous when used for COVID-19. It doesn’t make sense, but it seems to have worked. Were these acts carefully orchestrated? You decide.
Might these events have been planned to keep the pandemic going? To sell expensive drugs and vaccines to a captive population? Could these acts result in prolonged economic and social hardship, eventually transferring wealth from the middle class to the very rich?”
The fight over hydroxychloroquine may also have political underpinnings. As noted by investigative reporter Sharyl Attkisson in a May 18, 2020, Full Measure report, “never before has a discussion about choices of medicine been so laced with political overtones.”
Nass’ article17 lists what has occurred with regard to hydroxychloroquine so far, the intention being to keep it as a living document that will be added to as time goes on.
Nass says she wrote it in such a way that it might be read as a “to do list … to be carried out by those who pull the strings,” with the intention of suppressing use of the drug. At the time of this writing, Nass’ list18 contains 27 bullet point entries. I highly recommend reading through it, as I will only highlight a select few here.
Several items on Nass’ list detail the various ways in which safe and effective use of the drug were undermined, which allowed for a false narrative of danger to be crafted.
For example, Nass points out that three large, randomized multicenter clinical trials all used excessive dosages known to be toxic.19 These include the following. She also discusses these trials in other in-depth articles:20,21,22
• The U.K. Recovery Trial23,24,25 — Funded in part by the Bill & Melinda Gates Foundation, Wellcome Trust and the U.K. government through Oxford University,26 this study randomly assigned patients to usual care or to one of five primary drug treatments: lopinavir-ritonavir; a corticosteroid (low-dose dexamethasone); hydroxychloroquine; tociizumab; or azithromycin. They also used convalescent plasma.
Patients received 2,400 mg of hydroxychloroquine during the first 24 hours — three to six times higher than the daily dosage recommended27 followed by 400 mg every 12 hours for nine more day for a cumulative dose of 9,200 mg over 10 days. The trial ended its hydroxychloroquine arm on June 4, reporting “no benefit.”
• The Solidarity Trial28 — Launched by the World Health Organization and funded by 43 countries and 203,000 individuals and organizations,29 this trial also compares standard of care against four drug options, including hydroxychloroquine, among patients in 35 countries.
Strangely, the WHO does not specify the daily dosage used in the trial. However, the registration of the Canadian30 and Norwegian31 portions of the trial lists a dosage of 2,000 mg on the first day, and a cumulative dose of 8,800 mg over 10 days. This is only 400 mg less than the U.K.32 Recovery Trial’s toxic dose.
The hydroxychloroquine arm was halted May 25,33 following the publication of the Surgisphere study34 in The Lancet. June 3, after tremendous controversy had been raised over the veracity of the study, and a day before the study was retracted for using fabricated data,35,36 (and this despite having undergone peer-review), the hydroxychloroquine arm was restarted.37
June 17, 2020, the hydroxychloroquine arm was stopped again, this time “based on evidence from the Solidarity trial, U.K.'s Recovery trial and a Cochrane review of other evidence on hydroxychloroquine.”38
• The REMAP-CAP Trial (Randomized, Embedded, Multifactorial Adaptive Platform Trial for Community-Acquired Pneumonia)39 — Here, patients either received nothing, a combination of lopinavir and ritonavir, or hydroxychloroquine alone or in combination with lopinavir and ritonavir.
REMAP used the same toxic dose as the Recovery Trial but for six days instead of 10. What’s more, only critically ill hospitalized patients were included in this trial. Nass addresses other concerns as well in her June 19 blog40 about this study.
What possessed the study designers and investigators of these three huge clinical trials to use such exaggerated dosages? Hydroxychloroquine has been on the market for 65 years and both toxic and the effective dosages for a variety of ailments are well documented. Doctors who have reported excellent treatment results in the field stayed within the recommended hydroxychloroquine dosages.
Were they trying to purposely sabotage these trials using dosages known to be toxic? Doctors have also reported that best results are observed when the drug is administered early, while symptoms are still mild or moderate, yet in these trials the drug was not given until it was too late.
A July 1, 2020, retrospective analysis41,42,43 of 2,541 patients in the Henry Ford Hospital System in Detroit, Michigan, found use of hydroxychloroquine alone cut mortality by more than half, from 26.4% to 13.5%. (Hydroxychloroquine in combination with azithromycin had a mortality rate of 20.1%, and azithromycin alone had a mortality rate of 22.4%.)
More than 90% of the patients had received the drug or drugs within 48 hours of admission into the hospital. No adverse heart-related events were observed among those given hydroxychloroquine.
All three trials above that used toxic hydroxychloroquine doses — Recovery, Solidarity and REMAP — also failed to include zinc, which appears to be a key factor. As noted by Zelenko above, the hydroxychloroquine is really only used to drive the zinc in to the cells. Nass observes:44
“The conclusions to be drawn are frightening:
Aside from that, there are two additional facets of what’s going on that are not yet being discussed:
1. What we’re seeing happen right now is that patients are being turned into guinea pigs en masse. As of June 16, 2020, the U.S. Food and Drug Administration stated the only way a patient should receive hydroxychloroquine is by enlisting in a clinical trial.45
Similarly, in the U.K., treating physicians have been asked to enroll all hospitalized COVID-19 patients into the Recovery and REMAP trials. As of July 9, 2020, Recovery had enrolled more than 12,000 subjects.46
What this means is that thousands of patients are having their treatment selected via randomization by computer rather than by their own doctors' choice of treatment. The U.K., by the way, has one of the highest COVID-19 death rates in Europe already.47 By removing physician and patient choice of treatment, the death toll might end up being far worse than it needs to be.
Importantly, will this trend continue post-COVID? Now that doctors are being groomed to accept having their patients treated by randomization rather than with the treatment any given doctor believes to be best, will they sign up their future non-COVID patients as subjects just as easily?
2. Secondly, three recent papers48,49,50 argue that the excessive doses of hydroxychloroquine used in the Recovery Trial were not actually toxic. This creates a serious contradiction that has yet to be addressed. As noted by Nass in an email to me:
“For argument's sake, say they are right, and even high doses are safe. Well then, why are the FDA, European Medicines Agency, pharmacy boards, governors, etc. restricting this drug that is so safe you can even overdose it and be fine?
Either the drug is so toxic at normal doses that it can’t be used for a life-threatening illness, or it is perfectly safe at extremely high doses. You can’t have it both ways."
In conclusion, let us circle back to where we started — with the reports of treatment success. A study51 posted on the prepublication server medRxiv, May 8, 2020, compared outcomes in hospitalized COVID-19 patients treated with either hydroxychloroquine and azithromycin alone, or Zelenko’s triplet regimen of hydroxychloroquine, azithromycin and zinc.
While the addition of zinc sulfate had no impact on the length of hospitalization, ICU duration or duration of ventilation, univariate analysis showed it was associated with other positive effects:
As noted by the authors:52
“After adjusting for the time at which zinc sulfate was added to our protocol, an increased frequency of being discharged home (OR 1.53 …) reduction in mortality or transfer to hospice remained significant (OR 0.449 …). This study provides the first in vivo evidence that zinc sulfate in combination with hydroxychloroquine may play a role in therapeutic management for COVID-19.”
In short, to maximize effectiveness, you need zinc. As explained in “Is Quercetin a Safer Alternative to Hydroxychloroquine?” hydroxychloroquine acts as a zinc ionophore,53,54 meaning it shuttles zinc into your cells, and zinc appears to be a “magic ingredient” required to prevent viral replication.55
If given early, zinc along with a zinc ionophore should, at least theoretically, help lower the viral load and prevent the immune system from becoming overloaded. As noted in the preprint paper, “Does Zinc Supplementation Enhance the Clinical Efficacy of Chloroquine / Hydroxychloroquine to Win Todays Battle Against COVID-19?” published April 8, 2020:56
“Besides direct antiviral effects, CQ/HCQ [chloroquine and hydroxychloroquine] specifically target extracellular zinc to intracellular lysosomes where it interferes with RNA-dependent RNA polymerase activity and coronavirus replication.
As zinc deficiency frequently occurs in elderly patients and in those with cardiovascular disease, chronic pulmonary disease, or diabetes, we hypothesize that CQ/HCQ plus zinc supplementation may be more effective in reducing COVID-19 morbidity and mortality than CQ or HCQ in monotherapy. Therefore, CQ/HCQ in combination with zinc should be considered as additional study arm for COVID-19 clinical trials.”
So far, no major clinical trial has bothered to follow this rather commonsense advice. Unfortunately, due to the corruption and politicization of science on this matter, it’s hard to offer any clear recommendations. In the end, it probably comes down to who you trust.
That said, if you suspect you’ve contracted COVID-19, it probably wouldn’t hurt to give a version of Zelenko’s regimen a try, at the first sign of symptoms. As explained in “Is Quercetin a Safer Alternative to Hydroxychloroquine?” quercetin is also an ionophore and has the same mechanism of action as hydroxychloroquine — it improves zinc uptake by your cells.
So, you might not need the drug. You could also swap out the antibiotic for a natural antibacterial such as olive leaf or oregano oil. You can find more information about this in “How to Improve Zinc Uptake with Quercetin to Boost Immune Health.”
Personally, I’m taking quercetin and zinc at bedtime as a prophylactic each day. The reason it’s best to take them in the evening, several hours after your last meal, and before the long fast of sleeping, is because quercetin is also a senolytic (i.e., it selectively kills senescent or old, damaged cells) that is activated by fasting. So, why not maximize the timing and use of quercetin?
The COVID-19 pandemic has raised questions about the efficacy of wearing face masks to reduce the transmission of infectious disease. Health agencies are not always in agreement as to who should or should not be wearing masks. The World Health Organization currently states:1
“Medical masks should be worn by health workers and those caring for someone with COVID-19 symptoms, persons aged 60 and over and anyone with preexisting medical conditions as they are at greater risk of developing serious illness, and people who have symptoms suggestive of COVID-19.”
The Centers for Disease Control and Prevention clearly states that medical masks should be reserved for health care professionals and cloth masks should be worn by the public in areas where people congregate:2
“Cover your mouth and nose with a cloth face cover when around others. Do NOT use a facemask meant for a healthcare worker. Currently, surgical masks and N95 respirators are critical supplies that should be reserved for healthcare workers and other first responders.”
The CDC also states a cloth face mask will not prevent the wearer from getting sick but may keep the virus from spreading.3 Many medical and political leaders also support wearing masks in public, such as Dr. Anthony Fauci from the National Institute of Allergy and Infectious Diseases and past acting CDC director Dr. Richard Besser.4
Across the world, countries that have routinely embraced the use of face masks have posted lower numbers of COVID-19 transmissions.5 Whether this means the mask is reducing transmission or encouraging people to maintain social distancing are questions that still need to be answered.
Experts were debating the effectiveness of wearing masks to reduce the risk of infection long before COVID-19 came into the picture. Surgical masks were introduced nearly a century ago for the purpose of protecting patients during surgery. Yet, researchers continue to question whether this established routine is necessary.6
In one study published in 2016, scientists found no difference in the infection rates of patients undergoing “clean” surgery, whether the surgical team was masked or unmasked.7 A clean surgery was defined as one in which the lungs, gut, genitals and bladder were not involved.
Researchers have also questioned whether wearing masks during the cold season may cut down on the number of health care professionals who get sick.8 The researchers collected data for 77 consecutive days during cold season and determined whether a cold was present and if participants experienced symptoms based on their reports.
The intervention group wore masks at work and the control group did not. During the study period, one individual in the intervention and one in the control group got a cold. Although the study was small, the researchers felt there was not enough evidence to demonstrate benefits to health care workers in terms of preventing cold symptoms.
Investigations into the effectiveness of masks continued with a study published in BMJ.9 Since the results were released in 2015, the researchers have responded to their data in light of the COVID-19 pandemic. The study was aimed at comparing the effectiveness of cloth masks to that of medical masks in health care workers.
They evaluated 14 secondary and tertiary level hospitals in Hanoi, Vietnam, using 1,607 participants who worked full-time in high-risk units. Their measurement outcome was clinical demonstration of respiratory illness, flu-like illness or laboratory-confirmed respiratory infection.
The researchers found that those who wore cloth masks had a significantly higher rate of flu-like illness and all measured infections as compared to participants using medical masks. They cited moisture retention, reuse and poor filtration as potential reasons for the increased rates of infection.
They wrote, “… cloth masks should not be recommended for HCWs [health care workers], particularly in high-risk situations, and guidelines need to be updated.”10
In follow-up comments published in March 2020, the researchers pointed to critical shortages of personal protective equipment and stated that while those wearing cloth masks have a higher rate of infection, they may be better for health care workers than wearing no mask at all.11 They went on to say their research does not excuse health care workers from working unprotected.
Just prior to the pandemic reaching the U.S., a team evaluated the effectiveness of low-cost cloth face masks. The study was published in 2019 and was undertaken since these materials are commonly used in developing countries.12 The team evaluated 20 types of cloth masks and found pore size could range from 80 to 500 nanometers.
This is significantly larger than particulate matter with a diameter of 10 nanometers or less (PM10). They also found that the effectiveness was reduced by 20% after the mask had gone through the fourth cycle of washing and drying. Stretching of the surface altered pore size and washing reduced the number of microfibers within the pores, also altering the effectiveness of the mask.
Finally, the authors of a recently-released preprint study evaluated the effectiveness of reducing airflow in face covers with and without an outlet valve.13 The researchers measured airflow from a person during quiet and heavy breathing and coughing while using different types of face covers.
They found that face covers without an outlet valve reduced the flow of air forward by more than 90%. Individuals using surgical, cloth masks and face shields had intense back and downward flow, which may present a hazard.
In the study from Asia in which the symptoms of health care workers who wore face masks were compared to those who did not, researchers asked about headaches, among other things. Participants who wore masks were much more likely to complain of headaches than those who did not wear masks.14
In a more recent study published in the journal Headache, researchers sought to evaluate the factors associated with headaches resulting from the use of personal protection equipment.15
They also wanted to look into workers’ thoughts on how headaches affected their health and performance. The study team surveyed clinicians at a tertiary care hospital where they worked in areas taking care of COVID-19 patients.
Data were gathered from 158 health care workers including nurses, doctors and paramedical staff. During the study, 128 developed headaches associated with their personal protection equipment and 91.3%:16
“… of respondents with pre‐existing headache diagnosis either ‘agreed’ or ‘strongly agreed’ that the increased PPE usage had affected the control of their background headaches, which affected their level of work performance.”
The researchers did not question the origin of the headaches in the participants, but others have asked whether wearing a mask could reduce levels of oxygen or raise CO2 levels, which in turn could produce a headache.
This question was asked in 2008 by a team of researchers from Turkey who evaluated the oxygen saturation of 53 surgeons during surgical procedures.17 The team used a pulse oximeter before the procedure and immediately postoperatively. The results showed the surgeons experienced a decrease in oxygen saturation and a slight increase in pulse rate.
The decrease in oxygen saturation was more significant in surgeons over the age of 35. Due to the design of the study, the researchers were unable to determine whether the changes in oxygen saturation were from the face mask or stress during the surgery. Concerned about the consistent use of face masks, retired neurosurgeon Dr. Russell Blaylock warned that face masks:18
“… fail to protect the healthy from getting sick, but they also create serious health risks to the wearer. The bottom line is that if you are not sick, you should not wear a face mask.”
He expressed some frustration at the wholesale use of face masks for the vulnerable and healthy individuals, pointing out, “When a person has TB we have them wear a mask, not the entire community of noninfected.”
He referenced a study in 2006 in which researchers evaluated the development of headaches in health care workers who were using an N95 face mask.19 Using a survey, they found that 37.3% reported mask-associated headaches and 32.9% said that this happened more than six times per month.
During the study, 59.5% used analgesics for headache pain and 2.1% took preventive medications. The researchers concluded that the N95 face mask could increase the risk of headaches in health care providers and that using them for shorter periods of time could reduce the frequency and severity of their headaches.
Wearing an N95 mask for up to three hours could have also changed nasal function, making it more difficult to breathe after the mask was removed.20 Before Blaylock went on to discuss the new evidence suggesting coronaviruses may enter the brain, he pointed out:21
“There is another danger to wearing these masks on a daily basis, especially if worn for several hours. When a person is infected with a respiratory virus, they will expel some of the virus with each breath.
If they are wearing a mask, especially an N95 mask or other tightly fitting mask, they will be constantly rebreathing the viruses, raising the concentration of the virus in the lungs and the nasal passages. We know that people who have the worst reactions to the coronavirus have the highest concentrations of the virus early on.”
Based on past evidence,22 Blaylock questions whether wearing a mask could also reintroduce exhaled viruses deep into the nasal cavity, driving up the amount of virus in the upper respiratory tract and increasing the potential to enter the olfactory nerves and travel into the brain.23
Blaylock is not the only expert to react to the widespread use of masks. One group of experts writing in the New England Journal of Medicine said:24
“We know that wearing a mask outside health care facilities offers little, if any, protection from infection. Public health authorities define a significant exposure to Covid-19 as face-to-face contact within 6 feet with a patient with symptomatic Covid-19 that is sustained for at least a few minutes (and some say more than 10 minutes or even 30 minutes).
The chance of catching Covid-19 from a passing interaction in a public space is therefore minimal. In many cases, the desire for widespread masking is a reflexive reaction to anxiety over the pandemic.”
They go on to describe why masks may be critical to protect health care workers in close proximity to patients with active and symptomatic COVID-19. For those working in close quarters with health care workers who may be asymptomatic or who have a mild disease, a mask may at least lessen the risk for patients and other employees to get sick.
The authors of a paper published in the Journal of the American Medical Association agree that face masks should only be used by “individuals who have symptoms of respiratory infection such as coughing, sneezing, or, in some cases, fever.”25 The authors go on to say there's no evidence masks used by healthy people can prevent others from becoming sick.
Ultimately, the goal is to reduce transmission of infectious disease, including COVID-19. It’s apparent scientific evidence supporting or debunking face masks is far from conclusive. If you do choose to wear a face mask, here are strategies from the WHO for reducing the potential of infecting yourself:26
Even though the COVID-19 mortality curve has been flattened, mainstream media outlets continue to push doomsday predictions of an impending explosion of deaths. The New York Times, for example, published articles July 21,2 and July 3,3,4 2020, basically warning everyone to not get excited about plummeting mortality rates, as the trend could change at any moment.
