Year: 2020

Broccoli sprouts oppose effects of advanced glycation end products (AGEs)

gettingwell4 4-5 stars Advanced knowledge, Epigenetics, Hypothalamus, Immune system, Limbic system, Stress , , ,

This 2020 Australian/UK review subject was AGEs:

“AGEs are formed during cooking and food processing or produced endogenously as a consequence of metabolism. Deleterious effects of AGEs are underpinned by their ability to trigger mechanisms well known to elicit metabolic dysfunction, including activation of inflammatory pathways, oxidative stress and impaired mitochondrial oxidative metabolism. They have been widely implicated in complications of diabetes affecting cardiovascular health, the nervous system, eyes and kidneys.

Reactive carbonyl groups are constantly being produced via normal metabolism and when production overrides detoxification, AGEs accumulate. AGE formation may take several days or weeks to complete in the body.

Factors affecting AGE content of food depends on composition of protein, fat, and sugar and types of processing and cooking methods employed, predominantly on temperature and duration of preparation. Circulating free-AGEs concentrations are a good marker for dietary AGE intake while plasma protein-bound AGEs better represent endogenously produced AGEs.

Receptor for Advanced glycation end products (RAGE) signals via transcription factor NF-kB increasing gene expression of inflammatory mediators and production of ROS (reactive oxygen species).”

https://onlinelibrary.wiley.com/doi/abs/10.1002/mnfr.201900934 “The Role of Dietary Advanced Glycation End Products (AGEs) in Metabolic Dysfunction” (not freely available)

Let’s use the Australian 2019 Sulforaphane: Its “Coming of Age” as a Clinically Relevant Nutraceutical in the Prevention and Treatment of Chronic Disease as a reference for how sulforaphane may counter effects of AGEs:

1. “Activation of inflammatory pathways”

“Antioxidants in general and glutathione in particular can be depleted rapidly under conditions of oxidative stress, and this can signal inflammatory pathways associated with NF-κB. SFN [sulforaphane] has been shown to inhibit NF-κB in endothelial cells.

Two key inflammatory cytokines were measured at four time points in forty healthy overweight people [our model clinical trial, Effects of long-term consumption of broccoli sprouts on inflammatory markers in overweight subjects]. Levels of both interleukin-6 (Il-6) and C-reactive protein (CRP) declined over the 70 days during which sprouts were ingested. These biomarkers were measured again at day 90, wherein it was found that Il-6 continued to decline, whereas CRP climbed again. When the final measurement was taken at day 160, CRP, although climbing, had not returned to its baseline value. Il-6 remained significantly below the baseline level at day 160.”

OMCL2019-2716870.010

2. “When production overrides detoxification”

“SFN significantly activates Nrf2 and as such has the potential to modulate the expression of genes associated with redox balance, inflammation, detoxification, and antimicrobial capacity, all key components of the upstream cellular defence processes.

Toxins presented to Phase 1 enzymes produce intermediate compounds which are sometimes more toxic to cells than the initial toxin. It is therefore important that Phase 2 is sufficiently active that intermediate products cannot accumulate in the cellular environment.

As a monofunctional inducer, SFN has been described as an ideal detoxifier, as its effect on Phase 1 is minimal compared with its significant activity on Phase 2.”

3. “Oxidative stress”

“As a mediator for amplification of the mammalian defence system against various stressors, Nrf2 sits at the interface between our prior understanding of oxidative stress and endogenous mechanisms cells use to deal with it. Diseases known to be underpinned by oxidative stress are proving to be more responsive to amplification of cellular defences via Nrf2 activation than by administration of direct-acting antioxidant supplements.

SFN, with absolute bioavailability of around 80%, is capable of increasing several endogenous antioxidant compounds via transcription factor Nrf2.”

4. “Complications of diabetes affecting cardiovascular health, the nervous system, eyes and kidneys”

“Nrf2 is ubiquitously expressed with highest concentrations (in descending order) in the kidney, muscle, lung, heart, liver, and brain. Nrf2 was shown to prevent endothelial cells from exhibiting a proinflammatory state. Nrf2 is required for protection against glucose-induced oxidative stress and cardiomyopathy in the heart.

Well in excess of 500 genes have been identified as being activated by SFN via the Nrf2/ARE [Antioxidant Response Element] pathway, and it is likely that this underestimates the number as others are being discovered. Of available SFN clinical trials associated with genes induced via Nrf2 activation, many demonstrate a linear dose-response. More recently, it has become apparent that SFN can behave hormetically with different effects responsive to different doses.

