Illustrating the sadistic and predatory nature of those who claim to “keep us safe,” for five years, Pasquale Salas terrorized a young girl he met on Minecraft.
Dementia is a growing problem worldwide and the numbers are overwhelming. Alzheimer’s Disease International estimates the global number with dementia reached 46.8 million in 2015 and is predicted to grow to 75 million by 2030, and 131.5 million by 2050.1
In the U.S. there are more than 5 million people with Alzheimer’s, one form of dementia.2 This number is estimated to nearly triple to 14 million by 2050. One in 3 of older adults dies every year with some form of dementia, which is more than the numbers with breast cancer and prostate cancer combined.
To put it another way, from 2000 to 2018, the number who died from heart disease dropped 7.8%, while the number who died from Alzheimer’s rose 146%.
The economic costs have reached $305 billion and could rise to $1.1 trillion by 2050. Primary care doctors are overwhelmed by the number of patients in their practices and half believe the profession isn’t ready for the growing number.
The development of dementia and Alzheimer’s disease is likely due to a number of reasons. Researchers have identified several factors that impact cognitive impairment, including insulin resistance,3 certain drugs,4 lack of sleep5 and low levels of some vitamins.6
Cholinergic Dysfunction May Drive Dementia
As explained in a recently published paper, scientists analyzed the effect proton pump inhibitors have on the development of dementia. They recognized indicators pointing to cholinergic dysfunction in the development of dementia. In a review article from 1999,7 other scholars outlined data to support the hypothesis that cholinergic dysfunction contributes to Alzheimer’s.
By 2008,8 the research community had identified areas of the brain where cholinergic dysfunction may influence dementia. Subsequently, acetylcholine was recognized for the central role it plays in the nervous system.9 It requires an enzyme to synthesize from acetyl-COA and choline. That enzyme is choline acetyltransferase.
Cholinergic synapses are found throughout the brain, including the basal forebrain, which is severely damaged in those who have the disease. With further research,10 scientists found using cholinesterase inhibitors could increase acetylcholine in the brain, which has proven to be clinically useful in the treatment of Alzheimer’s dementia.
The use of anticholinergic drugs has a known side effect, though, of causing short-term cognitive impairment in the elderly.11 These medications act on the neurotransmitter acetylcholine, which is involved in sending messages that affect muscle contraction. They also act on parts of the brain that handle memory and learning.
Anticholinergic drugs have been used for decades to treat diarrhea, asthma, insomnia, motion sickness and even some psychiatric disorders. Some of the more common side effects include blurry vision, dizziness, confusion, hallucination and drowsiness.12
As described in study published in JAMA,13 scientists looked at whether exposure could increase the risk of dementia in people 55 years and older. The data revealed that those taking strong anticholinergic drugs, which affect acetylcholine, was associated with a greater risk of dementia.
Gastric acid secretion is regulated in part by acetylcholine. The development of proton pump inhibitors for chronic heartburn became a mainstay of treatment. This resulted in people taking the medication for long periods of time. The intended use of the drug was to inhibit the cellular proton pump that produces acid.
However, proton pump inhibitors are not specific to stomach cells and will inhibit any cell with a proton pump. This may be the trigger for the long list of side effects associated with the drugs, including kidney disease, dementia and liver disease.14 While researchers found an association between proton pump inhibitors and dementia, the mechanism had yet to be discovered.
One Drug Selectively Inhibits Synthesis of Acetylcholine
One team of researchers15 looked at all proton pump inhibitors approved by the FDA and found that the drugs negatively affected the production of acetylcholine in the body.
Using computer simulations, they evaluated how different substances in six proton pump inhibitors interacted with choline acetyltransferase.16 While the drug was designed to limit cellular proton pumps and reduce acid production, the simulations showed they could bind with the enzyme that synthesizes acetylcholine.
The effect of this was to reduce production of acetylcholine. The researchers believe new studies are needed to determine if the effects in the lab also happen in the body. One of the team members commented:17
“Special care should be taken with the more elderly patients and those already diagnosed with dementia. The same also applies to patients with muscle weakness diseases such as ALS, as acetylcholine is an essential motor neurotransmitter. In such cases, doctors should use the drugs that have the weakest effect and prescribe them at lowest dose and for as short a time as possible.”