"Why Virus Deaths Are Down but May Soon Rise," its July 2 headline states. The article goes on to claim "coronavirus trends in the United States are pretty dark right now" — based on surging case numbers, meaning positive test results, not hospitalizations or people exhibiting actual symptoms.
The article attributes the steady and relatively rapid drop-off in deaths to improved medical treatment and older people being more cautious, but warns that "Deaths may be on the verge of rising again," because "middle-aged and younger people are acting as if they're invulnerable" and have increased their social activities.
"Their increased social activity has fueled an explosion in cases over the last three weeks, which in turn could lead to a rise in deaths soon," The New York Times states,5,6 adding:
"With testing now more widespread, it's possible that the death data will lag the case data by closer to a month. (In a typical fatal case, the death comes three to five weeks after contraction of the virus.) If that's correct, coronavirus deaths may start rising again any day."
This, however, completely ignores data showing that the COVID-19 fatality rate for those under the age of 45 is “almost zero,” and between the ages of 45 and 70, it’s somewhere between 0.05% and 0.3%.7,8,9
In other words, the fact that young and middle-aged adults are testing positive in droves is not a warning sign of an impending onslaught of deaths, as the risk of death in these age groups is minuscule. If anything, it seems to show herd immunity is building which, ultimately, will help protect the most vulnerable among us.
The primary justification for the tyrannical governmental interventions of COVID-19 was to slow the spread of the infection so that hospital resources would not be overwhelmed, causing people to die due to lack of medical care. These interventions were not about stopping the spread or reducing the number of people that would eventually get infected.
It was only intended to slow it down so, eventually, naturally-acquired herd immunity — the best kind — would prevent its spread. Well guess what? They have changed the narrative. That is why you now do not hear anything about flattening the curve. Instead they transitioned the fear-mongering to alarm the public that the number of “cases” are increasing.
Bear in mind that you do NOT need any test to be classified as a COVID case. All you need is a simple upper respiratory infection and you can legally be classified as a COVID-19 case to artificially inflate the totals.
The fatality rate data given above were cited by Stanford University's disease prevention chairman Dr. John Ioannidis — an epidemiologist who has made a name for himself by exposing bad science — in a June 27, 2020, interview with Greek Reporter,10,11,12 in which he criticized global lockdown measures, saying they were implemented based on flawed modeling and grossly unreliable data.
"0.05% to 1% is a reasonable range for what the data tell us now for the infection fatality rate, with a median of about 0.25%," Ioannidis told Greek Reporter.13
"The death rate in a given country depends a lot on the age-structure, who are the people infected, and how they are managed. For people younger than 45, the infection fatality rate is almost 0%. For 45 to 70, it is probably about 0.05-0.3%.
For those above 70, it escalates substantially, to 1% or higher for those over 85. For frail, debilitated elderly people with multiple health problems who are infected in nursing homes, it can go up to 25% during major outbreaks in these facilities."
When asked whether the curve had indeed been flattened in the U.S., seeing how no health care system had been completely overwhelmed, Ioannidis answered:14
"The predictions of most mathematical models in terms of how many beds and how many ICU beds would be required were astronomically wrong. Indeed, the health system was not overrun in any location in the USA, although several hospitals were stressed. Conversely, the health care system was severely damaged in many places because of the measures taken …
Major consequences on the economy, society and mental health have already occurred. I hope they are reversible, and this depends to a large extent on whether we can avoid prolonging the draconian lockdowns and manage to deal with COVID-19 in a smart, precision-risk targeted approach, rather than blindly shutting down everything …
I hope that policymakers look at the big picture of all the potential problems and not only on the very important, but relatively thin slice of evidence that is COVID-19."
The fear-mongers also ignore recent Centers for Disease Control and Prevention statements15 saying the COVID-19 mortality — which had declined for the last 10 weeks straight — "is currently at the epidemic threshold," meaning if it slides down just a little more, COVID-19 will no longer meet the CDC's criteria for "epidemic" status.
The percentage of doctors' visits for influenza-like illness (ILI) for all age groups has also dropped below the 2019-2020 baseline, as seen in the CDC graph below, published July 3, 2020.16
The graph below shows the percentage of visits to emergency departments, specifically, related to suspected ILI and COVID-19-like illness (CLI). While ER visits for suspected COVID-19 have seen a slight uptick, it's not an extreme increase.
The video above reviews why the rise in COVID-19 "cases" is misleading at best, and not a viable measure of a public health threat. It presents a historical overview of what happened during the 2009 swine flu pandemic, and how it parallels the current COVID-19 pandemic.
In summary, fear of a novel illness — pandemic swine flu — led to a dramatic spike in testing, making it seem like a significant threat as many tested positive. Yet the death toll was insignificant. We're seeing the same thing happening now. Two things are driving the numbers of positive tests skyward: The sudden availability of tests, and widespread testing of asymptomatic people.
Put another way. The sharp increases in "cases" are not proof of disease spread but rather the spread of testing. When you don't have a test for the infection, you cannot tally positive cases. Hence it looked like there were virtually no COVID-19 cases in January 2020.
The sudden jump in cases in February correlates with the emergence of test kits sent out by the CDC. Once those test kits were used up, the number of "cases" again dried up. Then, once test kits became readily available again in early April, the number of cases skyrocketed — as you'd expect. But again, this doesn't mean the disease was spreading like wildfire.
It was probably in circulation throughout and countless people were already walking around with it, feeling no worse than normal. The only difference is that test kits became available and massive amounts of people — whether they had symptoms or not — were being tested.
In short, the graphs showing "cases" in large part simply illustrate the availability of testing. Granted, even this is an oversimplification and is not going to be exact, and there's more than one reason for this. For example, during the third week of May, the CDC admitted it had combined the results from viral and antibody tests in its national results.17
This provides a really inaccurate picture, since the two tests describe very different things. The viral test is supposed to identify active infections (regardless of whether you have symptoms or not), whereas the antibody test tells you if you've been exposed to the virus in the past and fought it off by developing antibodies. Hence, an antibody test should not be counted as an active infection or active "case."
Some data18 also suggest positive test results have declined even as testing has increased. The question is, could this be an indication that people who are being tested for active infection have already fought off the virus and have antibodies? Could it be a sign of rising herd immunity?
Unfortunately, COVID-19 test data has been so mishandled and the way the data is compiled has changed enough times that it's virtually impossible to make sense of it at this point. The quality and reliability of the tests themselves, both viral and antibody, also appear to be less than stellar.
The CDC has admitted that prior exposure to coronaviruses responsible for the common cold can result in a positive COVID-19 antibody test,19 and during an April White House Coronavirus Task Force briefing, Dr. Birx explained that COVID-19 tests are "not 100% sensitive or specific," and that when prevalence is low in the community, the false positive rate will be high.
"If you have 1% of your population infected, and you have a test that's only 99% specific, that means that when you find a positive, 50% of the time will be a real positive and 50% of the time it won't be," Birx said. In other words, if the prevalence of infection in the community is 1%, about half of all positive tests will be false positives.
Only as the overall infection rate gets higher does the viral test become increasingly reliable. Who knows, perhaps this is why some of the data suggest the number of positive tests is actually decreasing even as testing continues to increase?
As you may recall, early on, the media focused on the death toll and hospitalizations. We had daily news ticker tapes providing us with the numbers of severe and critical cases, and the number of deaths.
These statistics were used to justify draconian lockdown orders to prevent hospitals from becoming overwhelmed. Now you hear virtually nothing about hospitalizations or deaths.
It's all about the rising number of "cases," meaning infected individuals, which is to be expected when you test a population in which the virus has already infected the majority. But that doesn't mean it poses a threat, since deaths continue to drop.
It seems many are simply unwilling to accept the good news and allow the population to return to normal living. Instead, "rising cases" — especially among previous low-risk age groups — is now being used to justify continued stay-at-home orders, even though hospitals are at no risk of being overwhelmed since a vast majority of these cases are asymptomatic and need nothing in terms of health care.
In its April 13, 2020, issue, the German magazine Blauer Bote20,21 lists a collection of 75 expert opinions about the COVID-19 threat. Among them is a statement from Gerd Bosbach,22 professor emeritus of statistics, mathematics and empirical economic and social research, and author of the book, "Lying With Numbers," who said (translated from German to English using TranslationLookup.com23):24
"The tripling of the tests resulted in a little more than tripling the number of those who tested positive. This tripling was presented to the citizens as a tripling of the infected …
Far-reaching decisions require secure foundations. This is exactly what has been neglected so far. The repeated equation of the number of positively tested people with the number of infected clouded the view …
The government's standard of when measures should be weakened is based on an apparent number of infected people, which has nothing to do with reality …
So we have a muddle of terms, which is ultimately explained by the fact that we keep talking about infected people instead of positive people. The high numbers remain in memory, such as the mortality rate of 3.4% stated by the WHO. And that creates fear …
We should ensure that the media do not use the power of images to generate emotions that influence our judgment. If you get pictures of coffins and death departments from Italy or pictures of completely empty shelves, then their effects exceed the facts mentioned."
In related news, several recent studies suggest a majority of the population may already have immunity against COVID-19, via one mechanism or another. According to a Swiss study,25,26 SARS-CoV-2-specific antibodies are only found in the most severe cases — about 1 in 5. That suggests COVID-19 may in fact be five times more prevalent than suspected. This also means it may be five times less deadly than predicted. According to the authors:
"When symptomatic, COVID-19 can range from a mild flu-like illness in about 81% to a severe and critical disease in about 14% and 5% of affected patients, respectively."
They also found that even though people who had been exposed to COVID-19 had SARS-CoV-2-specific immunoglobulin A (IgA) antibodies in their mucosa, there were no virus-specific antibodies in their blood.
IgA is an antibody that plays a crucial role in the immune function of your mucous membranes, while IgG is the most common antibody that protects against bacterial and viral infections and is found in blood and other bodily fluids. As explained by the authors:27
"As with other coronaviruses, symptomatic SARS-CoV-2 disease causes an acute infection with activation of the innate and adaptive immune systems. The former leads to the release of several pro-inflammatory cytokines, including interleukin-6 …
Subsequently, B and T cells become activated, resulting in the production of SARS-CoV-2-specific antibodies, comprising immunoglobulin M (IgM), immunoglobulin A (IgA), and immunoglobulin G (IgG).
Whereas coronavirus-specific IgM production is transient and leads to isotype switch to IgA and IgG, these latter antibody subtypes can persist for extended periods in the serum and in nasal fluids. Whether SARS-CoV-2-specific IgG antibodies correlate with virus control is a matter of intense discussions."
Another study28,29 published in the journal Cell found 70% of samples from patients who had recovered from mild cases of COVID-19 had resistance to SARS-CoV-2 on the T-cell level. Curiously, 40% to 60% of people who had not been exposed to SARS-CoV-2 also had resistance to the virus on the T-cell level.
According to the authors, this suggests there's "cross-reactive T cell recognition between circulating 'common cold' coronaviruses and SARS-CoV-2." In other words, if you've recovered from a common cold caused by a particular coronavirus, your humoral immune system may activate when you encounter SARS-CoV-2, thus rendering you resistant to COVID-19.
May 14, 2020, Science magazine reported30 these Cell findings, drawing parallels to another earlier paper31 by German investigators that had come to a similar conclusion. That German paper,32 the preprint of which was posted April 22, 2020, on Medrxiv, found helper T cells that targeted the SARS-CoV-2 spike protein in 15 of 18 patients hospitalized with COVID-19.
Yet another study,33,34,35 this one by researchers in Singapore, found common colds caused by the betacoronaviruses OC43 and HKU1 might 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.
Two additional studies suggesting herd immunity is near were reported36 by Reason, July 1, 2020. These include a Swedish study,37,38 which found "SARS-CoV-2 elicits robust memory T cell responses akin to those observed in the context of successful vaccines, suggesting that natural exposure or infection may prevent recurrent episodes of severe COVID-19 also in seronegative individual." Similarly, a German study39 concluded:
"SARS-CoV-2-specific T-cell epitopes enabled detection of post-infectious T-cell immunity, even in seronegative convalescents. Cross-reactive SARS-CoV-2 T-cell epitopes revealed preexisting T-cell responses in 81% of unexposed individuals, and validation of similarity to common cold human coronaviruses provided a functional basis for postulated heterologous immunity in SARS-CoV-2 infection."
So far, many efforts to curb COVID-19 infection have proven to be ill advised. Evidence shows the illness spreads mostly indoors,40,41,42 for example, casting doubt on the sanity of closing parks and beaches, especially during the summer. As reported by The Baltimore Sun,43 scientists are now considering using ultraviolet light to eradicate SARS-CoV-2 in indoor air. Step outside, and you get that effect for free.
The total all-cause mortality is not significantly different than in previous years as discussed by my interview with Denis Rancourt. Many other deaths have been shifted to COVID-19, bringing a high spike in deaths, but when you look at the area under the curve for total deaths, it really doesn't differ from previous years.
This was also echoed by the American Institute for Economic Research.44 Back in April 2020 they referred to the COVID-19 pandemic as "An egregious statistical horror story" that resulted in "a vandalistic lockdown on the economy," which:
"… would have been an outrage even if the assumptions were not wildly astronomically wrong. Flattening the curve was always a fool's errand that widened the damage …
The latest figures on overall death rates from all causes show no increase at all. Deaths are lower than in 2019, 2018, 2017 and 2015, slightly higher than in 2016. Any upward bias is imparted by population growth.
Now writing a book on the crisis with bestselling author Jay Richards, [statistician William] Briggs concludes: 'Since pneumonia deaths are up, yet all deaths are down, it must mean people are being recorded as dying from other things at smaller rates than usual.' Deaths from other causes are simply being ascribed to the coronavirus.
As usual every year, deaths began trending downward in January. It's an annual pattern. Look it up. Since the lockdown began in mid-March, the politicians cannot claim that their policies had anything to do with the declining death rate.
A global study45 published in Israel by Professor Isaac Ben-Israel, chairman of the Israeli Space Agency and Council on Research and Development, shows that 'the spread of the coronavirus declines to almost zero after 70 days — no matter where it strikes, and no matter what measures governments impose to try to thwart it.'
In fact, by impeding herd immunity, particularly among students and other non-susceptible young people, the lockdown in the U.S. has prolonged and exacerbated the medical problem. As Briggs concludes, 'People need to get out into virus-killing sunshine and germicidal air.'"
Mechanical ventilators may cause more harm than good in a significant number of COVID-19 patients, which is a conundrum for physicians used to treating severe hypoxia — low blood oxygen — with such machines. In some cases, COVID-19 patients have oxygen levels that are so low they’re considered “incompatible with life,” yet the patients have no shortness of breath or labored breathing.1
The phenomenon has been dubbed “happy hypoxia,” a term medically known as silent hypoxemia, in which COVID-19 patients may have blood-oxygen saturation levels as low as 50% — normal blood-oxygen saturation is 95% or higher.
“There is a mismatch [between] what we see on the monitor and what the patient looks like in front of us,” Dr. Reuben Strayer, an emergency physician at Maimonides Medical Center in New York City, told Science.2
Typically, if a person has low oxygen saturation, they’ll be treated with breathing support in the form of continuous positive airway pressure, or CPAP, masks, which are often used to treat severe sleep apnea. CPAP devices regulate the pressure and level of oxygen that reaches the lungs,3 using mild air pressure to keep breathing airways open.
Bilevel positive airway pressure ventilators (BiPAP), another noninvasive device to supply pressurized air into the airways, may also be used. If oxygen saturation doesn’t increase, or in cases of acute respiratory distress syndrome (ARDS), a lung condition that’s common in severe COVID-19 cases, and which causes low blood oxygen and fluid buildup in the lungs, mechanical ventilation is often recommended.
However, research is revealing that COVID-19 patients placed on ventilators often don’t survive, leading experts to suggest the machines are being overused and patients may do better with less invasive treatments.
“Mechanical ventilation is the main supportive treatment for critically ill patients” infected with novel coronavirus 2019 (COVID-19), according to a February 2020 study published in The Lancet Respiratory Medicine.4 Yet, it’s quickly become apparent that invasively ventilated COVID-19 patients often don’t make it, and have a very high case fatality rate of more than 50%.5
The practice is widespread, nonetheless. In a case series of 1,300 critically ill patients admitted to intensive care units (ICUs) in Lombardy, Italy, 88% received invasive ventilation, but the mortality rate was still 26%.6
Further, in a JAMA study that included 5,700 patients hospitalized with COVID-19 in the New York City area between March 1, 2020, and April 4, 2020, mortality rates for those who received mechanical ventilation ranged from 76.4% to 97.2%, depending on age.7
Similarly, in a study of 24 COVID-19 patients admitted to Seattle-area ICUs, 75% received mechanical ventilation and, overall, half of the patients died between one and 18 days after being admitted.8
There are many reasons why those on ventilators have a high risk of mortality, including being more severely ill to begin with. However, given the poor outcomes, some physicians are now trying to keep patients off of ventilators as much as possible by using less-invasive alternative measures.
“Contrary to the impression that if extremely ill patients with Covid-19 are treated with ventilators they will live and if they are not, they will die, the reality is far different,” Dr. Muriel Gillick of Harvard Medical School told STAT news.9
There are risks inherent to mechanical ventilation itself, including impairment to the lung’s air sacs from high levels of oxygen and lung damage caused by the high pressure used by the machines. Long-term sedation from the intubation is another risk, one that’s difficult for some patients, especially the elderly, to bounce back from.
In cases of ARDS, the lung’s air sacs may be filled with a yellow fluid that has a “gummy” texture, making oxygen transfer from the lungs to the blood difficult, even with mechanical ventilation.
According to Gillick, “We need to ask, are we using ventilators in a way that makes sense for other diseases but not for this one? Instead of asking how do we ration a scarce resource [ventilators], we should be asking how do we best treat this disease?”10
In some cases, there’s evidence that a far less invasive nasal cannula may be sufficient to help COVID-19 patients. In a study of COVID-19 patients in China, most of the critically ill patients received high-flow nasal cannula (HFNC) oxygen therapy as a first-line treatment, and it was sufficient in the majority of cases.11
Although 41% did eventually require more intensive breathing support, noninvasive ventilation, such as BiPAP, was offered next and again succeeded in keeping most of the patients off mechanical ventilators. Ultimately, only four of the 27 patients with severe acute respiratory failure were intubated.
According to some physicians, COVID-19 patients display symptoms more in line with altitude sickness than pneumonia, such as having low levels of carbon dioxide in the blood, despite low oxygen, calling mechanical ventilation into further question.
