true story

This is the reason … why all the hype

Better understanding:

Here is a little more information on the virus that may help explain a few things that people don’t understand. This is from an immunologist at Johns Hopkins University.


Feeling confused as to why Coronavirus is a bigger deal than Seasonal flu? Here it is in a nutshell. I hope this helps. Feel free to share this with others who don’t understand…

It has to do with RNA sequencing…. I.e. genetics.

Seasonal flu is an “all human virus”. The DNA/RNA chains that make up the virus are recognized by the human immune system. This means that your body has some immunity to it before it comes around each year… you get immunity two ways…through exposure to a virus, or by getting a flu shot.

Novel viruses come from animals…. the WHO tracks novel viruses in animals, (sometimes for years watching for mutations). Usually, these viruses only transfer from animal to animal (pigs in the case of H1N1) (birds in the case of the Spanish flu). But once, one of these animal viruses mutates, and starts to transfer from animals to humans… then it’s a problem, Why? Because we have no natural or acquired immunity.. the RNA sequencing of the genes inside the virus isn’t human, and the human immune system doesn’t recognize it so, we can’t fight it off.

Now…. sometimes, the mutation only allows transfer from animal to human, for years it’s the only transmission is from an infected animal to a human before it finally mutates so that it can now transfer human to human… once that happens..we have a new contagion phase. And depending on the fashion of this new mutation, that’s what decides how contagious, or how deadly it’s gonna be..

H1N1 was deadly….but it did not mutate in a way that was as deadly as the Spanish flu. Its RNA was slower to mutate and it attacked its host differently, too.

Fast forward.

Now, here comes this Coronavirus… it existed in animals only, for nobody knows how long…but one day, at an animal market, in Wuhan China, in December 2019, it mutated and made the jump from animal to people. At first, only animals could give it to a person… But here is the scary part…. in just TWO WEEKS it mutated again and gained the ability to jump from human to human. Scientists call this quick ability, “slippery”

This Coronavirus, not being in any form a “human” virus (whereas we would all have some natural or acquired immunity). Took off like a rocket. And this was because Humans have no known immunity…doctors have no known medicines for it.

And it just so happens that this particular mutated animal virus, changed itself in such a way the way that it causes great damage to human lungs..

That’s why Coronavirus is different from seasonal flu, or H1N1 or any other type of influenza…. this one is slippery AF. And it’s a lung eater…And, it’s already mutated AGAIN, so that we now have two strains to deal with, strain s, and strain L….which makes it twice as hard to develop a vaccine.

We really have no tools in our shed, with this. History has shown that fast and immediate closings of public places have helped in the past pandemics. Philadelphia and Baltimore were reluctant to close events in 1918 and they were the hardest hit in the US during the Spanish Flu.

Factoid: Henry VIII stayed in his room and allowed no one near him, till the Black Plague passed…(honestly…I understand him so much better now). Just like us, he had no tools in his shed, except social isolation…

And let me end by saying….right now it’s hitting older folks harder… but this genome is so slippery…if it mutates again (and it will). Who is to say, what it will do next.

Be smart folks… acting like you’re unafraid is so not the right thing right now.

#flattenthecurve and share this to those that just are not catching on.

•Again, not a judgment this post, just posting this information I bumped into. 💕✌️

Just Because, opinion

Is Melatonin the answer to the corona crisis?

Melatonin is the reason why children under the age of 9 seldom exhibit severe symptoms. In fact, children may exhibit mild or even no symptoms at all, even though they have been infected by SARS-CoV-2 [73].  How significant is the difference in melatonin production between children, adults and the elderly?

For most people, peak melatonin production is between the hours of 2 am to 3 am.  The maximum melatonin levels measured in healthy adults between the ages of 65 to 70 years appeared to be around 49.3 picograms/ml (pg/ml).  Adults more than 75 years of age only have maximum production levels of 27.8 pg/ml [74].

Young children, on the other hand, have extremely high melatonin levels, compared to adults.  The maximum levels recorded for children showed a decline as age increased. Children between the ages of 1 to 5 had peak melatonin at 325 pg/ml, while those between the ages of 5 to 11 already declined to 133 pg/ml [76].