It [sulforaphane] is not only a potent Nrf2 inducer but also highly bioavailable so that modest practical doses can produce significant clinical responses. Other Nrf2 activators [shown in the above image] not only lack potency but also lack the bioavailability to be considered as significant intracellular Nrf2 activators.”

As mentioned in Changing an inflammatory phenotype with broccoli sprouts, per the above bolded part of section 3, I stopped taking N-acetyl-cysteine, the precursor to our endogenous antioxidant glutathione. I stopped taking curcumin last year due to no noticeable effects, probably because of its poor bioavailability. I may soon stop taking more vitamin E than the RDA, and β-carotene.

I changed my diet last summer to reduce AGEs, with mild effects. I expect stronger effects from also daily eating 60 grams of 3-day-old broccoli sprouts that yield 27 mg of sulforaphane after microwaving.

Reanalysis of findings from a senolytics clinical trial

gettingwell4 2-3 stars Required further work, Epigenetics, Stress

To follow up Preliminary findings from a senolytics clinical trial:

“The central hypothesis tested in our article is that a brief course of the senolytic drug combination, Dasatinib plus Quercetin (D+Q), can reduce senescent cell abundance in humans, specifically focusing on targeting adipose tissue in subjects with diabetes and kidney dysfunction, a condition in which adipose tissue senescent cell burden is known to be increased.

Although we reported a statistically significant decrease in skin senescent cells in the 9 subjects whose skin data were reported in the original article, that conclusion did not hold up upon reanalysis.

The overall conclusion of our article that D+Q can target senescent cells in humans holds upon reanalysis of the data, at least in adipose tissue and as reflected by a composite of blood SASP [senescence-associated secretory phenotype] factors, but we have not shown this in skin here.”

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6994619/ “Corrigendum to ‘Senolytics decrease senescent cells in humans: Preliminary report from a clinical trial of Dasatinib plus Quercetin in individuals with diabetic kidney disease’”

Reviewing clinical trials of broccoli sprouts and their compounds

gettingwell4 4-5 stars Advanced knowledge, Epigenetics , ,

This 2020 Spanish review analyzed recent clinical trials that used broccoli sprouts and their compounds. Stringent criteria for study selection resulted in few trials being considered:

  • “We reduced the timeframe to the last years, from 2012 to the present.
  • We focused our work on the data of studies carried out with human adults with different pathologies.
  • Articles [that] did not provide us with specific information about consumption of cruciferous foods or ingredients derived from Brassicaceae products, documents based on healthy volunteers, and patients with pathologies unrelated to our objective of study were also not included in the analysis.”

None of the 15 analyzed clinical trials were unqualified successes. Some of the problems noted were summarized in this critique of the largest study:

“The authors presented the results that there was a risk for T2DM [type 2 diabetes mellitus] with the intake of cruciferous foods and glucosinolates. However, this study presented big limitations because:

  • It did not review or consider the cooking procedures,
  • It did not quantify the amount of vegetables consumed on a daily or weekly basis, and
  • It did not quantify the glucosinolate contents in the different vegetables consumed. Besides,
  • The population sample was homogenous, because all of the participants were health-area workers, and the results are not extrapolatable to the general population. Finally, it should be highlighted that
  • Other nutrients and confounding factors were not considered in the study, and they could affect the development of these pathologies.”

“Figure 1 – General scheme of the glucosinolates (GSLs) and common hydrolysis products. ESP: Epithiospecifer proteins.”

https://www.mdpi.com/1420-3049/25/7/1591/htm “The Role of Brassica Bioactives on Human Health: Are We Studying It the Right Way?”

The reviewers’ answer to the title’s question “Are We Studying It the Right Way?” was NO. The 15 analyzed trials lacked one or more clearly defined measurements related to their target diseases:

“It is crucial that the outcome measure is of biological relevance; biomarkers or risk factors measured must be associated to the latter development of a disease. The degree of progression of the disease greatly influences the response observed.”

So: Why not consider Aging as a disease for clinical trials with broccoli sprouts and their compounds?

  1. “Lack of cure goes hand in hand with inability to accept that this [aging] is disease. It used to be that, please do not diagnose that there’s bacterial meningitis, because there is no cure. Whatever else you can come up with, do it first. Now, diagnose it as fast as possible, so we can put patients on antibiotics immediately. The same will happen to aging.”
  2. Several of the clinical trials’ methodological and statistical problems could be resolved with recognizing aging as a disease. “Healthy” old people who have no other diseases may be scarce, but there are large populations to sample control groups from among healthy and unhealthy young people, and unhealthy old people.
  3. The reviewers already have experience in using “healthy” 46 ± 6 year-old people in a clinical trial of broccoli sprouts and their compounds.
  4. A wide range of epigenetic clocks are available to test the efficacy of broccoli sprouts and their compounds with respect to human aging phenotypes.