Speaking with STAT, Dr. Scott Weingart, a critical care physician in New York and host of the “EMCrit” podcast, said, “we’ve had a number of people who improved and got off CPAP or high flow [nasal cannulas] who would have been tubed 100 out of 100 times in the past.”
But, he said, automatically putting patients on mechanical ventilators “is really bad,” adding “… I think these patients do much, much worse on the ventilator … I would do everything in my power to avoid intubating patients.”12
An April 2020 article by Drs. Luciano Gattinoni and John Marini describes two different types of COVID-19 presentations, which they refer to as Type L and Type H.13 In Type L, patients have “low lung elastance (high compliance), lower lung weight as estimated by CT scan, and low response to PEEP [positive end-expiratory pressure].” Many patients become stabilized at this stage and do not deteriorate further.
However, in some cases symptoms closer to ARDS develop. This type of presentation is defined as Type H, and includes “high elastance (low compliance), higher lung weight, and high PEEP response.”
Importantly, while one type benefits from mechanical ventilation, the other does not. Dr. Roger Seheult discusses this paper, as well as the comparison of COVID-19 to high altitude pulmonary edema, or HAPE, in the MedCram video above, once again suggesting it may turn out that mechanical ventilators are inappropriate for a majority of patients.
Meanwhile, doctors at University of Chicago (UChicago) Medicine reported “truly remarkable” results using high-flow nasal cannulas in lieu of ventilators.14 In fact, 24 COVID-19 patients who were in respiratory distress were given HFNCs instead of ventilators. All “fared extremely well,” and only one required intubation 10 days later.
Dr. Michael O’Connor, director of critical care medicine, called the team’s success “truly remarkable. At one point, the department had 137 COVID-19 patients, but only 27 were on ventilators. “The medical staff has avoided mechanical ventilation on 40% of patients, and extubated 50% of those who needed ventilators, O’Connor said in a news release. “It’s a phenomenal number, because in Italy, the number of extubations was much lower.”15
The team has also been combining the use of HFNCs with prone positioning, another alternative treatment that’s shown promise for treating COVID-19. Lying in the prone (face down) position, in which your chest is down and your back is up, has been shown to improve outcomes in people with severe ARDS,16 and oxygenation tends to be significantly better among patients in the prone position compared to the supine (face up) position.17
A study of critically ill COVID-19 patients in China’s Jiangsu Province recommended the use of awake prone positioning, which, the researchers noted, “showed significant effects in improving oxygenation and pulmonary heterogeneity.”18
It’s also been suggested that the physiological changes that occur with prone positioning may be even more favorable in spontaneously breathing patients than in those who are intubated.
A 2003 study found, in fact, that the prone position led to a rapid increase in partial pressure of oxygen, or PaO2, which is a measure of how well oxygen moves from the lungs to the blood, among patients with respiratory failure.19 All of the patients in the study were able to avoid mechanical ventilation.
Dr. Thomas Spiegel, medical director of UChicago Medicine’s emergency department, said, “The proning and the high-flow nasal cannulas combined have brought patient oxygen levels from around 40% to 80% and 90%, so it’s been fascinating and wonderful to see.”20
The UChicago Medicine team is using an approach they’ve dubbed “prevent the vent,” which involves using mechanical ventilation only as a last resort. “Avoiding intubation is key,” Spiegel said. “Most of our colleagues around the city are not doing this, but I sure wish other ERs would take a look at this technique closely.”21
Hyperbaric oxygen therapy (HBOT) is another treatment adjunct being explored against severe COVID-19. It works by supplying 100% oxygen in a pressurized chamber, which allows your body to absorb oxygen directly into your tissues. Since there's no airflow being forced directly into the lungs, it doesn’t cause the lung damage that mechanical ventilation can.
Dr. Kelly Thibodeaux with Opelousas General Hospital in Louisiana, which has a hyperbaric center, called HBOT “a less invasive way to deliver oxygen that doesn't require sticking a tube down the trachea.”22
Thibodeaux and colleagues explained, “Once intubated, mortality increases exponentially.”23 They’ve been deploying off-label compassionate use of HBOT as an alternative for patients that would otherwise have required ventilation, with promising results. In a case series of five patients, “dramatic improvement” was seen with HBOT. According to the article:
“All the patients recovered without the need for mechanical ventilation. Following HBOT, oxygen saturation increased, tachypnea [rapid breathing] resolved and inflammatory markers fell.
At the time of writing, three of the five patients have been discharged from the hospital and two remain in stable condition … Most importantly, HBOT potentially prevented the need for mechanical ventilation.”24
Ongoing research will be needed to determine the best course of action for individual COVID-19 cases, but it appears that starting with the least invasive options is beneficial in the majority of cases, while an increasing number of physicians are advising against mechanical ventilation whenever possible.
By now, you're probably aware that one of the lethal effects of COVID-19 is the virus' ability to trigger a cytokine storm. It makes sense then that many health practitioners are looking at ways to strengthen and improve immune function. The good news is there are several strategies that appear very helpful in this respect.
Supplements and strategies that have been identified as capable of modulating immune responses and suppressing cytokine storm include but are not limited to:
To this list, we can also add the omega-3 fats docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), long-chained omega-3 fats found in cold-water fatty fish like wild-caught Alaskan salmon, sardines, anchovies and krill, just to name a few.
According to the opinion paper "The Potential Beneficial Effect of EPA and DHA Supplementation Managing Cytokine Storm in Coronavirus Disease," published June 19, 2020, in the journal Frontiers in Physiology, EPA and DHA are known to affect biological pathways that "may have direct influence in the outcome of COVID-19":1
"To date, the molecular events that precipitate a 'cytokine storm' or the applicable therapeutic strategies to prevent and manage this process is not elucidated because of the complex nature of this problem.
Recent articles suggest that specific nutrients such as vitamin B6, B12, C, D, E, and folate; trace elements, including zinc, iron, selenium, magnesium, and copper may play a key role in the management of cytokine storm …
LC-PUFAs (long chain polyunsaturated fatty acids) such as EPA … and DHA … are noteworthy because of their direct influence in the immunological response to viral infections. Evidence suggests that n-3 LC-PUFAs can modulate the immune response and function in many ways.
Among these complex immunomodulatory effects, interleukin-6 (IL-6) and interleukin-1ß (IL-1β) — because of the suspected central regulatory role in the 'cytokine storm' — should be highlighted. These cytokines can be affected by dietary EPA and DHA intake (Figure 1).
In addition, poly(ADP-ribose) polymerase enzymes that have anti-inflammatory properties, translatable to human COVID-19 infection were shown to improve tissue levels of DHA and EPA, as well as the downstream anti-inflammatory metabolites of EPA and DHA further underscoring the applicability of DHA and EPA in COVID-19."
Figure 1: Main pathways for the metabolism of DHA and EPA yielding anti-inflammatory metabolites.
While not mentioned in this Frontiers in Physiology paper, animal-based omega-3 fats, especially DHA, have also been shown to prevent thrombosis (a blood clot within a blood vessel) by decreasing platelet aggregation. As discussed in "COVID-19 Critical Care," hypercoagulation is another complication of severe COVID-19 infection that can have lethal consequences. Omega-3 also:
Unfortunately, the authors recommend using "algae- or plant-based sources of EPA and DHA" rather than marine-based sources. I believe this is a mistake. While microalgae2 do contain DHA and EPA and are a viable source for strict vegetarians, as previously discussed in "The Critical Differences Between Omega-3 Fats From Plants and Marine Animals," most plant-based omega-3s actually do not contain any of the long-chain omega-3 fats, DHA and EPA.
As mentioned, ideal sources of DHA and EPA are marine-based and include cold-water fatty fish like wild-caught Alaskan salmon, sardines and anchovies. If you do not eat these fish on a regular basis, consider taking a krill oil supplement. To learn more about why krill oil is preferable over fish oil, see the infographic below.
As it pertains to the issue of cytokine storm, the authors of the Frontiers in Physiology paper3 point out there are at least three studies showing that by lowering triglycerides, the risk of developing a cytokine storm is diminished, and krill oil, specifically, has been shown to lower triglycerides more effectively than fish oil.4
Along with vitamin D testing, measuring your omega-3 level at least once a year is strongly recommended, as being low in this vital nutrient can spell trouble for your health in more ways than one.
One of the reasons why DHA and EPA are so crucial is because they're actually key structural elements of your cells; they're not just simple fuel. If you don't have enough DHA and EPA, your body's ability to repair and maintain healthy cell structures is seriously impaired.
The assay to measure omega-3 in your red blood cells was developed by William Harris, Ph.D., in 2004. The omega-3 index is expressed as a percent of all fatty acids in the red blood cell membrane.5 Data from studies Harris performed showed an ideal, healthy range of omega-3 is 8% to 12%.6,7
GrassrootsHealth co-founder Carole Baggerly commented on the Frontiers in Physiology paper in a personal email to me: "Based on this data, it is highly likely that the higher omega-3 would help prevent the cytokine storm … I would … get up to the index level of 8.1% at least."
Not only do you want to make sure you are getting sufficient omega-3, but it is also absolutely imperative you limit your omega-6 intake, especially from processed vegetable oils. I discuss this in greater detail in a section below. This is another benefit of the omega-3 index test, as it will show you precisely the levels of these potentially dangerous fats in your cells.
GrassrootsHealth, a nonprofit public health research organization, has several cost-effective testing options available as part of its consumer-sponsored nutrient research projects,8 the aims of which are to establish population-based nutrition recommendations based on science-backed data.
For example, ongoing research by GrassrootsHealth has established the ideal vitamin D range for disease prevention is between 60 and 80 ng/mL. It conducts the same kind of consumer-sponsored research for omega-3 and magnesium. For omega-3, you have four test options:
Each kit contains instructions for how to collect your blood sample. You then mail in your sample and fill out a quick online health questionnaire through GrassrootsHealth. Your test results will be emailed to you in about 10 to 20 days after your samples are received.
Based on your index result, you will then be able to use GrassrootsHealth's omega-3 index calculator9 to determine the dosage you may require to raise your current level to your chosen target level.
Avoid the temptation to assume that your omega-3 index is sufficient just because you're eating fish or taking a supplement. Many fish do not contain high omega-3 levels (you have to eat cold-water fatty fish to reap that benefit), and many fish oil supplements are synthetic with questionable efficacy.
As reported by GrassrootsHealth,10 of the first 135 participants in the D*action + Omega-3 home testing project, 85% had an omega-3 index below 8%, which is the lower threshold for sufficiency, putting them at increased risk for heart disease11 and other chronic diseases, as well as death from any cause. To learn more about the benefits of optimizing your level, see "How Much Omega-3 Do You Need?"
As reported by GrassrootsHealth:12
"In studies using a measurement called the Omega-3 Index test, individuals with a low Omega-3 Index were shown to have a 10-fold higher risk of death compared to those with a high index … An Omega-3 Index between 8% and 12% was associated with lower risk for death from cardiovascular disease, versus an index less than 4%."
Again, while many need a marine-based omega-3 supplement to get their level up, it's also crucial to limit your intake of omega-6 fats from vegetable oils. This even includes some healthy oils such as virgin olive oil.
Aside from the fact that a majority of olive oils are fake, even the real McCoy can cause trouble when consumed in too-high amounts, as it's loaded with omega-6 and therefore can skew your omega-3 to omega-6 ratio.
Ideally, this ratio should be close to 1-to-1, but because people eat so little omega-3 and excessive amounts of omega-6, it's not uncommon for this ratio to be closer to 1-to-25 of greater. When your consumption is this skewed, you may still have a hard time optimizing your omega-3 index, even when taking a supplement.
It's important to realize that your body metabolizes omega-3 and omega-6 polyunsaturated fatty acids (PUFAs) into eicosanoids, which are hormone-like substances. As a general rule, omega-3 eicosanoids are anti-inflammatory while omega-6 eicosanoids have proinflammatory effects.13
Part of the benefits of omega-3 fats is that they block the proinflammatory effects of omega-6 eicosanoids, but if your omega-6 intake is too great, you may still have high rates of inflammation. Omega-6 fats also:14
According to the 2017 U.S. Department of Agriculture report,15 "U.S. Trends in Food Availability," consumption of healthy saturated animal fats such as butter, lard and beef tallow fell by 27% between 1970 and 2014, while consumption of harmful vegetable oils rose by 87%. Intake of salad and cooking oils specifically rose by 248%.
As noted in "New Study Tells Why Chicken Is Killing You and Saturated Fat Is Your Friend," which features a podcast interview with Dr. Paul Saladino and Nina Teicholz, conventional chicken is also a hidden source of harmful omega-6 linoleic acid, due to the fact that they're fed corn. So, your best bet is to eat the eggs, not the chicken.
Compelling evidence suggests processed vegetable oils, rich in omega-6 polyunsaturated fatty acids, are likely the primary culprit in our modern diet, contributing to the development of just about all chronic diseases. I believe they take a greater toll on human health than high fructose corn syrup even.
Not only have vegetable oils been linked to heart disease, gastrointestinal diseases such as irritable bowel disorder and inflammatory conditions such as arthritis, they've also been linked to cancer, especially neuroblastoma, breast, prostate, colon and lung cancer.16
In a November 8, 2019, Medium article,17 Maria Cross, a nutritionist with a master of science degree, discusses the science behind vegetable oils and what makes them carcinogenic. She explains:
"There are two classes of PUFA: omega-6 and omega-3. Although functionally distinct and non-interchangeable, these two classes are perpetually engaged in a metabolic balancing act, pushing and pulling as they compete for absorption in the body.
There is nothing intrinsically wrong with omega-6 PUFAs: we need them … That's why scientists believe that it is not omega-6 per se that is to blame; it's the balance between the two groups of PUFA that is out of kilter and wreaking havoc on our bodies.
We evolved on, and are genetically adapted to, a diet that provides more or less equal amounts of omega-3 and omega-618 … Experimental data19 supports the theory that it is this skewed balance between the two PUFAs that influences the development of a tumor."
Similarly, the 2002 paper20 "The Importance of the Ratio of Omega-6/Omega-3 Essential Fatty Acids" points out that:
"Excessive amounts of omega-6 polyunsaturated fatty acids (PUFA) and a very high omega-6/omega-3 ratio, as is found in today's Western diets, promote the pathogenesis of many diseases, including cardiovascular disease, cancer, and inflammatory and autoimmune diseases, whereas increased levels of omega-3 PUFA (a low omega-6/omega-3 ratio) exert suppressive effects."
In addition to promoting chronic disease by throwing your omega-3 to omega-6 ratio off kilter, vegetable oils also have more direct toxic effects. One of the reasons for this is because they degrade when heated, forming extremely toxic oxidation products such as cyclic aldehydes.21
Cyclic aldehydes cause oxidized low-density lipoprotein (LDL) associated with heart disease. They also crosslink tau protein and create neurofibrillary tangles, thereby contributing to the development of neurodegenerative diseases.
As explained by Dr. Cate Shanahan in her book, "Deep Nutrition: Why Your Genes Need Traditional Food,"22 in order to understand how dietary fats affect your health you need to understand how fats oxidize.
The omega-6 PUFAs found in vegetable oils have highly perishable bonds that react with oxygen, creating a free radical cascade that turns normal fatty acids in your body into dangerous high-energy molecules that wreak havoc in a way similar to that of radiation.
What's more, many of the vegetable oils produced today — especially corn and soy oil — are genetically engineered and a significant source of glyphosate exposure, and glyphosate has also been linked to gut damage and other health problems.
Shanahan's book also expounds on the hazards of 4-hydroxynonenal (4HNE), which is the oxidized form of omega-6 vegetable oil and forms during the processing. 4HNE is highly toxic, especially to your gut bacteria, and consumption of 4HNE has been correlated with having an obesogenic balance of gut flora.
4HNE causes cytotoxicity and DNA damage, and instigates free radical cascades that damage the mitochondrial membrane. The omega-6 found in vegetable oils also damages the endothelium (the cells lining your blood vessels), allowing LDL and very low-density lipoprotein (VLDL) particles to penetrate into the subendothelium.
Importantly, these oils get integrated into your cell and mitochondrial membranes (just like healthy omega-3s), and once these membranes are impaired, it sets the stage for all sorts of health problems.
They also make cell membranes less fluid, which impacts hormone transporters in the cell membrane and slows your metabolic rate, and inhibit the removal of senescent cells — aged, damaged or crippled cells that have lost the ability to reproduce and produce inflammatory cytokines that rapidly accelerate disease and aging.
Vegetable oils also strip your liver of glutathione (which produces antioxidant enzymes), thereby lowering your antioxidant defenses,23 and inhibit delta-6 desaturase (delta-6), an enzyme involved in the conversion of short-chained omega-3s to longer chained omega-3s in your liver.24
Remember, omega-6 and omega-3 oils are polyunsaturated oils and highly susceptible to oxidation and becoming biologically damaged. This is why it is NOT as simple as merely adding omega-3 oils to your diet to improve your ratio. Merely increasing your omega-3 could actually make your health worse by increasing the oxidized fats.
The absolute key is to be assiduous in removing ALL vegetable oils. You simply should avoid them at all costs. Another source high in omega-6 oils is chicken meat. Chicken is very high in the omega-6 fat linoleic acid because they eat so many omega-6 rich grains.
One of the best ways you can get a handle on how many omega-6 oils you are eating is by using the incredible nutrient tracking app call Cronometer. If you use the app on your desktop, it is completely free. As long as you are accurately weighing your foods when you enter them, it will give you a fantastic estimate of how many omega-6 oils you are really eating.
This may be one of the most important and least expensive health strategies you can implement today.
Additionally, as noted in my recent interview with Dr. Chris Knobbe, omega-6-rich oils have a half-life of 600 to 680 days in your body. That means it can take quite a few years to empty your body stores of these damaging omega-6 fats. That said, eliminating them from your diet now will, over time, allow your body to rid itself of them, thus steadily improving your health.
In summary, as with vitamin D, optimizing your omega-3 index to a level of at least 8% may be a strategy that can help lower your risk of an adverse COVID-19 outcome, as omega-3 fats are important modulators of immune function25 and can help lower your risk of a cytokine storm.
Just remember that increasing your intake of omega-3 may not be sufficient. In all likelihood, you also need to limit your intake of vegetable oils, including corn-fed chickens. Together, these two strategies should allow you to achieve a healthy omega-3 to omega-6 ratio.
Vision is one of your five senses and protecting it has an impact on your overall physical and mental health. Your eye is a complex organ that takes in light bouncing off objects in the environment. Structures in the eye bend and change shape so your brain can interpret your surroundings.