Choline: Key Factor in Nonalcoholic Fatty Liver Disease?
Nonalcoholic liver disease (NAFLD) is one of the most common forms of liver disease in the U.S.18 It is initiated in part by obesity and insulin resistance. Scientists have found it may lead to fibrosis of the liver and then to cirrhosis or liver cancer.
There are two forms of NAFLD which are not associated with alcohol consumption. The first is simple fatty liver or nonalcoholic fatty liver (NAFL) in which there are fatty deposits in the liver but very little, if any, inflammation or cellular damage.
The second is called nonalcoholic steatohepatitis (NASH). This is a form of NAFLD in which you have fatty deposits in the liver and hepatitis, or inflammation of the liver. This results in liver cell damage that can lead to fibrosis, cirrhosis or liver cancer. Most people with the condition have simple fatty liver while only a small number have NASH.
The National Institute of Diabetes and Digestive and Kidney Diseases reports that between 30% and 40% of all adults in America have NAFLD. Those who have a higher risk are obese and have Type 2 diabetes. The condition can affect people of any age, race or ethnicity.
In one animal study, researchers found that by supplementing with choline they could normalize cholesterol metabolism, which appeared to help prevent NASH and improve liver function.19 As described in one paper, choline is necessary for liver health:20
“Humans must eat diets containing choline because its metabolite phosphatidylcholine constitutes 40–50% of cellular membranes and 70–95% of phospholipids in lipoproteins, bile and surfactants; it is needed to form acetylcholine, an important neurotransmitter; its metabolite betaine is needed for normal kidney glomerular function, and perhaps for mitochondrial function; and it provides one-carbon units, via oxidation to betaine, to the methionine cycle for methylation reactions.
When humans eat diets low in choline, fatty liver is one of the earliest adverse events, and in some people significant hepatic damage occurs (as assessed by release of hepatic enzymes into blood).”
According to Chris Masterjohn, Ph.D., choline deficiency may be a more significant in development of the condition than taking in too much fructose. His degree is in nutritional science and he believes the rise in fatty liver conditions is largely due to more and more people avoiding egg yolks and liver.
In his review of the medical literature, Masterjohn found a link between choline and fatty liver, which was initially discovered in research into Type 1 diabetes. He describes the relationship:21
“Physicians and researchers had started pinning the blame on alcohol abuse for fatty liver back in the 1800s, so while research was first highlighting the role of sucrose in fatty liver, other research was doing the same for alcohol.
In 1949, however, researchers showed that sucrose and ethanol had equal potential to cause fatty liver and the resulting inflammatory damage, and that increases in dietary protein, extra methionine, and extra choline could all completely protect against this effect.
Conversely, much more recent research has shown that sucrose is a requirement for the development of fatty liver disease in a methionine- and choline-deficient (MCD) model. The MCD model of fatty liver disease is the oldest and most widely used dietary model.
The MCD model produces not only the accumulation of liver fat, but massive inflammation similar to the worst forms of fatty liver disease seen in humans. What no one ever mentions about this diet is that it is primarily composed of sucrose and its fat is composed entirely of corn oil!
The picture that is clearly emerging from all of these studies is that fat, or anything from which fat is made in the liver, such as fructose and ethanol, are required for the development of fatty liver. But in addition to this [same] factor — overwhelmingly, it appears to be choline deficiency — must deprive the liver of its ability to export that fat.”
Choline Needed for Optimal Health
Your liver produces a small amount of choline,22 but the rest must be supplied through your diet. Unfortunately, nearly 90% of people living in the U.S. have a deficiency,23 which increases the risk of babies being born with neural tube defects.24
As I’ve written before, groups at particularly high risk for choline deficiency include pregnant mothers, endurance athletes, postmenopausal women, vegans, and those who consume high amounts of alcohol.
Choline serves several vital functions in the body.25 It’s used in the manufacture of some phospholipids essential to the development of your cell membranes. Choline is also a precursor for intracellular molecules used in cell signaling.
The neurotransmitter acetylcholine is synthesized from choline and involved in memory, circadian rhythm and muscle control. Each of these specific functions contribute to the impact it has on cardiovascular health, liver diseases, neural tube defects and cognitive health.
Seek Best Natural Sources of Choline First
The National Institutes of Health26 lists the adequate intake for choline provided in the Dietary Reference Intakes developed by the Institute of Medicine (IOM). At the time these were developed, there was not sufficient data to establish an estimated average requirement.