As far as I can tell, epigenetic clocks haven’t been used in the subject area thus far! The review’s reference [7] from 2015 didn’t mention them.

Reference [55] was the October 2019 Sulforaphane: Its “Coming of Age” as a Clinically Relevant Nutraceutical in the Prevention and Treatment of Chronic Disease, which I’ve been using as the most current and comprehensive of the subject todate. Its references of broccoli sprouts and their compounds with respect to aging included:

“Nrf2 [nuclear factor erythroid 2-related factor 2] transcriptional activity declines with age, leading to age-related GSH [reduced glutathione] loss among other losses associated with Nrf2-activated genes. This effect has implications, too, for decline in vascular function with age. Some of the age-related decline in function can be restored with Nrf2 activation by SFN [sulforaphane].

A potent Nrf2 activator is capable of inducing hundreds of genes simultaneously. Of the phytochemicals with Nrf2 inducer capacity, Brassica-derived SFN is the most potent naturally occurring biomolecule known at this time.”

However, it had only one reference of DNA methylation, the 2015 The Role of Sulforaphane in Epigenetic Mechanisms, Including Interdependence between Histone Modification and DNA Methylation. Even that was a review rather than a study, and it had no mention of epigenetic clocks.

Maybe broccoli sprouts and their compounds’ effects on human aging is an area that just hasn’t drawn attention and funding?

Understanding a clinical trial’s broccoli sprout amount

gettingwell4 4-5 stars Advanced knowledge, Epigenetics, Immune system

To follow up Week 2 of Changing an inflammatory phenotype with broccoli sprouts, I contacted the model clinical trial’s corresponding coauthor to clarify a citation. Our correspondence was as follows:

Hello Dr.! Could you further describe Citation 11 of your 2018 clinical study Effects of long-term consumption of broccoli sprouts on inflammatory markers in overweight subjects or say where it may be found? “Services, F. a. D. A. F. U. D. o. H. a. H., 2001.” was cited for 30 grams of fresh broccoli sprouts being a half-serving.

Ref. 11. Sulforaphane: translational research from laboratory bench to clinic CA Houghton, RG Fassett, JS Coombes – Nutrition reviews, 2013.

If you check in the table 2, about clinical trials, different studies using broccoli sprouts were establishing daily dosage around 60 g/day (e.g. 56 – 68, etc.). In a similar way, in our previous studies for bioavailability with broccoli sprouts (Domínguez-Perles et al.) we also considered 30 g and 60 g was 1/2 and 1 portion per day, respectively, of broccoli sprouts.

When we carried out tests with consumers, previous to the bioavailability studies (Domínguez-Perles et al., Baenas et al.), higher amounts per day, were not easy to consume and to get eaten by participants. The people or general public in Spain is not very familiar (yet) with these fresh sprouts as may be in USA, or UK, for example. That why we took a “realistic” amount of broccoli sprouts per day, to be incorporated in daily diet.

Of course, with higher amounts we could even probably see better results, but that would not be realistic for a food to be incorporated in daily diet – the purpose of the “prevention” perspective of this work.

I hope that I help you to understand why we selected that amount or the doubts about it. Thank you very much for your interest in the work.

Thank you very much Dr.! It’s encouraging that healthy people were the subjects of your 2018 clinical trial.

May I obtain your permission to use your excellent explanation as a follow up to my blog post?

I and several other people are using your study as the model to improve our health during this lockdown. There have been a lot of errors on my part, but our methods are improving.

Yes, you can use the information, of course. The participants were “healthy” overweight subjects (without medication or treatments of any disease, just adults with overweight). Please, keep safe and have a nice week.

Attached to the last email was his latest coauthored review The Role of Brassica Bioactives on Human Health: Are We Studying It the Right Way? published March 30, 2020, curated in Reviewing clinical trials of broccoli sprouts and their compounds.

“Figure 1 – General scheme of the glucosinolates (GSLs) and common hydrolysis products. ESP: Epithiospecifer proteins.”

Forcing people to learn helplessness

gettingwell4 4-5 stars Advanced knowledge, Beliefs, Brainstem, Cerebrum, Cortisol, Epigenetics, Hippocampus, Hypothalamus, Limbic system, Locus coeruleus, Lower brain, Memory, Neurochemicals, Stress , , , ,

Learned helplessness is a proven animal model. Its reliably-created phenotype is often the result of applying chronic unpredictable stress.