Light first enters through the cornea, which is a clear covering over the eye.1 This functions to protect the eye and to bend the light so it can pass through the dark pupil at the center of your iris, the colored part of the eye. The iris gets larger or smaller, which makes the pupil look smaller or larger, to regulate the amount of light.
Light passes through the lens, which also bends the rays to focus them on the retina at the back of the eye. This structure has tiny light-sensitive nerve cells called cones and rods. The cones are sensitive to color and are in the center of the retina, near the macula.
The rods are sensitive to light intensity and don't register color.2 They are located outside the macula, extending to the edge of the retina. The cones and rods convert the light into electrical impulses and send them to the brain where your brain perceives an image.
Visual loss or impairment has an impact on a person's mental and physical well-being. The American Academy of Ophthalmology writes that those with a visual impairment experience a higher risk of some conditions such as depression, social withdrawal and accidents.3
People with vision loss may also experience a higher risk of chronic health conditions such as high blood pressure, heart disease, kidney failure, hearing loss and arthritis.4 As the population ages, the number who have visual impairment or blindness also rises.
The primary causes of visual impairment appear to increase with age. These include cataracts, age-related macular degeneration, glaucoma and diabetic retinopathy.5 Loss of vision at night may not get as much attention as other eye conditions, but it is commonly found in those who are older.
In some, difficulty seeing at night starts around age 40 and may be associated with older individuals who are involved in car crashes.6 There are several reasons people may have impaired night vision, including age-related changes and eye disease:7,8
Smaller pupils — With aging the muscles that control the pupil, the area that allows light into the eye, do not react as quickly or may not be as strong. If the pupil doesn't dilate enough, you don't have enough light to see. This makes adapting to seeing out the windshield and back to a brightly-lit car dashboard difficult.
Eye lens — With age, the lens of the eye stiffens and may get less transparent. This doesn't let enough light pass through, which you experience especially at night.
Rods — The rods in the retina are necessary for sight but may be lost with aging.
Nearsightedness — This may make it hard to see down the road at night while driving.
Medications — Some can slow your pupil's ability to adapt to changing light conditions.
Nutritional deficiency — A vitamin A deficiency can impair your night vision.
Retinitis pigmentosa — This is a hereditary disease that causes permanent impairment of night vision and peripheral vision. Eventually it can cause significant visual loss in normal light conditions.
In the first-of-its-kind research in humans, a team from University College London led by Glen Jeffery was able to improve declining eyesight using simple light therapy.9 In this short video he describes the interaction between red light and mitochondria, which is the basis for sight improvement.
The researchers were aiming at improving the vision of the large number of seniors who suffer from physical decline and impaired eyesight. In 2020, the team wrote there were 12 million people in the U.K. over age 65, which is expected to increase by another 8 million by 2050.
They estimate all will experience some degree of impairment from aging of the cones and rods in the retina. In the video, Jeffery explains the retina of the eye has a greater energy demand and more mitochondria than other tissues in the body, including the heart. As reported in a press release, he said:10
"As you age your visual system declines significantly, particularly once over 40. Your retinal sensitivity and your colour vision are both gradually undermined, and with an ageing population, this is an increasingly important issue. To try to stem or reverse this decline, we sought to reboot the retina's ageing cells with short bursts of longwave light."
The team recruited 24 people ages 28 to 72 years. Each of them was given a device that emitted a red light at 670 nanometers. As Jeffery commented, the mitochondria have the ability to absorb light in longer wavelengths, from 650 nm to 1,000 nm to raise energy production.
However, when the wavelength is above 670 the light is difficult for the human eye to see, which could potentially impact compliance. As a result of the high energy demands, the mitochondria in the retina age faster than other areas of the body. This causes a significant reduction in function.11 The participants took a device home, which they used for three minutes each day for two weeks.
Their rod and cone sensitivity were tested before and after the intervention. They found participants younger than 40 exhibited no difference in sensitivity. However, those older than 40 showed some significant improvement in color contrast and the ability to see in low light. Jeffery concluded:12
"Our study shows that it is possible to significantly improve vision that has declined in aged individuals using simple brief exposures to light wavelengths that recharge the energy system that has declined in the retina cells, rather like re-charging a battery.
The technology is simple and very safe, using a deep red light of a specific wavelength, that is absorbed by mitochondria in the retina that supply energy for cellular function. Our devices cost about £12 to make, so the technology is highly accessible to members of the public."
It’s important to remember that not all light is the same. In fact, artificial light at the wrong time of the day can significantly impact sleep quality. It's called light pollution and it can result in sleep deprivation that ultimately affects your immune system. There is a steep cost to sleep deprivation, including obesity, high blood pressure, diabetes, heart attack and depression.13
One of the side effects of spending hours indoors is a lack of exposure to the sun. The bright light emitted by LED lights and streetlamps is not full-spectrum: Full-spectrum light comes from the sun.14
Hormones and bodily functions operate on a circadian rhythm, which is attached to a 24-hour day-night cycle and light. Your hormones that regulate digestion, metabolism and sleep are affected by your circadian rhythm.15 Ultimately, your circadian rhythm is affected by exposure to sunlight.
For example, the hormone melatonin should rise at night to encourage quality sleep.16 Exposure to bright sunlight in the morning helps regulate the release of melatonin and affects your sleep cycle. In a recent preprint paper, researchers suggest that lockdowns instigated by COVID-19 have mitigated the protective role of ultraviolet light from the sun by up to 95%.17
There is a link between blue light and circadian rhythms.18 The sun provides a full spectrum of light, and thus includes blue light. A reduction in the intensity of sunlight during the winter months may suppress melatonin and result in feelings of listlessness, sleepiness and in some, depression.
As well as reducing your exposure to full spectrum light, including infrared light from 650 nm to 1000 nm, spending hours indoors increases your exposure to blue light. Although blue light in the early hours of the day helps shut off melatonin production, continued exposure after sunset has deleterious effects on health.
With the production and distribution of energy-efficient LED lights, many are exposed for longer hours to blue light without a balance of red or near-infrared light. For this reason, incandescent lights are safer as they emit the longer wavelength red and near-infrared light and only emit a bit of blue.19
The damage blue light does to the retina has been known for years. In one study published in 1995, researchers wrote, “Exposure of the eye to intense light, particularly blue light, can cause irreversible, oxygen dependent damage to the retina.”20
More recently, data from a study involving animals has suggested that blue light increases retinal damage and apoptotic cell death. In this study, the damage induced greater cone cell death than rod cell death.21 The blue light emitted by LED lights is the main component scientists are concerned with regarding vision and the health of the retina.
Experts find that the blue light component in energy-efficient LED lights is “the major cause of retinal damage,” inducing “oxidative stress and retinal injury” as well as “photoreceptor death by necrosis and apoptosis.”22
Researchers from Oregon State University in collaboration with The Ohio State University found prolonged exposure to blue light may also affect your brain, even when blue light is not shining through your eyes.23
There are some important steps you can take to protect your eyesight and overall health. While it's important to get blue light first thing in the morning to shut off melatonin production, it's just as important to reduce exposure after 7 p.m. when the sun naturally begins to set.
There are several ways to accomplish this, depending on your personal preferences. Many digital devices have software that can reduce the blue light emitted by the screen. When you do this on all electronic devices and you replace all LED lights with incandescent bulbs, you won't need blue blocking sunglasses indoors.
However, if you don't have control over lighting, then it's important to strongly consider using blue-blocking glasses after 7 p.m. This will help regulate your internal clock and reduce damage to your eyes.
Outdoor street lighting and alarm clocks are other ways you're exposed to light after dark. The quality of sleep you get is linked to resting in total darkness. Consider removing all light-emitting devices and using a sleep mask and room-darkening blinds.
On the other hand, during the daylight hours, it's important to get sensible sun exposure for eye health and to help raise your vitamin D production. If you find it difficult to fall asleep and stay asleep, you may need to make a few more changes using strategies I suggest in “Top 33 Tips to Optimize Your Sleep Routine.”
Your body functions best when it’s in balance; the biological term for this is homeostasis. Basically, this means that while a little of something may be good, a lot of the same thing can be bad.
Your body also functions optimally when it is under some stress. For instance, your muscles grow and strengthen when they are asked to perform. Your immune system creates antibodies when it is exposed to a pathogen. You experience personal growth and development only when you step past the edge of your comfort zone.
Yet, with too much stress, your body can get overwhelmed and damaged. Being exposed to too many free radicals is one example. This leads to oxidative stress, which is an imbalance between free radicals and antioxidants.1 Reactive oxygen species (ROS) are free radicals that are the by-products of metabolism and they play an important role in cell signaling.
Your body constantly produces ROS. When there aren't enough antioxidants to keep the number in check, it can result in oxidative stress. This can lead to several health conditions such as neurodegenerative disease, gene mutations, cancer, heart disease and inflammatory diseases.2
At the molecular level, free radicals have an unpaired electron. This makes them highly unstable, damaging your cellular structures. The damage happens when the free radicals steal an electron from another molecule. This process is called oxidation.3 You can see the visible signs of oxidation when you cut into an apple and let it sit on the counter and watch as the flesh begins to turn brown over the next couple of hours.
In small amounts, free radicals help fight infections, inhibit aging and start wound healing. But in larger amounts they are damaging. Your body has a built-in mechanism to help fight the damage from ROS using antioxidants. These molecules are different since they can donate an electron and remain stable, thus reducing the damage from free radicals.
More than one type of antioxidant is in play when it comes to our defenses. In one group are exogenous antioxidants: These are molecules that are formed in foods and can be absorbed when eaten. Examples I’ve talked about are vitamin C, astaxanthin, flavonoids and polyphenols. Keeping a balance between damaging ROS and antioxidants may also help your body fight infectious diseases, such as flu and COVID-19.
Your body can also form endogenous antioxidants, including superoxide dismutase, glutathione peroxidases, glutathione and catalase. While getting enough external antioxidants from your food is important, it is the endogenous antioxidants like superoxide dismutase (SOD) that are the first line of defense against ROS.4
Glutathione plays a crucial role in health and fitness. It is an intracellular antioxidant that can improve the activity of other antioxidants like vitamins C and E, CoQ10 and alpha lipoic acid.5 Since glutathione is poorly absorbed from foods,6 it may be beneficial to raise your levels using the precursor N-acetyl L-cysteine (NAC).7
Another powerful antioxidant made inside your body is SOD, which plays a role in a variety of physiological and pathological conditions such as cancer, rheumatoid arthritis, diabetes and inflammatory diseases.8 During metabolism, an aggressive superoxide radical is created. SOD breaks this down to hydrogen peroxide and molecular oxygen.9
The accumulation of hydrogen peroxide in the cells is also damaging. At this point in the reaction catalase, another endogenous antioxidant, breaks down the hydrogen peroxide into water and oxygen.
SOD is found in every cell of your body as well as between the cells.10 When adequate amounts of this enzyme are produced, you are powerfully protected against the ravages of oxidative stress. However, levels of SOD go down as you age.11 In one review, researchers discussed its importance to overall health and wellness, writing:12
“It has been suggested that proper daily SOD supplementation will protect the immune system and significantly reduce one’s chances of diseases and ultimately slow down aging process.”
SOD is a metalloenzyme, which means it needs a metal ion to work. The ions that researchers have found most commonly bound to SOD include zinc, iron, manganese and copper. Large amounts of extracellular SOD (SOD3) can be found in nearly all human tissue.13 Several places, including the heart, have the ability to transcribe SOD3 RNA from SOD DNA, raising the level of production.14
By reversing the loss of SOD, scientists may be able to have a powerful effect on reducing oxidative stress and therefore lower the potential risk of many chronic diseases. There are two ways to increase it:
Enter the Aronia berry. In parts of the country they are known as chokeberries, in reference to their sour flavor.15 They come in red and black colors, with the red berries being slightly sweeter than the black. They are a native, perennial, deciduous shrub in North America.16
In a study from the U.S. Department of Agriculture (USDA), researchers found that chokeberries had 50% more antioxidant activity than other, more common berries.17 In addition to high levels of exogenous antioxidants, Aronia berries can activate nuclear factor erythroid 2–related factor 2 (NRF2), a key regulator of antioxidant action,18 to boost the production of SOD.19
Supplementation with Aronia berry extract reduced oxidative stress in the fruit fly so significantly that it extended the life of the fly by 18%.20 It also reduced oxidative stress and the pathogenesis of colitis in an animal model.21
The berry extract modulated mitochondrial antioxidant activity and upregulated antioxidant enzymes, preventing depletion of reduced glutathione and glutathione peroxidase.
In the search for ways to raise SOD levels, nearly 35 years ago scientists pulled it from the blood of livestock and injected it directly into the joints of people with osteoarthritis. The results showed significant improvement.22 However, other research showed disappointing results and it was not developed for commercial purposes.
When intraperitoneal and oral administration of SOD was compared to naproxen and dexamethasone in an animal model, the results revealed that oral SOD lowered lipoperoxidation.23 In the animals that received the drugs, 20% of those getting naproxen died of hemorrhages in the gastrointestinal tract and 50% of those getting dexamethasone died of pulmonary infections.
The question has remained as to how to naturally increase the amount and activity of SOD in the body. Although some plants naturally produce it, once consumed, the harsh environment of the gastrointestinal tract destroys it.24
It appears that consuming Aronia berry extract could actually increase SOD levels. In one study, researchers engaged 47 participants; 22 were healthy and 25 had metabolic syndrome. The participants with metabolic syndrome were given 100 mg of Aronia extract three times a day for two months.25 This group saw reductions in their blood pressure and cholesterol levels while their SOD levels were significantly raised.
Researchers have also learned that curcumin supplementation can increase SOD, catalase and glutathione peroxidase, all important endogenous antioxidants.26 This same effect was also found in the fruit fly.27
Remember, SOD has to have metal ions to function properly. This is an important consideration for our time, as some people may be taking zinc to protect against COVID-19, flu and other infectious conditions. In a discussion of the importance of the zinc/copper balance, Chris Masterjohn, Ph.D., writes:28
“The negative effect of zinc on copper status has been shown with as little as 60 mg/d zinc. This intake lowers the activity of superoxide dismutase, an enzyme important to antioxidant defense and immune function that depends both on zinc and copper.
Notably, the maximum amount of zinc one could consume while staying in the acceptable range of zinc-to-copper ratios and also staying within the upper limit for copper is 150 mg/d."
Molecular hydrogen is yet another important antioxidant. Among the many benefits of using it is the ability to selectively decrease excessive oxidative stress and inflammation.29
As discussed earlier, it's important to remember that the body requires balance in all its processes, including stress. By inhibiting excessive oxidative stress and damage, molecular hydrogen helps to maintain homeostasis. This means the goal is to neutralize excessive free radicals, but not all of them.
In my interview with Tyler W. LeBaron, founder of the science-based, nonprofit Molecular Hydrogen Institute, he talked about the selective elimination of free radicals. You can see the entire interview in my article, “Molecular Hydrogen — Is it the Best Antioxidant You Can Take?” He comments:30
"Sometimes antioxidants can even exacerbate oxidative stress because they can increase Fenton reaction cycles and redox cycling and end up being potent pro-oxidants. So, it is very complicated, and we have to be very cautious …
One of the reasons we know hydrogen gas could be so safe is because it simply does not have the reductive power or potential to neutralize or react with some of these critical important signaling oxidants, such as hydrogen peroxide, singlet oxygen, superoxide radicals and nitric oxide. It just does not have the ability to react with these, even in vitro, if you just put the two together, they don't react."
Molecular hydrogen will react with hydroxyl radical, which is the most reactive and oxidative radical in the body. It is turned into harmless water.31 Molecular hydrogen is inexpensive, has no risk and its potential upside is tremendous. Use the article link above to read more about its benefits.
Molecular hydrogen is absorbed in gas form. As LeBaron and I discuss in our interview, easiest way to get it into your system is to dissolve molecular hydrogen tablets in pure water and drink it. It is important to be sure the concentration is high enough and that the frequency is not continuous.
As LeBaron explained, when exposure to molecular hydrogen is continuous, it is less effective. At this time, further study is needed to determine the best frequency.
Until then, customizing the dose to your personal circumstances may be appropriate. For example, if you live in non-stressful circumstances and are not exercising much, once a day may be enough. On the other hand, if you exercise vigorously, it may be more appropriate to take it a couple of times a day.
The normal dose is one tablet in 500 mL or 16 ounces of water. You want to drink the whole glass as soon as the tablet dissolves and before the cloud of hydrogen gas dissipates. The rate the tablet dissolves will depend on the water temperature. Ideally, use room temperature water so there's more gas in the water by the time the tablet is fully dissolved.
It’s important to use plain water and not sparkling water, which contains carbon dioxide that will disperse the hydrogen gas faster. The water will take on a milky look from the dissolved hydrogen gas. You'll want to drink it as quickly as possible while the hydrogen is suspended in water.
1 Which of the following supplements may be of particular benefit in the treatment of COVID-19, thanks to its ability to improve pneumonia, modulate immune responses and inhibit virus-induced cytokine storms?
2 Which of the following substances was recently found to pose an unnecessary risk to vulnerable subpopulations, especially children, in a landmark trial?
3 Which of the following edible oil industries has recently been identified as being rife with food fraud?
4 Which of the following strategies appear to be the most effective for lowering your risk of severe COVID-19 infection and death?
5 What percentage of all COVID-19 deaths in the U.S. have occurred in nursing homes and other long-term care facilities for the elderly?
6 Which of the following is essential for proper nutrition, including vitamins and minerals?
7 Which of the following substances has been shown to increase the risk of ADHD in children by nearly 300%?
As every year during our annual Fluoride Awareness Week, Fluoride Action Network (FAN) founder Dr. Paul Connett is here to provide us with a progress update. FAN has been instrumental in reducing fluoride exposure in North America and in many countries throughout the world over the past 20 years.
As in previous years, we ask that you consider donating to this worthy organization that is spearheading the daunting task of eliminating water fluoridation around the world. As usual, Mercola.com will match your donation, dollar for dollar, up to $25,000 during Fluoride Awareness Week.
From the very beginning, one of Connett’s driving concerns was the possibility that fluoride might be lowering children’s IQ.
“Two Chinese studies were published in 1995 and 1996, in English. I was very concerned, and felt strongly that if there was any evidence that fluoride lowered intelligence of children, then there's no way you would put benefits to teeth above that and continue water fluoridation,” Connett says.