This is a number that’s usually used to determine the amount of nutrients needed to adequately supply diets for 50% of healthy individuals. Instead, the Food and Nutrition Board of the IOM established adequate intakes for all ages they believe would prevent the development of liver damage.
To date, men 19 years and older who get 550 mg per day and women who take in 425 mg per day have an adequate intake. This rises to 450 mg per day during pregnancy and 550 mg per day while breastfeeding. These are suggested values and may vary depending on your diet, age, ethnicity and genetic makeup.
It is best to first seek healthy natural sources for your nutrients. For instance, a single hardboiled egg weighing approximately 50 grams may contain from 113 mg27 to 147 mg28 of choline. This is 25% to 30% of your daily requirement. Only grass fed beef liver has more, with per 50 grams per serving.29 As noted in the Fatty Liver Diet Guide:30
“Eggs rank very high on the list of foods that are high in either lecithin, which converts to choline, or in choline itself. Note that this is the egg yolks only, not egg whites, which only have traces of this micronutrient.
Choline is essential in the production of phosphatidylcholine, a fat molecule called a phospholipid. But wait! Isn’t all fat bad? No — especially if it is essential to overall health and in particular, liver health. Simply put — if you don’t have enough choline, your liver can’t move out fat. It instead begins to collect within your liver, creating fatty liver.”
That said, supplementation is a potential option if you don’t eat eggs, salmon or other foods with ample amounts of the nutrient. The tolerable upper intake for an adult is 3.5 grams per day.32 Be careful not to take too much, as side effects of excessive choline include low blood pressure, sweating, diarrhea and a fishy body odor.
N-acetylcysteine (NAC) is a precursor to reduced glutathione, and both of these play important roles in health and fitness. NAC has a long history of use as a first-aid remedy for acetaminophen (known as paracetamol in Europe) poisoning.
It’s given in cases when you’ve taken an overdose of Tylenol or other acetaminophen products. It neutralizes the toxic effects of the drug by recharging glutathione, thereby preventing liver damage.
NAC and glutathione may also be important in COVID-19, as explained by pulmonologist Dr. Roger Seheult in the MedCram lectures above. The reason for this is because of the role they play in combating oxidative stress, which is a main cause of inflammation and disease in general, and the cytokine storm associated with COVID-19 in particular. NAC may also combat the abnormal blood clotting seen in many cases.
As explained and illustrated by Seheult, when you add an electron to an oxygen (O2) molecule, you get superoxide (O2), a reactive oxygen species (ROS). When you add another electron (for a total of two electrons), you get hydrogen peroxide (H2O2). An oxygen molecule with three electrons added becomes hydroxyl (O3), and oxygen with four electrons added becomes water (H2O).
Oxygen is the most oxidized form, while water is the most reduced form. Your body has built-in defenses against oxidative stress like1 superoxide dismutase (SOD). SOD converts damaging superoxide into hydrogen peroxide. Another is catalase, which converts hydrogen peroxide into oxygen and water. A third is glutathione peroxidase (GSHPX).
GSHPX does two things simultaneously. While reducing hydrogen peroxide into water, it also converts the reduced form of glutathione (GSH) into glutathione disulfide (GSSG), which is the oxidized form of glutathione. In other words, as GSHPX turns hydrogen peroxide into harmless water, glutathione becomes oxidized.
The oxidized GSSG is then “recharged” or regenerated by NADPH (the reduced form of NADP+), turning it back into GSH (the reduced form of glutathione). NADPH is also converted into NADP+ through an enzyme called GSH reductase.
The reason this is important is because superoxide plays a crucial role in the oxidative stress occurring in the chronic illnesses identified as comorbidities for COVID-19, such as obesity, heart disease and diabetes.
As noted by Seheult, serious COVID-19 infection triggers a perfect storm of superoxide-driven oxidative stress, as SARS-CoV-2 attaches to the ACE2 receptor, triggering angiotensin 2 (AT-2), which stimulates superoxide. Simultaneously, there’s a deficiency of AT-1,7, which inhibits superoxide. So, this deficiency allows superoxide to accumulate further.