Compared to healthy adult seniors, a young child can easily have TEN TIMES the amount of peak melatonin levels.  But even then, the actual physiological concentration is extremely low. How much is one picogram, exactly?

To give you some perspective, most melatonin supplements are around 3 to 5 mg per capsule or tablet.  One milligram equals 1,000,000,000 picograms. That is why the physiological dosage generally recommended for melatonin supplementation is around 0.3 milligrams [75].

The fact that young children have such high melatonin levels explains why they show very mild symptoms after COVID-19 infections.


Melatonin is a potent inhibitor of NLRP3 inflammasomes.

Generally referred to as the “hormone of darkness”,  the ability of melatonin to regulate both pro- as well as anti-inflammatory cytokines in different pathophysiological conditions has only been extensively studied in the past several years.

Controlling cytokine storms is one of the major challenges in the treatment of sepsis [82].  The NLRP3 inflammasome has an interesting nickname of “Pandora’s Box for Sepsis” [83]. Yet nature provides all the solutions to difficult health challenges.

NLRP3 inflammasomes is a direct target of melatonin.  Animal models of sepsis showed melatonin’s ability to maintain mitochondrial homeostasis, reduce reactive oxygen species and lower production of proinflammatory cytokines. Melatonin was shown to inhibit NLRP3 inflammasomes in mice with myocardial septic conditions, transforming severe myocardial inflammation into milder symptoms, preventing cardiac failure, and significantly enhanced survival rates of septic mice [77, 78].

An excellent study by Volt et al (2016) showed that chronic low doses of melatonin in aged mice could prevent increase in inflammation, ROS and mitochondria impairments reflective of inflammaging [79, 80]. Volt et al. also showed that acute administration of melatonin could counteract severe inflammatory responses [81].

It is therefore not surprising to find that melatonin is able to prevent ARDS/ALI through suppression of NLRP3 inflammasomes.

In rodent acute lung injury (ALI) models, melatonin was found to markedly reduce pulmonary injury, lower infiltration of macrophages and neutrophils into lungs. Melatonin protected mice from acute lung injuries by inhibiting the activation of NLRP3 inflammasomes through the suppression of extracellular release of histones and blocking histone-induced NLRP3 inflammasome activation [84].

In rodent models of acute respiratory distress syndrome (ARDS), combined treatment of melatonin and mitochondria significantly attenuated progression of ARDS [85].

Melatonin Protects Lung Injury from Mechanical Ventilation Interventions

COVID-19 patients with ARDS/ALI often require intubation with mechanical ventilation.  Even though the intervention may help patients, in many instances, patients develop ventilator-induced lung injury as a result of mechanical ventilation [86].  In particular, high ventilation pressures and high tidal volumes required to maintain proper oxygenation and CO2 elimination can cause lung damage and impair gas exchange.

A study released on March 6, 2020 by Geng-Chin Wu et al. demonstrated that by increasing melatonin with the use of a melatonin receptor agonist, damaging effects of ventilator-induced lung injury could be prevented in rodent models [87].

The full therapeutic potential of melatonin in its ability to modulate the immune system, especially the critical function of suppressing cytokine storms to prevent progression of acute respiratory distress syndrome (ARDS) and respiratory failure in infected patients was clearly demonstrated in a study by Huan]g et al. (2019).  Huang et al. infected rodents with the highly lethal and infectious H1N1 influenza A virus. Co-treatment of these infected rodents with melatonin and an antiviral drug significantly increased their survival rates compared to mice treated only with antivirals alone [88]!

It is no wonder that none of the pregnant mothers infected by COVID-19  admitted to Zhongnan Hospital of Wuhan University, Wuhan, China,  developed severe pneumonia or died; nor were their babies infected by COVID-19 [89]. Why?

Melatonin secretion in the third trimester of pregnancy is more than doubled compared to the first trimester.

COVID-19, Pneumonia & Inflammasomes – The Melatonin Connection

#FOWC, Weekend Writing Prompt

Wake Up — Pray to LOVE TRUTH!

Wanting to write something about “Truth”, I BROWSED the internet looking for a quote.  I like this one —> “Facts are stubborn things” by Ronald Reagan

If you care you too can BROWSE the internet to find profound quotes about the subject of TRUTH.

Another Truth; is Trump and his administration perfect?    NO!