Ten years later, in 2006, the National Research Council looked at the toxicology of fluoride.1 At that time, there were six IQ studies and, based on those six studies along with many animal studies, the NRC concluded that fluoride did in fact pose a threat to the brain. By 2008, there were 18 such studies.
In 2012, a distinguished team, partly from Harvard University, did a review2 of 27 IQ studies; 25 from China and two from Iran. Strikingly, 26 of the studies showed children with higher fluoride exposure had lower IQ than the children with lower fluoride exposure.
“The bombshell came in 2017. Up to that point, we had about 60 studies that had shown a lowering of IQ, most of them from China, but also some from India, some from Iran, some from Mexico,” Connett says.
The bombshell study3,4 Connett refers to, known as the “Bashash study” (named after the lead author, Morteza Bashash, Ph.D.), was funded by the National Institutes of Health, the National Institute of Environmental Health Sciences and the Environmental Protection Agency.
It followed pregnant women and their babies for 12 years. They measured the fluoride in their urine, which reveals total exposure, regardless of the source or sources, and they found a strong relationship between the fluoride level in mothers’ urine and IQ scores in their children at the ages of 4, and between 6 and 12.
It’s important to realize that it’s not the concentration of fluoride in the water (measured in mg per liter) that is significant for health. What matters is the dose you get in milligrams per day, and the dosage (mg/day divided by the individual’s body weight), and these depend on a variety of fluctuating factors.
“The NIH is a parent of the Public Health Service, so they've been promoting fluoride for years and years (since 1950). So, I believe they put a lot of money into this study thinking that it would prove, once and for all, that crazy people like me and others were absolutely wrong about the notion that fluoride lowers IQ in children.
But lo and behold, they gave us very, very strong evidence that it is. And that the most susceptible age, as far as fluoride's impact on the brain, is during fetal development.
It turns out the placenta does not protect the fetus from fluoride, and, as you know, up to about six months of age, the blood-brain barrier is not fully formed in the baby. So, the fetus is very susceptible to this impact of fluoride.”
The first response of the American Dental Association was that the findings didn’t apply to the United States, since it was done in Mexico City. However, this ignored the fact that human beings are human beings, by measuring fluoride in the urine they had a measure of total exposure, regardless of the source. It really doesn’t matter if the fluoride comes from water, other beverages, food or toothpaste.
In 2019, the NIH study was replicated in Canada,5 and they too found that higher fluoride levels in maternal urine were associated with lower IQ in their offspring. The only major difference was that based on maternal urine levels only boys appeared to be affected, not the girls. But when the mothers’ fluoride exposure was calculated from ingestion (i.e. from food and beverages) there was a relationship between that and the children’s IQ for both boys and girls,
“Now, this study, unlike the first one, the Bashash study, got a certain amount of coverage,” Connett says. “[It] was published in the journal of the American Medical Association, Pediatrics. That's one of the major pediatrics journals in the world, and the editors of this journal went to extreme lengths.
They knew this was controversial. Hats off for them to take it on. They knew it was going to be consequential, so they doubled up on the peer review process, they double checked the statistics, so they were confident when they launched it. They even ran an editorial saying the steps they'd taken.
They had two of their editors, the editor of JAMA in total and the editor of JAMA Pediatrics did a 20-minute podcast explaining how astounding the results were. They said, ‘Oh, we had no idea that fluoride caused any problems to health.’ I don't know what they'd been reading. But anyway … it was a bombshell for them to suddenly find that fluoride could be damaging the brain of the fetus.
They also ran an editorial from David Bellinger, one of the world's experts on lead's neurotoxicity, and he said ‘The measurements here are akin to what's happening with lead.’ In other words, it’s very, very serious, and that got a lot of coverage around the world.
But the other side was organized and they quickly got some ‘experts’ — none of them actually experts on fluoride or toxicology or neurotoxicity — who said all the right things to dampen people's concern about this study.”
“There are four studies that people need to know about,” Connett says. To learn more about each, see Connett’s video commentaries on FluorideALERT.org FAN.tv page. Aside from the two already mentioned, the two other ones are:
November 22, 2016, a coalition including FAN, Food & Water Watch, Organic Consumers Association, American Academy of Environmental Medicine, International Academy of Oral Medicine and Toxicology, Moms Against Fluoridation and several individuals, filed a petition6,7 calling on the EPA to ban the deliberate addition of fluoridating chemicals to U.S. drinking water under Section 21 of the Toxic Substances Control Act (TSCA).
As explained by Connett, the TSCA allows citizens and nongovernmental organizations to petition the EPA to remove toxic substances found to pose a threat (an unreasonable risk) either to the general population or a subset of that population.
The petition was made on the grounds that a large body of research demonstrates fluoride is neurotoxic at doses within the range now seen in fluoridated communities, and included over 2,500 pages of scientific documentation detailing these health risks.
The EPA denied the petition8 February 27, 2017, on the grounds that it had failed to present “a scientifically defensible basis” to conclude that anyone had in fact suffered neurotoxic harm as a result of fluoride exposure. In response, FAN and its coalition partners filed a lawsuit in the U.S. District Court for the Northern District of California, legally challenging the EPA’s denial of their petition.
This interview was taped June 2, 2020. FAN was scheduled to begin arguments in front of a judge June 8. FAN will explain the neurotoxicity of fluoride shown in these and other studies, and then the EPA’s industry experts, paid consultants who have also defended glyphosate and other toxins, will present their evidence. (see FAN’s web site FluorideAlert.org for a summary of the trial)
“But we have, for our lawsuit … some of the leading experts on neurotoxicity in the world,” Connett says, “including a couple that were involved in the studies I've been talking about.” That includes Bruce Lanphear, the EPA’s go-to person for information about the neurotoxicity of lead. Lanphear worked with Till on the JAMA Pediatrics article and the bottle feeding study listed above. Howard Hu, lead author of the Bashash study, is another expert FAN witness, as is Philippe Grandjean.
“I am very optimistic. [The EPA] doesn’t have the science. We do. And not only do we have the science, but we have some of the world's best experts testifying for us. So, unless these crafty lawyers for the EPA are able to muddy the waters, I think we'll have no trouble in demonstrating three things: One, that the preponderance of evidence that fluoride is neurotoxic is overwhelming.
Second, that it is a risk at the levels at which we add fluoride to the water. And thirdly, it's an unreasonable risk. Because even if your number one focus was reducing tooth decay, there are other ways of delivering fluoride, instead of this ridiculous notion of putting it in the drinking water and forcing it on your whole population.
I think we can demonstrate those three things. And I'm happy to tell you that my son, who started our webpage in 2000 and developed the largest health database in the world, bigger than other fluoridating governments, by the way, is going to be the lawyer fighting this case,” Connett says.
You can now view the transcript of Michael Connett's brilliant summary statement
If victorious, the EPA will likely appeal, as this is a classic stall tactic. “There's no agency in the United States that is better at dragging its feet on controversial issues,” Connett says.
“They dragged their feet for over 18 years on the reassessment of dioxin, an issue I was very close to, and they still didn't resolve the issue. They're very subject to industry pressure, and their way of resolving issues is just delay, delay, delay.
But, I do believe that if a federal court, having heard both sides, declares that fluoride poses an unnecessary risk, an unreasonable risk to the developing brain of our children, that that news will ricochet around the fluoridating world — Australia, New Zealand, Ireland, Canada, Israel, Malaysia, and a few other countries where they still fluoridate. It's going to have a huge impact.
And I think the citizens will be able to use this as ammunition to say to their health departments, ‘Come on. Why are you doing this? Why are you doing this when you've got this scientific information … done by top notch scientists. Why on earth would you continue this practice when you know that if you want fluoride, you can simply brush it on your teeth and spit it out. What is your rationale for continuing this?
By the same token, to the professional bodies, to the AMA, the ADA, the APHA and all those other organizations that have endorsed fluoridation for years and years and years, why would you continue to support this? Why would you reveal to the public that you have no scientific credibility?
That you don't read the science, that you don't keep up with the science on an issue like this? When you're going to the public and saying again and again and again that fluoridation is safe and effective, when you've got this evidence right there in front of you?
One more thing … Possibly the most important agency for reviewing the toxicology of toxic substances is the National Toxicology Program (NTP). Back in 2016, FAN asked the NTP to do a systematic review of the neurotoxicity of fluoride. This was before the court case and before we went to court.
After three and a half years they came back, having reviewed all the animal data and the human data, and in their draft they said, ‘Based upon the literature, the presumption is that fluoride is a neurotoxic substance. Based upon studies done on children in several different countries, the presumption is that it is neurotoxic.’
Not that it's definite; but you would have to presume, based upon all the literature, that this is a neurotoxic substance. So, that’s a huge vindication for our case. But, because it's a draft and not a final version, we can't actually use it in the court case. Still, this is very useful for us going forward, in addition to whatever the court rules.”
While FAN has successfully ended water fluoridation in many areas, it’s still very difficult. One of the reasons for this is because those who want it to continue always point to reviews by government agencies “which, as bogus as they are and unscientific as they are, carry a lot of weight,” Connett says.
In Ireland, they refer to the expert committee. In New Zealand, they refer to the ministry of health and in Australia to the National Health and Medical Research Council. In the United States, they refer to the Centers of Disease Control and Prevention.
All of these agencies have promoted water fluoridation and are not good judges of whether there are problems or not. Hopefully, a court win against the EPA will facilitate and speed up the process of getting fluoride out of drinking water. A win would also set another important precedent:
“We've been able to bring this to court under the Toxic Substances and Control Act, which has a clause [stating] that any group or individual can petition the EPA to remove, to ban, any particular use of a particular chemical in the United States if they can show it's an unreasonable risk to the population, or even a subset of the population.
We … along with Food & Water Watch are the first groups to ever do this. So, it's establishing a very important precedent, which is really worrying the chemical industry. It’s a big concern of ours, because behind the scenes I'm sure they're trying to muddy the waters in every way they can. But it's a huge precedent. I hope that our victory will also shoot adrenaline into the veins of all these other [health safety] groups …”
In our interview, Connett also discusses the fluoride pollution released during recycling of lithium ion batteries, such as those used in electric cars. Lithium ion batteries contain fluorinated polymers like polyvinylidene difluoride (PVDF) and an electrolyte called lithium hexafluorophosphate (LiPF6).
When heated during the recycling process, these fluorinated compounds break down to produce hydrogen fluoride, and many fluorinated byproducts which are toxic and difficult to capture. Like PFOS, these chemicals stick around for so long they’re known as “forever chemicals.”
As it happens, a lithium ion battery incinerator is being built near Connett’s home, across the road from a residential area and adjacent to a little league baseball field. “It is an absolutely insane, unethical siting,” Connett says, noting that there really is no safe place for such facilities. It’s the recycling process itself that needs to be modified, which is what Connett is fighting for now.
“What this has done is fortuitous. It has brought together nearly all the strands of our activism. I've had 35 years fighting incineration and dioxins [and] 24 years fighting fluoridation. Now we're meeting hydrogen fluoride and fluorinated by-products in spades. At the very least the problem will be: What do you do with the sodium fluoride that's left over in the effluent, the waste water?
I hope someone doesn't suggest putting it in the drinking water. Because also in that waste water you'll have a PFAS, a polyfluorinated alkyl substance (used in some of the batteries), and my wife has spent many, many years maintaining a database on these PFAS … She's been concerned with that for a long time. So, we've been able to draw on three different strands of our activism to help our local community.”
Eliminating water fluoridation will go a long way toward protecting the health of all people, but especially children. Sacrificing children’s brain function for a theoretical benefit of less tooth decay is unconscionable.
Aside from making sure you do not drink fluoridated water, or use fluoridated water to mix infant formula, to reduce your exposure, avoid drinking excessive amounts of tea, which tends to be high in fluoride.
“Mix it up,” Connett says. “If you must drink tea, then drink tea, drink coffee, drink herbal tea. Mix it around. Not too much tea. Also, avoid animal bones. Don't eat the bones from sardines and pilchards. Don't eat the bones from chicken. Avoid mechanically deboned meat.”
Again, for more details on the four studies Connett highlights in this interview, see his video commentaries on FAN.tv page. There you can also find a webinar lecture by FAN’s senior scientist, Chris Neurath, in which he explains the neurotoxicity of fluoride. To help spread the word, you can print out a FAN pamphlet to share with family, friends and local community bulletin boards.
In closing, if you’re concerned about the health effects of fluoride, please support FAN with your tax-deductible donation today. Mercola.com will match your donation, dollar for dollar, up to $25,000 during Fluoride Awareness Week.
Dr. Mercola Interviews the Experts
This article is part of a weekly series in which Dr. Mercola interviews various experts on a variety of health issues. To see more expert interviews, click here.
Jonathan Latham, Ph.D., is a molecular biologist and a virologist, which is a great skillset to help us understand the origins of SARS-CoV-2. Latham reviews some really intriguing evidence in this interview. He’s also the editor of Independent Science News.
By and large, the mainstream media are still protecting the narrative that SARS-CoV-2 is a zoonotically transmitted virus originating in bats. Much of the evidence for this comes from Shi Zhengli, a researcher at the biosafety 4 laboratory in Wuhan, China.
As the leading Chinese bat coronavirus researcher, her career has been focused on studying bat coronaviruses for over a decade. In a recent article,1 Latham and Allison Wilson, Ph.D., dissect research showing this theory simply doesn’t hold water.
“Our article doesn't dispute that it came from a bat at some point, I think that is the strongest data, but what we do dispute is the mechanism by which it came from the bat,” Latham says.
Latham’s article lays out several different lab origin hypotheses. The simplest one is that researchers from the Wuhan Institute of Virology or another virology BSL-2 lab that's even closer to the wet market speculated to be the origin of SARS-CoV-2. In that process, one of them got infected and then passed it on to coworkers or family, either because they didn’t properly quarantine or didn’t realize they were infected.
This is not the most likely of hypotheses for the simple reason that few naturally occurring bat coronaviruses identified have the ability to bind to human ACE2 receptors, which is what allows them to infect human cells in the first place. In order for this theory to work, the virus would have to circulate among many people, evolving slightly with each pass.
Another theory is that the researchers were cloning a bat virus similar to SARS-CoV-2 in the lab in an effort to make a more infectious clone. Perhaps they placed the virus in monkey cells, humanized mice cells or human cells with an ACE-2 receptor expressed in them. A researcher may then have been accidentally infected.
“There have been lab escapes of viruses in which people fail to decontaminate samples and then they give the samples to someone else, or they throw them out with the trash, or some mishap arises,” Latham says.
“So, the virus is either identical to the one that was collected from the wild or very little altered by the lab, but then it escapes because there's some failure in the lab. That would be a second possibility.”
A third possibility is that they were collecting samples and looking at genetic sequences in order to find a virus they could then alter, giving it more interesting properties. Perhaps they found some with the spike protein that had a greater affinity for the ACE2 receptor. By combining it with another virus, they may have been able to create — through genetic engineering — a more infectious virus.
The reason for mixing and matching viruses in the lab in this way is to identify potential pandemic pathogens (PPP). Meaning, two wild viruses, if they come in contact with another, might mutate into something deadly to humans.
“For example, we will swap spike proteins and see if the viruses that we have circulating in bats, really all they need to do is evolve better spike protein and all of a sudden, they can become pandemic pathogens,” Latham says.
Many who defend the all-natural zoonotic origin story justify their stance by saying there are no signs of genetic manipulation. Like several other scientists, Latham points out there are ways you can manipulate a virus without leaving telltale markers. He explains the basics of the genetic engineering process:
“The standard thing, historically, was you find a restriction site in two different viruses, or you may manufacture a restriction site. That gives you a cutting place in the genome … Let's say you start with virus A and you cut a bit out and you put that into virus B. Of course, you've got to remove the bit from virus B that it already has.
So, you're basically swapping things and you're using restriction enzymes, which are basically enzymes that cut DNA in specific places. That's kind of the old-fashioned way.
There are newer methods with PCR and so forth that are slightly more complicated. It means you're not restricted to restriction sites to do that. There are very simple cutting and pasting [methods], but it doesn't necessarily leave a scar or a mark. This is the really important point here.
There are also passaging experiments. Passaging experiments are when you take a virus — say, for example, you take a virus that originally came from a bat and you put that into monkey cells, or human cells … What you normally observe with that virus is that it doesn't work too well in those cells because it's not adapted to them. It's a bat virus, so it doesn't work too well.
But what virologists have learned to do is to, essentially as the viral infection is failing, take a little sample of what is inside the cell and put that into another cell. Then, when that infection builds up … you take another sample.
This is called passaging. It allows the virus to evolve into a more pathogenic form against the cells that you are now putting into. So, you're always putting into the same species of cell. You can also do this with whole organisms.”
As noted by Latham, until the passaged virus has been genetically sequenced, there’s no telling exactly what it looks like, or how it might act. It’s fairly random in that sense. Latham explains:
“It may have recombined, it may have mutated; there's been a genetic change, but you don't know what it is until you research it, clone it and make a new infectious clone. And so, you have the possibility that what escaped from the lab is actually not known to the people in the lab. They don't actually know what it was that they evolved.
And, if they were doing those kinds of experiments, putting the live bat viruses into cells of different species — and historically we know that they were doing those kinds of experiments — then they could also develop a new virus.
You can also have a combination of those experiments. So, you can have researchers who passage recombined molecules, they did the cutting and pasting part, and then they put back the cut and pasted virus into novel cells like human cells, and then they passage back, and then you evolve an infectious clone in that way.”
In this way, you can create a virus with high affinity for human cells, even though it wasn’t infectious to humans in the beginning. One of the key features of SARS-CoV-2 is its spike protein has high affinity for the human ACE2 receptor. The question is, how did this affinity arise?
“One of the obvious answers to that question is that it was being passaged inside these human cells or that somebody cut and pasted a spike protein bound to these human receptors that they already knew worked particularly well.
So, my hypothesis is that either they were cutting and pasting, or they were passaging, or they were doing some combination of both, and then that basically led to somebody in the lab becoming infected through some kind of careless event,” Latham says.
The wild H1N1 virus that caused the 1918 flu pandemic was extinct for decades. However, in 1977, there appears to have been a biosafety lab leak in China or Russia in which that virus escaped, causing a global pandemic.
“Essentially what happened is the virus went extinct and then a new version of the virus appeared in 1977 in China, and it was basically identical to one that had existed 20 years before … No one can explain how a virus could appear — it was basically identical — but had been somehow hidden.