SARS-CoV-2 also attracts polymorphonuclear leukocytes (PMNs), a type of white blood cell, which also produces superoxide in its efforts to destroy pathogens. All of that superoxide is then converted into other ROS that destroy endothelial cells.
This down-spiral can be inhibited by N-acetylcysteine (NAC), which boosts GSSG. As illustrated by Seheult, when you add two GSH molecules and hydrogen peroxide together, you end up with oxidized glutathione and harmless water, thus alleviating the oxidative stress.
NAC Boosts GSH and Protects Against Influenza
Seheult cites research showing low GSH and oxidative stress are associated with a range of nose, ear and throat conditions, affecting tissues both locally and systemically. The good news is that glutathione can be recharged with NAC, an inexpensive and readily available over-the-counter supplement.
Research2 has in fact demonstrated that NAC can attenuate symptoms of influenza and improve cell-mediated immunity. According to the authors:
“N-acetylcysteine (NAC), an analogue and precursor of reduced glutathione, has been in clinical use for more than 30 yrs as a mucolytic drug. It has also been proposed for and/or used in the therapy and/or prevention of several respiratory diseases and of diseases involving an oxidative stress, in general.
The objective of the present study was to evaluate the effect of long-term treatment with NAC on influenza and influenza-like episodes. A total of 262 subjects of both sexes … were enrolled in a randomized, double-blind trial … randomized to receive either placebo or NAC tablets (600 mg) twice daily for 6 months.
Patients suffering from chronic respiratory diseases were not eligible, to avoid possible confounding by an effect of NAC on respiratory symptoms. NAC treatment was well tolerated and resulted in a significant decrease in the frequency of influenza-like episodes, severity, and length of time confined to bed.
Both local and systemic symptoms were sharply and significantly reduced in the NAC group. Frequency of seroconversion towards A/H1N1 Singapore 6/86 influenza virus was similar in the two groups, but only 25% of virus-infected subjects under NAC treatment developed a symptomatic form, versus 79% in the placebo group …
Administration of N-acetylcysteine during the winter, thus, appears to provide a significant attenuation of influenza and influenza-like episodes, especially in elderly high-risk individuals. N-acetylcysteine did not prevent A/H1N1 virus influenza infection but significantly reduced the incidence of clinically apparent disease.”
NAC Is a Potent Antiviral in Its Own Right
As noted by Seheult, the number needed to treat (NNT) in that study3 is 0.5, which means for every two people treated with NAC, one will be protected against symptomatic influenza. (Remember, you can be infected with a virus yet not become ill, i.e., symptomatic, if your immune system is strong enough.)
That’s significantly better than influenza vaccines, which have an NNT, or NNV (number needed to vaccinate) of 71,4 meaning 71 people must be vaccinated to prevent a single case of confirmed influenza. It’s even better than vitamin D, which has an NNT of 33.5 (Among those who were severely vitamin D deficient at baseline, taking vitamin D still had an NNT of 4.)
NAC has also been shown to inhibit viral replication and expression of pro-inflammatory cytokines, such as interleukin-6 (IL-6), in cells infected with highly pathogenic H5N1 influenza virus.6 According to the authors:
“The antiviral and anti-inflammatory mechanisms of NAC included inhibition of activation of oxidant sensitive pathways including transcription factor NF-kappaB and mitogen activated protein kinase p38 …
NAC inhibits H5N1 replication and H5N1-induced production of pro-inflammatory molecules. Therefore, antioxidants like NAC represent a potential additional treatment option that could be considered in the case of an influenza A virus pandemic.”
NAC in Acute Respiratory Distress Syndrome
NAC has also been shown to reduce acute respiratory distress syndrome (ARDS),7 which is a serious complication associated with acute lung injury (ALI). One meta-analysis8 of five randomized controlled trials found a significant reduction in intensive care unit (ICU) stays among patients treated with NAC, even though there was no significant difference in short-term mortality risk.
Another earlier study9 found NAC improves ARDS by “increasing intracellular glutathione and extracellular thiol molecules” along with general antioxidant effects. According to this study:
“In acute respiratory distress syndrome (ARDS), there is extensive overproduction of free radicals to the extent that endogenous antioxidants are overwhelmed, permitting oxidative cell damage.
The present study examined the benefit of the anti-oxidant compound N-acetylcysteine (NAC) in the management of ARDS by measuring patient’s intracellular glutathione (inside red blood cells) and extracellular (plasma) anti-oxidant defense biomarkers and outcome.