There was a theory that it had been in the permafrost and somebody had dug up a person from the permafrost who had died with H1N1 flu, but that was the best theory people had until they realized that it probably came from a lab that was making a vaccine.”
The H1N1 virus was temperature sensitive, and one of the things you use when you're making vaccine is a temperature-sensitive virus — a partially disabled virus.
“Basically, there is no other explanation than that this came from a lab and that there were labs who had stored stocks of it, but no lab has really come forward and said, ‘It was us.’ So, this has been kind of deduced from sequence information from the location in which it appears and so forth, but it's widely accepted by virologists,” Latham says.
Naturally, the notion that a biosafety lab leak would be responsible for a lethal pandemic is an uncomfortable one, especially for virologists doing that kind of work. An outbreak of equine encephalitis in Venezuela has also been traced back to a laboratory leak. Then there’s the H1N1 swine flu pandemic of 2009. Latham says:
“There's a scientific paper by a friend of mine, Adrian Gibbs ... written with two other virologists. He's a famous virologist and he says, ‘This came from a vaccine. The swine flu is actually not readily accountable by the specific circulating viruses that happened to be in North American and European and South American pigs at that time.’
Basically you can't explain it by that method, but you can explain it perfectly well by the idea that there was a manufacturer who was making bits of H1N1, one from European sequences and North American sequences, and South American sequences, and stuck them all together to make a universal vaccine, and somehow they failed to inactivate it.
So, they gave it to pigs in Mexico and that became the swine flu, the second H1N1 pandemic, and that second pandemic killed probably close to 300,000 people. We have a whole series of examples of lab escapes of viruses, so when people treat the lab escape thesis as being somehow ridiculous or outrageous or improbable, to me it just demonstrates their ignorance of the history of virology.”
Latham also addresses suspicions that HIV AIDS came from a polio vaccine, so for more details, listen to the interview. This was described in the book “The River: A Journey Back to the Source of HIV and AIDS,” by Edward Hooper, and reviewed in a British Medical Journal article that you can read for free.2
SIV from infected monkey kidney cells that were used to create polio vaccines and used on hundreds of thousands of Africans are also suspected of being the cause of certain cancers.
Many safety breaches have been documented at biosafety labs around the world, including the Wuhan lab. Several were documented by U.S. Embassy officials who visited the Wuhan Institute of Virology in 2018.
“I mean I think they're important data points but … we think it's more important that people from within China have raised questions about the bio security of this lab. Firstly, it's newly opened, so that's automatically a bit of a red flag. Secondly, there were violations cited by the internal overseeing agency in China of the kind of standards they would expect from a BSL facility.
They've been trying to set up the certification systems and so forth for their labs because they're trying to set up a whole network — a whole system of animal experiments and collection stations and so forth … So, they're setting up the certification schemes and they've already been cited, according to these reports, as having violations …
In the end, let me add something: One of the basics should be that you don't site these labs in the middle of a big city. So, we already have what I would say a violation to the basics. They should be in a desert or something like that, they should be in Antarctica, in remote areas.”
There can be no doubt that biosafety level 4 labs pose a tremendous threat to public health, seeing how they house the most dangerous pathogens in the world, and leaks are inevitable. The question is, are these risks worth it?
As noted by Latham, the existence of these laboratories drive the vaccine agenda while old-fashioned commonsense hygiene strategies such as hand-washing and protective gear fall by the wayside. The risks posed by these labs also fit right into the surveillance capitalism now getting a hard push through the roll-out of disease tracking and tracing mechanisms.
“An interesting thing happened the other day. Seventy-seven Nobel laureates, most of them molecular biologists, wrote a letter to the president protesting the cutting of the grants to the Wuhan lab that were emanating from the NIH. Well the man leading this effort [is] Richard Roberts. What is his scientific position?
He is on the board of directors of New England Biolabs, one of the biggest suppliers of molecular biology equipment. So, they're corralling together all these Nobel Prize winners to support all this molecular biology research that costs big bucks — hundreds of millions of dollars a year to do this kind of research, money that could be going to PPE and so forth.”
That money could also go to more basic strategies such as vitamin D supplements to build up the population’s immune system.
Latham and Wilson are also planning to write about what they believe is a cover-up at the Wuhan Institute of Virology. The nearest living ancestor of SARS-CoV-2 is a viral sequence currently stored in the Wuhan lab. It’s said to have been kept frozen for the past seven years and nothing has been done with it.
This sequence came from bats living in a mine, and people who have worked in the mine have died of viral infections. In other words, they’ve had a strong reason to look into that virus sequence, and that one also happens to be the closest relative to SARS-CoV-2. Shi published one of the first viral sequences of SARS-CoV-2.
“Three papers came out in three days, all saying this is ‘The sequence of the SARS-CoV-2 virus,’” Latham notes. Yet “her paper makes no reference to this longstanding sequence that they'd had in her lab. Zero reference. Instead, they say they've taken a sample from that freezer and they've sequenced it, and this is the nearest living relative.
But this obscures the fact that for seven years they'd had another virus, which basically came from the same tube … But it looks like when you go searching the DNA databases, it makes it look like this virus has just been with us since December.
It really hasn't, it's been sitting in that lab, supposedly unresearched. So, the question is, what were they doing with this viral sequence for seven years that may have killed three miners back in 2013?”
In a nutshell, SARS-CoV-2 is quite possibly not a new virus. A highly conserved close ancestor was already in the database under the name BtCoV/4991. It was already in the published literature. However, when the Wuhan Lab resequenced the mineshaft sample following the COVID-19 outbreak, they simply renamed that old virus that’s been on ice for seven years.
“Giving it a new name basically obscures the old history. They don't even acknowledge that it came from the same tube, which they now have been forced to acknowledge … It’s the same virus. The sequence identity between the two samples is 100%.
So, if there were one base pair different, you could maybe make a scientific argument that we should give them a different name, but there's no difference between them whatsoever. It's the same virus from the same tube, collected from the same place — the mine where the miners died … from a viral infection of pneumonia.”
Shi’s genetic sequencing paper basically pretends the 4991 sequence never existed. “They've forgotten all about it; that would be the interpretation of reading their paper,” Latham says. A second paper released within that three-day span identifies 4991 as the nearest living relative, and states that it comes from the Wuhan Institute of Virology.
The third sequence paper does a complicated phylogenetic analysis of the SARS-CoV-2 virus, yet it too fails to mention that the nearest living relative is 4991 and held in the Wuhan lab.
“What's really interesting is that everyone who sequence [SARS-CoV-2] — there was a bunch of labs that sequenced the virus around the same time — they all would have searched the database and come up with this 4991 sequence … They all would have done that.
What you have to imagine is that they just get on the phone with the Wuhan Institute of Virology and say, ‘Oh, the virus broke out in your town just down the road from you, walking distance, and you are the keepers of the nearest known viral sequence. Have you had a lab accident?’ You can imagine dozens of labs phoning them up and say, ‘How do you handle a lab accident?’ …
What I'm offering is evidence of a cover-up, but we don't know exactly what they were covering up. They could have been covering up something a little different, but the very obvious thing to be covering up is simply that you are researching a virus that looks uncomfortably like SARS-CoV-2 …
We only have a partial sequence [of 4991]. We don't have the whole genome of this original sample. They only provided a sequence of 370 base pairs, but it is 98.7% identical to SARS-CoV-2 on nucleotides and the 370 base pairs.
This is considered the most conserved part of the genome, so it doesn't necessarily extrapolate to the whole thing. What is quite possible is that, that sample comes from something that is way closer than anything we've been told about.”
Even if 4991 isn’t a 100% match to SARS-CoV-2 (which sequencing of the whole genome would reveal), it could be close enough that you wouldn’t even need a whole lot of gain-of-function experiments to end up with a highly transmissible virus. According to Latham, “That's exactly the kind of thing that could have happened.”
In closing, as noted by Latham, the big picture question is, do we really want to be spending taxpayer money on all of these public health models that rely on biosafety/bioweapons research?
The justification for doing this kind of research on viruses is to prepare us for potentially devastating outbreaks, should the viruses evolve and mutate in the wild. Yet, that same research ends up being the source of our most dangerous outbreaks. As noted by Latham:
“These people have not managed to predict anything so far. What they've done is these incredibly dangerous experiments and then find out that the next virus comes from somewhere they didn't anticipate, or certainly didn't warn us about …
This research is not really predictive, but if enough virologists get together and say that this is how we predict the next pandemic, what is the government to do? If they all say, ‘That's how we should do it,’ then who's going to contradict them? …
I mean, you want to continue gainful employment, so why not push an agenda that's going to keep you employed, even though it doesn't serve the public good necessarily …
What [should] we spend our public health money on? Do we target these individual diseases and make New England Biolabs and the Gates Foundations investors rich, or do we invest in public health in a sense that benefits everybody — prevention and nutrition?
Also, the big issue too that we haven't really touched on is, why are we blaming the wildlife trade here? This is a really important question to ask because Peter Daszak, head of the EcoHealth Alliance, has been in all the media; he's been on Democracy Now!, the New York Times, Scientific American, Science Magazine, all these different outlets, basically ubiquitously blaming the wildlife trade, saying categorically it's not a lab escape.
Well, he is an interested party, right? His nonprofit is funding this research. The media cannot go and ask the person who's funding it whether it came from their lab or not. It's ridiculous. But that's what they're doing and they're treating us like idiots.”
As Latham points out, the reason some wild viruses emerge is because we’re destroying rainforest and building roads into remote areas. People end up catching the viruses because animals are fleeing the destruction of the forest.
So, why are we blaming the wildlife trade? If anything, we need to address the destruction of the animals’ native habitats. That, however, would be very bad for Daszak’s business because the EcoHealth Alliance is in partnership with the palm oil industry.
“We find that science — if you understand the science well enough — really helps you understand who's lying,” Latham says. “When you understand that part, you got a really strong anchor to base in analysis of what's really going on in the bigger picture.
If you can see that a very obvious thing — the possibility here is a lab escape —and then you've got one or a few people wandering around the media saying, ‘A lab escape is an impossibility, it never happened, there's no chance of it at all’ — you know that they're not speaking science, that they have some kind of ax to grind. And then you see who else repeats the message, who supports them and who doesn't and so forth.”
In the video podcast above, Dr. Paul Saladino and science journalist and author, Nina Teicholz — who is also an adjunct professor at NYU's Wagner Graduate School of Public Service and the executive director of The Nutrition Coalition — review the evidence against chicken, and why saturated fat really qualifies as a health food.
Teicholz' book, "The Big Fat Surprise," challenged the conventional wisdom on dietary fats, especially saturated fat. Saladino, meanwhile, is releasing the second edition of his book, "The Carnivore Code," August 4, 2020.
As noted by Saladino, while consumption of red meat is on the decline, thanks to the vilification of red meat and saturated fat, people are eating more and more chicken.
Long thought of as a healthier type of meat, primarily because it's leaner than red meat, the problem with conventional chicken is that they're fed corn — typically GMO varieties that are farmed with glyphosate.
Increasingly, we're finding that trans fats and polyunsaturated fat from vegetable oils are far worse for your health, and a greater contributor to chronic disease, than added sugar even. And what happens when chicken is fed corn? The meat becomes high in omega-6 linoleic acid, as corn is high in this type of fat.1
As Saladino points out, high chicken consumption actually adds to your vegetable oil consumption. While you need some omega-6, the amounts obtained from a standard American diet high in processed foods are far too high for health. High omega-6 intake also skews your omega-3 to omega-6 ratio, which ideally would be close to 1-to-1.
As noted by Saladino and Teicholz, 60% of the U.S. population has chronic disease, nearly 70% are overweight or obese, and recent NHANES data2 reveal 87.8% of Americans are metabolically unhealthy, based on five parameters. That data is over four years old now, so the figure is clearly greater than 90% of the population today.
That means virtually everyone is at risk for Type 2 diabetes and all the chronic diseases associated with insulin resistance, which run the gamut from cancer to Alzheimer's. Simply assuming you are one of the 12.2% (from the 4-year-old figures) that are metabolically healthy would be risky business.
Part of why chronic ill health is so widespread is this persistent idea that saturated animal fats are unhealthy, and should be replaced with industrial vegetable oils.3
On the upside, Teicholz reviews a recent paper4 in the Journal of the American College of Cardiology, published online June 17, 2020, which actually admits the long-standing nutritional guideline to limit saturated fat has been incorrect. This is a rather stunning admission, and a huge step forward. As noted in the abstract:
"The recommendation to limit dietary saturated fatty acid (SFA) intake has persisted despite mounting evidence to the contrary. Most recent meta-analyses of randomized trials and observational studies found no beneficial effects of reducing SFA intake on cardiovascular disease (CVD) and total mortality, and instead found protective effects against stroke.
Although SFAs increase low-density lipoprotein (LDL)-cholesterol, in most individuals, this is not due to increasing levels of small, dense LDL particles, but rather larger LDL which are much less strongly related to CVD risk.
It is also apparent that the health effects of foods cannot be predicted by their content in any nutrient group, without considering the overall macronutrient distribution.
Whole-fat dairy, unprocessed meat, eggs and dark chocolate are SFA-rich foods with a complex matrix that are not associated with increased risk of CVD. The totality of available evidence does not support further limiting the intake of such foods."
In the podcast, Saladino and Teicholz review the history of the demonization of saturated fat and cholesterol, starting with Ancel Keys' flawed hypothesis5 that saturated fat causes heart disease in 1960-1961, and how the introduction of the first Dietary Guidelines for Americans in 1980 (which recommended limiting saturated fat and cholesterol) coincided with a rapid rise in obesity and chronic diseases such as heart disease.
They also discuss the reasons why this myth has been allowed to persist, despite the scientific evidence against it. In short, the low-fat, low-cholesterol myths promulgated by Keys in the '60s rapidly led to dramatic changes in the food and drug industries, and these behemoths are incredibly reluctant to relinquish what have become highly profitable businesses.
Acknowledging that saturated animal fats are healthy, and processed industrial vegetable oils and grains are not, would decimate the processed food industry, as it relies on vegetable oils and grains. The healthy alternative is real food, and there's no big industry profits to be made from that.
Saladino and Knobbe are both equally convinced that the massive increase in linoleic acid (omega-6 polyunsaturated fat found in industrial vegetable oils) is a key metabolic driver of obesity, heart disease, cancer and other chronic disease. They review several studies6,7,8,9,10,11,12 demonstrating the truth of this.
Historically, humans got an estimated 2% polyunsaturated fat from their diet. Today, that percentage is between 10% and 20% — and conventional poultry is a hidden source of harmful polyunsaturated fat as well.
Importantly, they also review the incorrect belief that high LDL is a risk factor for heart disease, and that by lowering your LDL, you lower your risk of a heart attack. The science simply doesn't bear this out, and the reason for this is because not all LDL particles are the same.
By cutting down on red meat and saturated fat and eating more vegetable oil and chicken for example (which again will count toward your vegetable oil or polyunsaturated fat intake), your LDL may go down, but those LDLs are now going to be oxidized, and no one is testing for oxidation. Oxidized LDL, Saladino explains, will in turn trigger insulin resistance and related problems, including heart disease.
Eating saturated fat, on the other hand, may raise your LDL, but those LDL particles will be large and "fluffy," and do not cause any arterial damage. Many studies have demonstrated that high LDL has nothing to do with heart disease. High LDL does not raise your risk of heart disease per se, but oxidized LDL do.
Teicholz also makes another important point, in that the saturated fat myth has been one of the most thoroughly and comprehensive hypotheses in the history of nutritional science, and it has failed miserably.
She also details how avoiding saturated animal fats causes you to end up with nutritional deficiencies, as animal foods and fats are also rich in micronutrients. Industrially processed vegetable oils are not. As noted by Teicholz, "foods high in saturated fats are the most nutrient-dense foods on the planet." These nutrients are also highly bioavailable.
Meanwhile, the diet recommended by our Dietary Guidelines for Americans do not actually meet nutritional goals. As a result, the most disadvantaged among us — impoverished school children who rely on school meals, hospital patients and the elderly who are in long-term care facilities for example — are being disproportionally harmed, as they have few if any options to make healthier food choices.
In addition to saturated fat and the vitamins and minerals it contains, red meat is also an important source of carnosine, a dipeptide (two amino acids put together) made up of beta-alanine and histidine. Carnosine is only found animal products. It serves as a scavenger or sink for reactive carbonyl groups — intermediaries that go on to form advanced lipoxidation end-products.
If you can grab these carbonyls before they attack proteins and fats, you can essentially stop the vicious cycle resulting in catastrophic peroxidation. Diets that exclude animal products and meat will lower your carnosine level, and carnosine is a really important nutrient to limit the damage from oxidation products. It's also important for mitochondrial function.
Toward the end of his podcast, around one hour and 44 minutes in, Saladino offers a comprehensive summary of the entire discussion. Here's a quick review of his key points:
As discussed in my recent interview with Knobbe (above), the polyunsaturated fats from vegetable oils, seed oils and trans fats are mostly stored in your fat cells (opposed to being used for fuel), and have a half-life of 600 to 680 days.13
They also get incorporated into tissues, including your heart and brain. Who in their right mind would want a highly oxidizable oil saturating their organs for years? One result of this could be memory impairment and increased risk of Alzheimer's disease, which is exactly what they found with canola oil.14 As reported in one 2017 study:15
"Our findings do not support a beneficial effect of chronic canola oil consumption on two important aspects of AD pathophysiology which includes memory impairments as well as synaptic integrity. While more studies are needed, our data do not justify the current trend aimed at replacing olive oil with canola oil."
In the interview above, Knobbe explains the harms of vegetable oils and, like Saladino and Teicholz, reviews why they are a root cause behind virtually all chronic diseases.
According to the featured BBC Documentary “The Power of Meditation,”1,2 originally aired in 2008, more than 10 million Westerners practice daily meditation. More recent statistics3 suggest people are turning to meditation in droves, with the number of practitioners tripling since 2012. As of 2019, an estimated 200 million to 500 million people meditate regularly around the globe.
Considering its many psychological and physical benefits, this is good news, especially in light on the pandemic we are all going through. There is a large body of evidence demonstrating the mind-body connection is real, and that your mind has a direct impact on your physical health.
For example, brain imaging has revealed meditation alters your brain in a number of beneficial ways — such as increasing gray matter volume in brain regions involved in the regulation of emotions, memory, learning and self-referential processes4 — and studies show meditative practices even alter your genetic expression.5,6,7,8
Indeed, one study9 found meditation practice altered the expression of no less than 2,209 different genes. Examples of genetic effects include the down-regulation of genes involved in inflammation and stress.10,11
According to a study in PLOS ONE,12 many of these genetic changes — such as reduced oxidative stress and increased antioxidant production and telomerase stability — are the result of activating the body’s relaxation response. The relaxation response also influences your energy metabolism, which can have bodywide benefits. As explained by the authors:13
“Upregulating ATP synthase — with its central role in mitochondrial energy mechanics, oxidative phosphorylation and cell aging — RR [the relaxation response] may act to buffer against cellular overactivation with overexpenditure of mitochondrial energy that results in excess reactive oxygen species production.
We thus postulate that upregulation of the ATP synthase pathway may play an important role in translating the beneficial effects of the RR.”
Findings such as these prove you cannot separate your health from your emotional well-being, and if you want to prevent chronic illness, you’d be wise to incorporate this knowledge.
Clinically, mindfulness-based meditation practice has been demonstrated in randomized trials to improve depressive symptoms in women with fibromyalgia14 and to have lasting anti-anxiety effects after only eight weeks of group practice.15
In “The Power of Meditation,” professor Kathy Sykes begins her investigation of meditation by visiting a Buddhist monk in Nepal, who teaches her basic Buddhist meditation, which involves sitting comfortably, with your spine straight, concentrating on a single focal point, such as your breath.
When a thought arises, you simply refocus your attention on your breath. Over time, this kind of meditation fosters inner calm, happiness, relaxation and emotional equanimity, although results can often be felt rather quickly. “Meditation is not just a hobby,” the monk says. “It’s something that is going to change the very way you experience every moment of your life.”
I’ve already mentioned a number of studies demonstrating the benefits of meditation. “The Power of Meditation” cites16 additional evidence showing it can help a wide range of health problems, including cardiac arrhythmias, bronchial asthma, cold sores, cough, ulcers, diabetes, constipation, infertility, high blood pressure, psoriasis, pain and much more.
Research17 even suggests total medical costs for primary care could be drastically reduced simply by practicing meditation and other relaxation techniques.
To reach this conclusion, the researchers analyzed data from 4,452 people who received eight weeks of relaxation response training and 13,149 controls who did not meditate. The intervention group also worked on building resiliency using social support, cognitive skills training and positive psychology. Results showed:
“At one year, total [health care] utilization for the intervention group decreased by 43%. Clinical encounters decreased by 41.9%, imaging by 50.3%, lab encounters by 43.5%, and procedures by 21.4% … The intervention group’s Emergency department (ED) visits decreased from 3.6 to 1.7/year and Hospital and Urgent care visits converged with the controls.
Subgroup analysis (identically matched initial utilization rates—Intervention group: high utilizing controls) showed the intervention group significantly reduced utilization relative to the control group by: 18.3% across all functional categories, 24.7% across all site categories and 25.3% across all clinical categories.
Conclusion: Mind body interventions such as 3RP [relaxation response resiliency program] have the potential to substantially reduce healthcare utilization at relatively low cost and thus can serve as key components in any population health and health care delivery system.”
The researchers estimate the average patient could save between $640 and $25,500 a year in health care costs by implementing this kind of relaxation response training.
While the mind-body connection has long been ignored by conventional medicine, the American Heart Association in 2017 issued its first scientific statement and guidelines on seated meditation,18 suggesting it can be a valuable adjunctive intervention for cardiovascular disease. As noted in the AHA’s scientific statement:19
“Novel and inexpensive interventions that can contribute to the primary and secondary prevention of cardiovascular disease are of interest. Numerous studies have reported on the benefits of meditation.
Meditation instruction and practice is widely accessible and inexpensive and may thus be a potential attractive cost‐effective adjunct to more traditional medical therapies …
Neurophysiological and neuroanatomical studies demonstrate that meditation can have long-standing effects on the brain, which provide some biological plausibility for beneficial consequences on the physiological basal state and on cardiovascular risk …
Overall, studies of meditation suggest a possible benefit on cardiovascular risk … Given the low costs and low risks of this intervention, meditation may be considered as an adjunct to guideline‐directed cardiovascular risk reduction by those interested in this lifestyle modification …”
As noted in “The Power of Meditation,” there are many different kinds of meditation techniques. Common forms of seated meditation suggested in the AHA’s guidelines include:20
Samatha (focused attention technique)
Vipassana (insight meditation; an “open monitoring” technique that encourages a broader awareness of your environment or train of thought, allowing feelings you might normally suppress to rise to the surface)
Zazen (Zen meditation)
Metta (loving-kindness meditation)
Transcendental meditation (TM)
Relaxation response practice
“The Power of Meditation” interviews Dr. Robert Schneider, a medical doctor who conducts research on the health benefits of Transcendental Meditation.21 According to Schneider, there are several hundred studies showing TM “evokes a deep state of rest and an orderliness of the brain and nervous system, and this results in improved mental health, physical health and even improved social health.”
He goes on to discuss the scientifically demonstrated benefits of TM on cardiovascular diseases specifically. This includes lowering high blood pressure and reducing death rates from heart attacks and strokes.
In the 2014 Talks at Google video above, meditation expert Emily Fletcher22 explains the differences between two popular styles of meditation, directed attention (mindfulness) meditation and nondirected attention meditation (which she refers to as “self-induced transcendence” meditation), and explains how each meditation style affects your brain.
She also discusses the similarities between meditation and caffeine. Both have the effect of energizing you and boosting your productivity, but meditation accomplishes this without any adverse effects.
Caffeine stimulates neural activity in your brain that triggers the release adrenaline, a stress chemical involved in the fight-or-flight state. Meditation, on the other hand, energizes you and makes you more productive without triggering an adrenaline rush.
The reason for this is because meditation de-excites your nervous system rather than exciting it further. This makes it more orderly, thereby making it easier for your system to release pent-up stress. It also makes you more productive. In fact, she notes that many are now starting to recognize meditation as a powerful productivity tool.
Contrary to popular belief, taking the time to meditate can actually help you gain more time through boosted productivity than what you put into it.23 According to Fletcher, meditating for just 20 minutes equates to taking a 1.5-hour nap, and provides your body with rest that is two to five times deeper than sleep. This is why even a short period of meditation each day can help you feel more refreshed and awake.
So, just how does different types of meditation styles impact your brain? Here’s a summary of some of the neuroplastic changes induced by three popular sitting meditation practices:
• Transcendental meditation24 causes your brain to switch into primarily alpha frequency, corresponding to a relaxed yet aware state akin to daydreaming.
As the left and right hemisphere of your brain enter into coherence, endorphin production increases, inducing a sense of happiness and bliss. Over time, this kind of meditation expands your sense of self beyond bodily limitations, resulting in a more integrated personality.
• Mindful meditation25 and samatha — focused attention techniques in which you concentrate on your breath or a single object, thought, mantra, sound or visualization — activate the executive mode of your brain.
The idea behind mindfulness is to remain in the present moment by focusing your attention in the now. The brainwave frequency here typically responds to the gamma range.
Long-term, this type of meditation tends to enlarge your hippocampus, which is where your memories are stored, while shrinking the amygdala, the emotional center and the site of your fight-or-flight instinct. This is in part why mindfulness training tends to be helpful for depression and anxiety, as it helps improve the regulation of emotions.
• Self-induced transcendence (discussed by Fletcher in the video above) is a nondirected style of meditation in which you access a fourth state of consciousness that is different from waking, sleeping and dreaming. Transcendence style meditation strengthens your corpus callosum, the bridge between your two brain hemispheres.
Your left brain is in charge of the past and the future, language, math and critical thought, while your right brain is in charge of “right now,” intuition, inspiration, connectedness, creativity and problem-solving.
By strengthening the connection between your right and left hemispheres, you gain access to more creative problem-solving and increase your productivity without adding stress.
Sykes also investigates the benefits of meditation on mental health, for which there is perhaps even more evidence. She visits a woman named Carol, who struggled with severe depression after the death of her husband.
Her psychiatrist suggested meditation, in which you focus on your breathing — similar to the Buddhist meditation described earlier. “It stopped me from living in my head with my thoughts,” Carol says, “and it’s given me a better picture of what it’s like to be alive, really.”
The program Carol enrolled in, called MBCT, which stands for mindfulness-based cognitive therapy, was developed by professor Mark Williams, described as a leader in the field of clinical depression. MBCT is a mix of about 80% mindfulness meditation and 20% cognitive therapy, which is a widely used psychological technique.
As explained by Williams, mindfulness meditation teaches you to see your problems or thoughts clearly, without trying to change or fix anything. In other words, you learn to view your thoughts as “just thoughts,” be they positive, negative or neutral, rather than something with intrinsic meaning or something that you need to do anything about.
According to Sykes, four different trials have demonstrated that MBCT reduces the risk of recurrent depression by 50% in people who have had three or more depressive episodes.
Williams also points out that mindfulness meditation can really benefit everyone, as it helps us deal with expectations, judgments (of self and others), paralyzing self-analysis and the feeling that we’re just not good enough.
“All of these things are just thoughts,” he says. “They will come up in meditation, and learning to recognize what they are — thoughts — and let them go, can be enormously empowering.”
While it's not unusual for the most experienced meditators to have spent decades, even a lifetime, perfecting the art of meditation, you can gain benefits just from meditating in your home for 20 minutes a day.
If you'd like to give meditation a try, there are many classes and group sessions available if you want a structured group setting, and free guided meditation apps you can use on your own wherever you are.
The UCLA’s Mindful Awareness Research Center26 is a helpful resource where you can download free guided meditations in English and Spanish. The following suggestions can also help you get started:
• Set aside 20 to 30 minutes to meditate each day. Choose a quiet place where you can sit comfortably without being disturbed or interrupted. Simply close your eyes and focus on your breath. You don’t need to control your mind or breathe in any unnatural way. When thoughts arise — and they will — simply let them pass through without judgment and return your attention to the breath.
• As you meditate, you will notice thoughts, sensations and sounds. The next step is to take note of the presence or “witness” that is doing the actual noticing. You’ll find that this presence cannot be pinned down to any particular place inside you. As you continue, simply abide in this presence and be the witness.
In the book, “The Untethered Soul, the Journey Beyond Yourself,”27 Michael Singer asserts that happiness and freedom are the result of cultivating “witness consciousness,” a state of willfully observing your mind, emotions and behaviors, rather than feeling that you actually are these things.
• The more you meditate, the easier it will become to quickly enter into a state of calm and relaxed yet focused awareness. It will also become easier to remain in meditation for longer periods of time. The after-effects will also last longer the more you meditate, allowing you to go through your day in a calmer more focused state.
Early on in the pandemic it became clear that older individuals were at disproportionate risk of severe COVID-19 infection and death.
According to an analysis1 conducted by the Foundation for Research on Equal Opportunity, which included data reported by May 22, 2020, an average of 42% of all COVID-19 deaths in the U.S. had occurred in nursing homes, assisted living and other long-term care facilities. This is beyond extraordinary, considering this group accounts for just 0.62% of the population.
Avik Roy, president of the Foundation for Research on Equal Opportunity, wrote an article2 about their findings in Forbes, pointing out that “42% could be an undercount,” since “states like New York exclude from their nursing home death tallies those who die in a hospital, even if they were originally infected in a long-term care facility.” Roy also testified before Congress June 17, 2020, about racial disparities in COVID-19 and the health care system.3
Disturbingly, some states have nursing home mortality rates that are significantly higher than the national average of 42%. Minnesota4 tops the list in this regard, with 81.4% of all COVID-19 deaths having occurred in nursing homes and assisted living facilities. Ohio comes in second, with a rate of 70%.
As reported by Roy:5
“Another way to cut the data is to look at nursing home and assisted living facility deaths as a share of the population that lives in those facilities. On that basis, three states stand out in the negative direction: New Jersey, Massachusetts, and Connecticut.
In Massachusetts and Connecticut, COVID deaths per 10,000 nursing home and assisted living facility residents were 703 and 827, respectively. In New Jersey, nearly 10 percent of all long-term care facility residents — 954 in 10,000 — have died from the novel coronavirus.”
By and large, nursing homes are ill equipped to care for COVID-19 infected patients.6 They’re set up to care for elderly patients, whether they are generally healthy or have chronic health problems, but they’re not typically equipped to quarantine and care for people with highly infectious disease.
It’s logical to assume that comingling infected patients with noninfected ones in a nursing home would result in exaggerated death rates, as the elderly are far more prone to die from any infection, including the common cold.
March 17, 2020, Stanford epidemiologist John Ioannidis wrote an op-ed in STAT news,7 stating that “even some so-called mild or common-cold-type coronaviruses have been known for decades [to] have case fatality rates as high as 8% when they infect people in nursing homes.”
In other words, we should not be surprised that COVID-19 disproportionally affects older people. Most elderly are frail and have underlying health problems that make them more prone to death from any infection whatsoever. Since this is common knowledge, why did some states decide to violate federal guidelines and send COVID-19 patients back into nursing homes?
Democratic governor of New York, Andrew Cuomo, appears to have been among the most negligent in this regard. March 25, 2020, instructions from the New York Department of Health stated nursing homes were not allowed to deny admission or readmission of a COVID-19-positive patient.
Nursing homes were even “prohibited from requiring a hospitalized resident who is determined medically stable to be tested for COVID-19 prior to admission or readmission.” As reported by Roy:8
“As recently as April 23, Cuomo declared9 that nursing homes ‘don’t have a right to object’ to accepting elderly patients with active COVID infections. ‘That is the rule and that is the regulation and they have to comply with that.’
Only on May 10 — after the deaths of nearly 3,000 New York residents of nursing homes and assisted living facilities — did Cuomo stand down and partially rescind his order.”
Cuomo’s order seems particularly dubious considering the Navy hospital ship USNS Comfort was docked in New York City harbor. The ship, which had a 1,000-bed capacity, was barely used.10 It departed NYC on April 30, having treated just 182 patients.11
A temporary hospital facility at the Javits Convention Center was also erected to deal with predicted hospital overflow. It had a capacity of 2,500, and closed May 1, 2020, having treated just over 1,000 patients.12 With all that available surplus space equipped for infectious disease control, why were COVID-19 patients forced back into nursing homes where they would pose a clear infection risk to other high-risk patients?
June 22, 2020, Centers for Medicare and Medicaid Services administrator Seema Verma condemned the actions of Cuomo and “other Democrat governors” — including Pennsylvania Gov. Tom Wolf, New Jersey Gov. Phil Murphy, Michigan Gov. Gretchen Whitmer and California Gov. Gavin Newsom — who contradicted federal guidelines for nursing homes in their own state guidance.
“Our guidance was absolutely crystal clear,” Verma said in an exclusive interview with Breitbart reporter Matthew Boyle, adding:13
“Any insinuation to the contrary is woefully mistaken at best and dishonest at worst. We put out our guidance on March 13 … It says … ‘When should a nursing home accept a resident who is diagnosed with COVID-19? …
A nursing home can accept a resident diagnosed with COVID-19 and still under transmission-based precautions,’ which means if this person is infectious you have to take precautions.
It says ‘as long as the facility can follow CDC guidance for transmission-based precautions.’ It says: ‘If a nursing home cannot, it must wait until these precautions are discontinued,’ meaning if you are not able to care for this patient — somebody is still positive and you’re not equipped to care for the patient, then you shouldn’t accept the patient into your care.
That’s really important because longstanding discharge — when you’re discharging a patient from the hospital, longstanding guidelines require when you transfer them somewhere you transfer them to a place that can take care of their needs whether they’re going home or they’re going to a nursing home or some other facility …
I just don’t think we should ever put a nursing home in a situation or a patient where we force them to take a patient they are not prepared to care for. That not only jeopardizes the patient but it jeopardizes the health and safety of every single resident in that nursing home.”
While Cuomo has tried to deflect criticism for his devastating nursing home directive, the facts seem to speak for themselves. ProPublica published an investigation14 June 16, 2020, comparing a New York nursing home that followed Cuomo’s order with one that refused, opting to follow the federal guidelines instead. The difference is stark.
According to ProPublica,15 by June 18, the Diamond Hill nursing home — which followed Cuomo’s directive — had lost 18 residents to COVID-19, thanks to lack of isolation and inadequate infection control. Half of the staff (about 50 people) and 58 patients were also sickened.
In comparison, Van Rensselaer Manor, a 320-bed nursing home located in the same county as Diamond Hill, which refused to follow the state’s directive and did not admit any patient suspected of having COVID-19, did not have a single COVID-19 death. A similar trend has been observed in other areas. As reported by ProPublica:16
“New York was the only state in the nation that barred testing of those being placed or returning to nursing homes. In the weeks that followed the March 25 order, COVID-19 tore through New York state’s nursing facilities, killing more than 6,000 people — about 6% of its more than 100,000 nursing home residents …
In Florida, where such transfers were barred, just 1.6% of 73,000 nursing home residents died of the virus. California, after initially moving toward a policy like New York’s, quickly revised it. So far, it has lost 2% of its 103,000 nursing home residents.”
Florida Republican Gov. Ron DeSantis actually took the opposite position with regard to nursing homes. Not only were hospitals not permitted to discharge COVID-19 patients into nursing homes, but all nursing home workers were also required to be screened for symptoms before entering facilities each day, and ensuring availability of personal protective equipment was prioritized.
In California, Los Angeles County nursing homes are such a hotspot, and local leaders describe the situation as a “pandemic within a pandemic.”17 There, the fact that many of the facilities are unusually large appears to be part of the problem.
They also have a higher percentage of people of color — another high-risk group — both working and residing in these facilities. Low pay, poor quality of care and inferior infection control add to the problem.
Overall, COVID-19 transmission appears to be rampant within our health care system in general, not just in nursing homes. As noted in “20% of COVID Patients Caught Disease at Hospital,” British data suggests 1 in 5 COVID-19 patients actually contracted the disease at the hospital, while being treated for something else.
SARS-CoV-2 is being transmitted not only between patients but also from health care workers to patients. When you add it all together, nursing homes and nosocomial infections (i.e., infections originating in or acquired from a hospital18), plus the spread from workers to family members, likely account for a vast majority of all COVID-19 deaths.