Twenty-seven ARDS patients were recruited from the intensive care unit of a teaching Hospital and randomly divided into two groups. Both groups were managed similarly by regular treatments but 17 patients received NAC 150 mg/kg at the first day that followed by 50 mg/kg/day for three days and 10 patients did not receive NAC.
Treatment by NAC increased extracellular total anti-oxidant power and total thiol molecules and also improved intracellular glutathione and the outcome of the patients. In conclusion, patients with ARDS are in a deficient oxidant-anti-oxidant balance that can get a significant benefit if supplemented with NAC.”
NAC Improves Lung Function
Other studies that have shown NAC eto be beneficial in the treatment of lung-related problems include the following:
• A 1994 study10 found NAC enhances recovery from ALI, significantly regressing patients’ lung injury score during the first 10 days of treatment, and significantly reducing the need for ventilation.
After three days of treatment, only 17% of those receiving NAC needed ventilation, compared to 48% in the placebo group. According to the authors:
“Intravenous NAC treatment during 72 h improved systemic oxygenation and reduced the need for ventilatory support in patients presenting with mild-to-moderate acute lung injury subsequent to a variety of underlying diseases.”
• A 2018 study11 found NAC reduces oxidative and inflammatory damage in patients with community-acquired pneumonia.
• Another 2018 study12 found NAC also improves post-operative lung function in patients undergoing liver transplantation.
NAC Protects Against Blood Clots and Stroke
Importantly, with regard to COVID-19, NAC may protect against the coagulation problems associated with this illness. Many COVID-19 patients experience serious blood clots, and NAC counteracts hypercoagulation in the blood as well.13,14,15
As noted in one of these studies,16 “NAC has anticoagulant and platelet-inhibiting properties.” Another study points out that:17
“… diabetes exacerbates stroke-induced brain injury, and that this correlates with brain methylglyoxal (MG)-to-glutathione (GSH) status. Cerebral injury was reversed by N-acetylcysteine (NAC).
Here we tested if the pro-thrombotic phenotype seen in the systemic circulation and brain during diabetes was associated with increased MG-glycation of proteins, and if NAC could reverse this …
NAC treatment partly or completely reversed the effects of diabetes. Collectively, these results show that the diabetic blood and brain become progressively more susceptible to platelet activation and thrombosis.
NAC, given after the establishment of diabetes, may offer protection against the risk for stroke by altering both systemic and vascular prothrombotic responses via enhancing platelet GSH, and GSH-dependent MG elimination, as well as correcting levels of antioxidants such as SOD1 and GPx-1.”
A fourth paper,18 published in 2017, found NAC has potent thrombolytic effects, meaning it breaks down blood clots. The authors concluded that “NAC is an effective and safe alternative to currently available antithrombotic agents to restore vessel patency after arterial occlusion.” (Restoring vessel patency means the blood vessel is now unobstructed so that blood can flow freely.)
Seheult cites two additional papers19,20 showing the same thing. As noted by Seheult, many COVID-19 cases have blood clots in addition to excessive oxidative stress, and NAC addresses both of these problems.
NAC for COVID-19
Last but not least, a report21 reviewing the evidence for using NAC in the treatment of COVID-19 was published April 14, 2020, by The Centre for Evidence-Based Medicine at the University of Oxford.
This report focuses on acute respiratory disorders, and we now know that COVID-19 is not just a respiratory disorder but also a blood disorder. This is a significant shortcoming of this report, as there’s significant evidence that NAC can break down the blood clots responsible for the hypoxia (cellular deprivation of oxygen) in COVID-19.
May 5, 2020, a trial was posted to ClinicalTrials.gov, for the study of NAC in patients with COVID-19, sponsored by the Memorial Sloan Kettering Cancer Center.22 The study aims to enroll 86 patients with severe or critical illness to investigate whether NAC, in addition to other supportive treatments, can reduce ICU stays and prevent the need for mechanical ventilation. Here, they are giving 6 grams (6,000 milligrams) of NAC a day for up to three weeks.
Seheult’s hypothesis for why NAC may be useful in COVID-19 treatment can be summarized as follows:
SARS-CoV-2 attaches to and reduces the ACE2 receptor, which causes AT-2 to increase and AT-1,7 to decrease. This in turn increases damaging superoxide that causes oxidative stress and endothelial cell dysfunction.