Without doubt, if nursing homes don’t start getting this right, they eventually won’t have enough patients to stay in business. Unfortunately, rather than tackle the problem head-on and implement sensible safety measures across the board, the nursing home industry is instead seeking immunity from COVID-19 related lawsuits. I discussed this in “COVID-19 and Nursing Homes: The No. 1 Place Not to Be.” According to NBC News:19
"So far at least six states have provided explicit immunity from coronavirus lawsuits for nursing homes, and six more have granted some form of immunity to health care providers, which legal experts say could likely be interpreted to include nursing homes …
Of the states that have addressed nursing home liability as a response to the outbreak, two — Massachusetts and New York — have passed laws that explicitly immunize the facilities. Governors in Connecticut, Georgia, Michigan and New Jersey have issued executive orders that immunize facilities."
In other words, New York not only issued rules requiring COVID-19 infected patients to be admitted into nursing homes, and barred them from testing, it also granted nursing homes immunity against lawsuits.
Talk about triple injury. Clearly, New York nursing home patients have gotten ill and died due to willfully negligent directives. On top of that, families have been deprived of due process and any legal recourse for these beyond-reprehensible criminal actions.
While several states have failed to protect their most vulnerable, New York’s actions stand out as being particularly egregious and, so far, no sound justifications have been forthcoming.
June 15, 2020, House Minority Whip Steve Scalise, R-La., and four Republican members of the Select Subcommittee on the Coronavirus sent letters20 to the governors of New York, Michigan, California, New Jersey and Pennsylvania, demanding answers:21
“Why did they give those orders? Why did they go against the safety guidelines that were issued from CMS? And why won't they give us all the disclosure of the patient information that they were giving and then all of a sudden when we started discovering this they clammed up and they’re not letting the public see what these numbers really are?” Scalise said.
Curiously, Select Subcommittee Democrats not only declined to join Republicans in the proposed nursing home oversight effort, they also refused Scalise’s call to “get to the bottom of what motivated these decisions” in New York, Michigan, California, New Jersey and Pennsylvania, and they did not sign the letters to the governors of those states.22
In a press release by Scalise, Select Subcommittee member Jackie Walorski (R-Ind.) is quoted saying:23
“Just about the worst possible thing to do is knowingly introduce coronavirus to the most vulnerable populations, yet that's exactly what several states did by mandating nursing homes accept infected patients.
These misguided policies deserve close scrutiny, and the leaders who put them in place have a lot of tough questions to answer. Now is not the time to look the other way while placing blame for this crisis on states that are taking a measured, responsible approach to reopening our economy and protecting our communities.”
While the death toll from COVID-19 in the U.S. has sharply declined since its peak in mid-April — declining from 2,666 deaths the week of June 13, 2020, to 906 deaths for the week of June 20, 2020,24 — authorities predict a reemergence this fall.
We can significantly blunt any reemergence by optimizing our vitamin D levels, and making sure this information reaches nursing homes and other long-term care facilities.
For more information, see “Your Vitamin D Level Must Reach 60ng/mL Before the Second Wave.” To facilitate the public information campaign, I’ve created two vitamin D reports — one comprehensive science report and one summary review — both of which can be downloaded below.
I urge everyone to share this information with friends, family and community at large, so that we can minimize a second outbreak. If you have a family member or know anyone that is an assisted living facility, you could meet with the director of the program, share these reports and encourage them to get everyone tested or at least start them on vitamin D.
Additionally, you could speak to pastors in churches with large congregations of people of color — who are also at disproportionate risk — and help them start a program getting people on vitamin D. Doing so could help save many lives, far more than any vaccine program.
The hope of living longer and healthier lives has been a focus of attention for centuries. In 1513, Juan Ponce de Leon left Puerto Rico and landed in Florida. He was said to be searching for the fabled Fountain of Youth, which people thought would confer everlasting life.1
While history would eventually tell a different story, with some now thinking his trek was more about politics than philanthropy, what hasn’t changed is our fascination with living longer, healthier lives.
Today, researchers and skin experts are in search of products that give the appearance of youth and vitality — qualities which are highly valued in society. In 2019, Forbes reported that the beauty industry, built on helping women look younger and more attractive, was worth $532 billion across the globe.2
Fifteen years ago, researchers from the west coast of the U.S. discovered that old mice that shared blood with younger mice performed as if they were younger.3 The University of California-Berkeley team decided to pursue the matter and have recently published details of their new study in the journal Aging.4 They were determined to find the factor involved in the results from their first study, so they designed a follow-up to see if plasma had an influence on aging.
Using a process to exchange blood in small animals, the team removed half of the plasma in mice and replaced it with a saline solution and albumin. They called this intervention neutral aged blood exchange (NBE). The process essentially diluted plasma factors and replenished albumin.
Just one round of this was enough to assist with muscle repair, lower liver adiposity and fibrosis, and help with brain functioning in older mice. An analysis of the blood after transfusion showed elevated levels of proteins that would be present with tissue maintenance and repair.
Researchers did not believe albumin added to the saline solution was the sole reason for the outcomes. They concluded that the process helps to forward understanding of rejuvenation and suggests a new approach for therapeutic plasma exchange in humans that may improve the health of older individuals.
Importantly, the data from this experiment moves the needle away from investigating young blood for antiaging effects and toward the potential for removing harmful factors in blood that could contribute to antiaging.
The researchers on the 2005 study, led by a husband and wife team, found that blood from younger mice could reverse signs of aging in older animals.5 They created conjoined mice using one old and one young animal. The animals shared blood and certain organs.
Their findings sparked interest in the scientific community and generated other research into whether transfusing young blood could reduce the signs of aging and essentially serve as a “fountain of youth.” As told by the lead scientist,6
“There are two main interpretations of our original experiments: The first is that, in the mouse joining experiments, rejuvenation was due to young blood and young proteins or factors that become diminished with aging, but an equally possible alternative is that, with age, you have an elevation of certain proteins in the blood that become detrimental, and these were removed or neutralized by the young partners.
As our science shows, the second interpretation turns out to be correct. Young blood or factors are not needed for the rejuvenating effect; dilution of old blood is sufficient.”
A therapeutic plasma exchange has been approved in the U.S. for the treatment of some autoimmune diseases. The process is also called plasmapheresis. Currently, the research team is finalizing plans for the next step, which is a clinical trial to explore modified plasma exchange in humans to improve the health of older adults.
In a separate study, scientists compared the actions and performance of older animals on tests of spatial memory. Special attention was paid to the hippocampus, an area of the brain crucial for forming memory and recognizing spatial patterns. The researchers concluded:7 “Our data indicate that exposure of aged mice to young blood late in life is capable of rejuvenating synaptic plasticity and improving cognitive function.” This was published in the journal Nature Medicine.
They are also evaluating the potential this intervention may be used to treat muscle wasting, immune deregulation and Type 2 diabetes.8 Another scientist on the team said this study may divert attention away from using plasma and other blood products from young people:9
“I think it will take some time for people to really give up the idea that young plasma contains rejuvenation molecules, or silver bullets, for aging. I hope our results open the door for further research into using plasma exchange — not just for aging, but also for immunomodulation.”
The point is that while positive effects from transfusing blood products from younger animals is possible, the practice is not necessary.
The aging process is associated with changes in physiological, biological and psychological processes. Some changes are innocuous, while others result in declining function or disability.10 The leading causes of death in the U.S. related to disease or illness include:11
Influenza and pneumonia
Stroke (cerebrovascular diseases)
Chronic lower respiratory diseases
Nephritis, nephrotic syndrome, and nephrosis
Many of these conditions are highly influenced by nutrition and lifestyle choices. In other words, while you could possibly develop heart disease or cancer as an older adult, you may delay or entirely prevent the disease through smart life choices.
After a lifetime of smoking, metabolic dysfunction or lack of physical activity you may be discouraged, but it is still possible to make an impact on your health. Even small changes made later in life can change overall health.12
A moderate amount of activity may help older adults retain independence, reduce blood pressure, improve pain from arthritis and improve mental health.13 Addressing potential health issues before they are overwhelming eases the challenges even further.
Geneticist and author David Sinclair, Ph.D., is a thought leader in how to improve health span. One important strategy that helps to slow your biological clock is calorie restriction and intermittent fasting. You’ll find more information in “Revolutionary Science of Aging and Longevity.”
Results from animal studies have suggested that the younger a person is when they start intermittent fasting, the better the results. Of course, it would be foolhardy to put an infant or young child on a fasting regimen. Teens and young adults are also not good candidates, as Sinclair says, “… there’s still a lot going on in their bodies and their brains.”14
However, after the age of 30, regular fasting is likely to lengthen life, based on the research. Time-restricted eating or intermittent fasting generally involves fasting for 12 to 16 hours each day. Typically, you either eliminate breakfast or dinner. If you choose to eat dinner, be sure it's at least three hours before bedtime.
As Sinclair and I talk about in the video above, this is because late-night eating increases your nicotinamide adenine dinucleotide (NAD+) levels which are important in a variety of bodily functions. It also reduces nicotinamide adenine dinucleotide phosphate (NADPH), an essential energy component for your cells.
If you’re eating too close to bedtime, your body cannot use the NADPH to burn calories and instead they are stored as fat. Additionally, you may try exercising while fasting. This means you'll workout just before your first meal, after a 16 or 18 hour fast. This raises your growth hormone levels to reach maximum benefit for mitochondrial biogenesis.
Sinclair's goal is to identify ways to reprogram cells in the body, so they don't just act younger, but literally are younger on a molecular level. To learn more about Sinclair’s research, the science behind aging and the potential for reversing its effects, be sure to pick up a copy of his book, “Lifespan: Why We Age — and Why We Don’t Have To.”
The foundations to good health and a long life are good nutrition, exercise, sensible sun exposure, quality sleep and hydration. Of course, there are other factors as well, but these are a good place to start.
Your body needs quality nutrition to deliver optimal health. Practicing intermittent fasting while eating junk food or processed foods will not accomplish your goal. Your body has micro- and macronutrient requirements for health that you must meet in order to thrive at the cellular level.
Since you can't out-exercise the amount of food you’re eating, you have to make sure you’re eating highly nutritious foods. Shop around the perimeters of the grocery store aisles to find whole foods you can cook at home. You’ll find more information about the sun and vitamin D, the importance of quality sleep to mitochondrial health and how to stay well-hydrated in the articles listed below:
Rosemary is an evergreen shrub native to the Mediterranean that’s revered for its culinary and therapeutic uses alike. Its pungent aroma and sharp lemon-pine flavor make it popular in French, Italian and other cuisines, and it’s been used for centuries as a tool to strengthen memory.1
A member of the mint family along with oregano and basil, rosemary is as versatile in medicine as it is in cooking. With potent antibacterial and antioxidant properties, rosemary is often used to help extend the shelf life of perishable foods, and rosemary extract is approved as a natural antioxidant for food preservation in the European Union.2
Among its many other pharmacologically validated uses in medicine are anticancer, antidiabetic, anti-inflammatory and hepatoprotective properties, but it’s also notable for its ability to improve cognitive function.3 In fact, it’s said that in ancient Greece, students would wear rosemary garlands while studying and would eat the herb to improve memory.
“Herball,” a classic plant reference written by English botanist John Gerard and published in 1597, even described rosemary as a “comfort” to the brain useful for improving memory and inward senses while being “especially good for infirmities of the head and brain.”4 Numerous modern studies support rosemary’s brain-boosting potential, courtesy of polyphenolic diterpenes such as carnosic acid.
What is perhaps most exciting about rosemary is that benefits have been demonstrated at very low amounts, such as those you might use while cooking. In a study of 28 adults with a mean age of 75 years, dried rosemary leaf powder was blended with tomato juice in order to study its effects on cognitive function in older people.5 The subjects received juice with either no rosemary, which served as a placebo, or a dose of:
The lowest dose led to improvements in speed of memory, which may be a predictor of cognitive function during aging, compared to placebo, while the highest dose led to a memory impairment. This suggests that using rosemary at “culinary” doses may be best for your brain.
“In conclusion, rosemary powder at the dose nearest normal culinary consumption demonstrated positive effects on speed of memory … The result points to the value of future studies on effects of low doses of rosemary on memory and cognition over the longer term,” the researchers noted.6
What’s more, the subjects also subjectively reported “significantly less impairment to their alertness compared with placebo” at the lowest dose, which the researchers said “strengthens the findings, particularly as there is research suggesting that mood is an underlying driver of cognitive function.”7
Carnosic acid is one of the active ingredients in rosemary, and researchers believe it helps protect the brain by staving off free radical damage that may lead to stroke and neurodegenerative conditions.
In fact, researchers from Iwate University in Japan and colleagues found that carnosic acid activates a signaling pathway that protects brain cells from free radicals and is activated by the free radical damage, which means it’s innocuous until it’s needed.8,9 Researchers detailed this impressive process in Advances in Experimental Medicine and Biology:10
“Carnosic acid, one of the major phenolic constituents of rosemary, is a pro-electrophile specifically activated by the oxidative stress pathological state resulting in its conversion from the hydroquinone to the oxidized quinone form, before it activates the Keap1/Nrf2 pathway leading to gene induction of the antioxidant response element (ARE) and gene products that protect against oxidative stress.”
Rosemary diterpenes are also known to inhibit neuronal cell death and are multifunctional in nature, offering antioxidant-driven neuronal protection against brain inflammation and amyloid beta formation, which may be implicated in Alzheimer’s disease.11
The amount of carnosic acid in dried leaves is thought to range from 1.5% to 2.5%, although higher amounts have been recorded. Environmental factors, including sunlight and water exposure, are known to affect the concentration of carnosic acid and other diterpenes in rosemary.12
Drug companies have promoted off-label usage of anti-inflammatory COX-2 inhibitor drugs for treating Alzheimer’s, but rosemary does this naturally. "If a synthetic COX-2 inhibitor could prevent Alzheimer's disease, so could a natural COX-2 inhibitor," said the late Jim Duke, an emeritus member of the American Botanical Council Board of Trustees.13 Rosemary contains numerous natural COX-2 inhibitors, including:14
A 2011 review also concluded that "carnosic acid [in rosemary] may be useful in protecting against beta amyloid-induced neurodegeneration in the hippocampus" and reduced cellular death in certain brain regions.15
It’s possible that rosemary compounds, including not only carnosic acid but also carnosol and rosmarinic acid, could be protective against a range of neurological disorders, including Alzheimer’s and other forms of dementia, Parkinson’s disease, epilepsy and migraines, wrote researchers in Natural Bio-active Compounds, who noted:16
“… R. officinalis L. [rosemary] and its bio-active metabolites [have a protective role] against various neurological disorders via targeting amyloid-beta (A-β) aggregation, neuronal cell death, acetylcholinesterase (AChE), neuroinflammation, β-secretase (BACE-1) activity, mitochondrial redox status, etc.
Based on the multifunctional nature due to effective bio-active secondary metabolites, R. officinalis can be a terrific alternative therapeutic source against many neurodegenerative diseases.”
Speaking of migraines, a 2013 study published in Food Chemistry points to rosemary as having a long history in tradition for treating headaches due to the potent anti-inflammatory and pain-relieving compounds it contains.17
To use rosemary essential oil for migraine headache relief, try adding one or two drops to a cup of tea, water or soup and drinking it. You can also mix two drops of rosemary oil with two drops of peppermint oil and a teaspoon of coconut oil to massage your forehead, temples and the back of your neck.
Rosemary may also be useful for improving cognitive function in healthy adults. In one example, eight healthy adults consumed either 250 milliliters (8.4 ounces) of rosemary water or plain mineral water, then completed a series of cognitive tasks.
Multiple statistically significant beneficial effects were noted among those who drank the rosemary water, including increased levels of deoxygenated blood in the brain, an indication that rosemary may facilitate oxygen extraction during times of cognitive demand — a previously unknown finding.18
In addition, those who consumed rosemary had a 15% average boost compared to the placebo group when it came to performing working memory tasks. The benefits were described as similar to those previously demonstrated via the inhalation of the aroma of rosemary essential oil. Study author Mark Moss of the U.K.’s Northumbria University said in a news release:19
"[R]osemary offers a number of interesting possible health promoting applications, from antioxidant and antimicrobial to hepatoprotective and antitumorigenic activity …
The results of this research show there are statistically reliable improvements in memory function thanks to the ingestion of … Rosemary Water. In fact, I'd say that the shots act like a turbo charger for the brain."
If you’re not fond of rosemary’s flavor, you can still get a quick boost simply by inhaling its scent. The aroma of rosemary essential oil led to a significant enhancement of performance in memory quality and secondary memory factors in a study of 144 people.20
Rosemary’s characteristic scent comes from 1,8-cineole, which is also found in bay leaves, wormwood, sage and eucalyptus. It’s possible that 1,8-cineole, a common monoterpene found in many essential oils, is responsible for some of its aroma benefits, as its been linked to performance on cognitive tasks.
When 20 volunteers performed a series of math problems and other cognitive tasks while in a cubicle diffused with the aroma of rosemary, their performance improved in relation to higher concentrations of 1,8-cineole, levels of which were measured via blood testing. Both speed and accuracy improved in association with 1,8-cineole concentrations.
“These findings suggest that compounds absorbed from rosemary aroma affect cognition and subjective state independently through different neurochemical pathways,” the researchers, which included Moss, explained.21
A small study in 2009 also found that 28 days of aromatherapy involving rosemary, lemon, lavender and orange essential oils helped enhance cognitive function, especially in Alzheimer's patients, with no side effects.22
Beyond your brain, rosemary also offers a host of additional benefits that extend bodywide. This powerful herb may help heart health, including after a heart attack, while favorably affecting body weight and dyslipidemia. Rosemary also offers pain-relieving qualities and the potential to fight infection, while also protecting your liver, fighting the proliferation of tumor cells and even reducing stress and anxiety.23
Rosemary, in fact, “may control physiological disorders similar to or superior to the usual medications,” according to a review in the Journal of Biomedical Science.24 While you can find rosemary in a variety of forms, from extracts and supplements to teas and essential oils, one of the best ways to enjoy the benefits of this perennial plant is to grow it in your own garden. Then, you’ll have access to fresh rosemary whenever you need it.
Fortunately, rosemary is easy to grow and thrives on little care. In warmer climates it grows quicker, so you'll want to plant them at least 3 feet apart to allow ample room for growth. If you live in northern climates and commonly experience freezing weather lower than 15 degrees F, you'll want to grow your rosemary in a pot and bring it in during the winter months.
When harvesting rosemary, snip the tender end shoots that aren't woody, as they’re best for cooking. It’s simple to strip the leaves once the stems are dry simply by running your fingers along the stem. Feel free to use rosemary generously in your cooking, as well as diffuse the essential oil around your home, especially when you feel like you need a brain boost.