This then increases von Willebrand factor from the endothelial space, causing thrombosis (blood clots), and it is this thrombosis that appears to cause the hypoxia in the lungs. NAC — which recharges glutathione — not only reduces superoxide (oxidative stress) but also appears to reduce von Willebrand factors that form blood clots.
Glutathione for COVID-19
In the second MedCram video (second in the playlist), Seheult reviews the blood clotting aspects of COVID-19. He also discusses the potential effectiveness of simply taking glutathione, opposed to its precursor, NAC.
A recent case report23 — which simply reviews one or more medical cases and is not an actual study — reports that two patients with COVID-19 and a history of Lyme disease (coinfection) treated with 2 grams of intravenous glutathione “improved their dyspnea within one hour of use.” Dyspnea is the medical term for shortness of breath. According to the authors:
“Oral and IV glutathione, glutathione precursors (N-acetyl-cysteine) and alpha lipoic acid may represent a novel treatment approach for blocking NF-?B and addressing ‘cytokine storm syndrome’ and respiratory distress in patients with COVID-19 pneumonia.”
He also cites a Russian paper24 stating that glutathione deficiency may be “the most likely cause of serious manifestation and death” in COVID-19 patients. The paper, which is a preprint and has not yet undergone peer review, presents a hypothesis “based on an exhaustive literature analysis and own observations.” According to the author:25
“The major risk factors established for severe COVID-19 infection and relative glutathione deficiency found in COVID-19-infected patients with moderate-to-severe illness have converged me to two very important conclusions:
(1) oxidative stress contributes to hyper-inflammation of the lung leading to adverse disease outcomes such as acute respiratory distress syndrome, multiorgan failure and death;
(2) poor antioxidant defense due to endogenous glutathione deficiency as a result of decreased biosynthesis and/or increased depletion of GSH is the most probable cause of increased oxidative damage of the lung, regardless which of the factors aging, chronic disease comorbidity, smoking or some others were responsible for this deficit.
The hypothesis provides novel insights into the etiology and mechanisms responsible for serious manifestations of COVID-19 infection and justifies promising opportunities for effective treatment and prevention of the illness through glutathione recovering with N-acetylcysteine and reduced glutathione.”
As noted by Seheult, we still do not have any trials demonstrating that NAC will benefit COVID-19 patients specifically, “but if we connect the dots, it looks promising.” What’s more, NAC is very safe and many studies have shown there are no serious adverse effects associated with its use.
The same can be said for glutathione. Seheult points out it would be interesting to see what the effect might be using a combination of both glutathione and NAC. Overall, the more we learn about this disease, the more we realize there may be simple and inexpensive ways to treat this perplexing illness, and NAC in particular looks like a good candidate for consideration.
Of course, both also have many other important health benefits. To learn more, see “Glutathione and NAC Play Crucial Roles in Health and Fitness,” and “The Many Benefits of NAC — One of the Most Important Supplements You’ve Likely Never Heard Of.”
1 Which of the following owns the equity firm that manages Gannett, the largest media company in the U.S. with more than 260 dailies, including USA Today, under their umbrella?
2 Which of the following is “the smoking gun” proving SARS-CoV-2 was lab-created?
3 What are human gammaretroviruses?
4 Who is the most visible mastermind behind the plan to vaccinate the global population with an experimental COVID-19 vaccine, despite the fact that coronavirus vaccines have a decades’ long history of causing a “paradoxical immune enhancement” that turns lethal when exposed to wild coronavirus?
5 In the past, coronavirus vaccine development has been hampered by which of the following problems?
6 What is the biggest risk of Amazon’s gigantic empire?
7 Who identified the 1978-1980 Zimbabwe anthrax outbreak as a case of biological warfare?
Countries across the world have been in lockdown for months in response to the coronavirus pandemic. The costs are enormous in terms of life, liberty and the economy.
One of the ideas for how extraterrestrial (i.e. Anunnaki) beings might try to reach out to humans is through the universal language of mathematics.
By Michael Snyder,
Can anyone explain how we are going to motivate unemployed workers to go back to work when most of them can actually make more money camped on their sofas watching Netflix? Over the past couple of months, 36.5 million Americans have filed new claims for unemployment benefits, and Congress understandably wanted to do something to address this unprecedented spike in unemployment. But by giving all of these unemployed workers a repeating 600 dollar bonus on top of existing unemployment benefits, Congress has actually created a very powerful incentive for Americans to be unemployed and to stay unemployed for as long as the bonuses last. According to a group of prominent economists at the University of Chicago, 68 percent of those that are currently unemployed can now bring home more money than when they were actually employed…
A new analysis by Peter Ganong, Pascal Noel and Joseph Vavra, economists at the University of Chicago,1 uses government data from 2019 to estimate that 68 percent of unemployed workers who can receive benefits are eligible for payments that are greater than their lost earnings. They also found that the estimated median replacement rate — the share of a worker’s original weekly salary that is being replaced by unemployment benefits — is 134 percent, or more than one-third above their original wage.
Of course you don’t have to be bringing home 100 percent of your former income for there to be an incentive to stay unemployed.
For example, if you had a job that you really hated, you would almost certainly jump at the chance to stay home every day and still make 90 percent of what you formerly earned.
So yes, those that had very high paying jobs will be motivated to get back to work, but everyone else will be highly tempted to ride the gravy train for as long as it lasts.
And the less you made when you were actually working, the more intense that temptation will be.
Just consider what restaurant and hotel workers must be thinking about now. According to CNBC, the average unemployed worker in that industry is now eligible to collect “182% of their previous wages”…
The average worker in this industry, which employs 14 million people, makes $13.45 an hour — the lowest compared with other industries.
These workers would benefit most under the unemployment system when compared to others — collecting 182% of their previous wages, according to a CNBC analysis of Bureau of Labor Statistics and Labor Department data.
Do you think that those workers are going to be eager to get back to their former jobs?
I don’t think so.
Of course the truth is that many of their jobs are never coming back. According to the Atlantic, “hundreds of thousands of companies” have already collapsed during this economic downturn…
Small-business activity has plunged nationwide by nearly 50 percent. Hundreds of thousands of companies have already failed. Big retailers such as J.Crew and Neiman Marcus have filed for bankruptcy, while others, including Macy’s, are teetering. By some measures, scarcely one-third of Americans say they are working. Next month’s jobs report will likely show that, for the first time since World War II, a majority of Americans aren’t officially employed.
So the cold, hard reality of the matter is that there simply is not going to be enough jobs for everyone in the United States for the foreseeable future.
And moving forward, a lot more businesses are going to be failing.
Just recently, Facebook conducted a survey of “86,000 small and medium-sized business owners”, and the results of that survey were quite startling…
About a third of small businesses forced to close due to the coronavirus pandemic say they won’t be able to reopen due to an inability to pay bills or rent, a Facebook survery has found.
More than half of the business owners surveyed by Facebook have also said they don’t expect to be able to rehire the same amount of workers that they employed prior to the pandemic.
More specifically, the survey discovered that just 45 percent of all small and medium-sized business owners plan to rehire the same number of employees that they previously had.
So that means that millions upon millions of jobs are gone for good.
And of course the environment of fear that COVID-19 has created is going to paralyze new hiring for a long time to come. If you are an existing business and you are concerned that you may not be able to keep the employees that you already have, that is going to make you extremely hesitant to add anyone new.
The bottom line is that it is going to be exceedingly difficult to find jobs in the months ahead, and the long-term outlook for the newly unemployed is not good at all.
For the moment, those newly unemployed workers are being taken care of by the federal government, but the $600 bonuses are set to expire in July.
If we get to July and those benefits are not extended, we could have a massive national temper tantrum on our hands.
Of course there are many in Congress that are quite eager to extend those benefits, but that would also mean borrowing and spending billions upon billions more dollars that we do not have.
And what happens when an even bigger crisis than COVID-19 comes along? We are just experiencing the early winds of “the perfect storm” that I portrayed in “The Beginning Of The End”, and most Americans are completely and utterly unprepared for what is coming.
So let’s not be mad at those that have lost their jobs just because they are getting a windfall for a few months. Instead, let us hold our national leaders accountable for getting us into this mess in the first place.
For decades, our national leaders have been leading us down a road that leads to national oblivion, and now it appears that we are rapidly approaching the end of that road.
By Anna Von Reitz
By Anna Von Reitz