As we’re finding out worldwide, forcing humans to learn helplessness works in much the same way, with governments imposing what amounts to martial law. Never mind that related phenotypes and symptoms include:

  • “Social defeat
  • Social avoidance behavior
  • Irritable bowel syndrome
  • Depression
  • Anxiety
  • Anhedonia
  • Increased hypothalamic-pituitary-adrenal (HPA)-axis sensitivity
  • Visceral hypersensitivity” [1]

Helplessness is both a learned behavior and a cumulative set of experiences. Animal models demonstrate that these phenotypes usually continue on throughout the subjects’ entire lifespans.

Will the problems caused in humans by humans be treated by removing the causes? Or will the responses be approaches such as drugs to treat the symptoms?

A major difference between our current situation and the situation depicted below is that during communism, most people didn’t really trust or believe what the authorities, newspapers, television, and radio said:

Image from Prague’s Memorial to the Victims of Communism

[1] 2014 GABAB(1) receptor subunit isoforms differentially regulate stress resilience curated in If research provides evidence for the causes of stress-related disorders, why only focus on treating the symptoms?

Week 2 of Changing an inflammatory phenotype with broccoli sprouts

gettingwell4 4-5 stars Advanced knowledge, Epigenetics, Immune system, Memory, Stress

To follow up Changing an inflammatory phenotype with broccoli sprouts:

1. My traveling companion used a kitchen scale to measure the weight of broccoli sprouts at Day 3. She started them from one tablespoon of broccoli seeds, and they weighed 60 grams!

The model clinical trial [1] used 30 grams to produce great results:

“The intervention consisted of a 10-week period which included daily consumption of a portion (30 g) of raw, fresh broccoli sprouts. This amount is consistent with a half-serving.”

I asked the study’s corresponding coauthor for clarification of “a half-serving.” Our conversation is at Understanding a clinical trial’s broccoli sprout amount.

Eating a 60 gram “full serving” of 3-day-old broccoli sprouts yielding 27 mg of sulforaphane after microwaving [2] fits [3]‘s guidelines:

“The daily SFN [sulforaphane] dose found to achieve beneficial outcomes in most of the available clinical trials is around 20-40 mg.”

2. My current microwaving time for 60 grams of 3-day-old broccoli sprouts in 100 ml of water with a 1000 W microwave on full power is 35 seconds. Their temperature gets up to 57°C. YMMV.

I immediately cool down the microwaved broccoli sprouts in a colander. See Enhancing sulforaphane content for changes. Go up to the 60°C cliff but don’t fall into the 70°C 65°C canyon:

cliff

The desired range [2]:

“In the temperature range of 50–60°C, a positive correlation was observed between GLR [glucoraphanin] or SFR [sulforaphane] contents and temperature. However, these two physiochemical contents were negatively correlated with temperature when it increased to 70°C.”

3. I had several days of failed crops during Week 2. I switched over to Russian-doll glass bowls with success:

I’d guess that failures were related to excess moisture, which broccoli sprouts hate, hate, hate! Look closely at the top left Day 0 tray below:

Notice concentric raised ribs that are about 1/16″ high. Their effects may have either kept broccoli seeds too wet over a 3-day period, or promoted bacterial growth (although I ran them through a dishwasher after Day 3).

4. I started to put items on the edge of my microwave’s carousel because they don’t heat evenly when placed in the center. I thought uneven heating was a problem that was solved a long time ago, but not for the microwave I bought (Sharp model SMC1131C, which was the least expensive at Best Buy on the day I needed a carousel microwave oven.)

[1] 2018 Effects of long-term consumption of broccoli sprouts on inflammatory markers in overweight subjects curated in How much sulforaphane is suitable for healthy people?

[2] 2020 Microwave cooking increases sulforaphane level in broccoli curated in Microwave broccoli to increase sulforaphane levels and Growing a broccoli sprouts Victory Garden

[3] 2019 Sulforaphane: Its “Coming of Age” as a Clinically Relevant Nutraceutical in the Prevention and Treatment of Chronic Disease curated in How much sulforaphane is suitable for healthy people?

Flatten the Panic Curve April 13-17, 2020

gettingwell4 4-5 stars Advanced knowledge, Amygdala, Beliefs, Brainstem, Immune system, Limbic system, Lower brain, Memory, Primal Therapy, Stress , , ,

To better understand our internal origins of panic, here’s Dr. Arthur Janov’s interpretation of a 2013 Iowa study Fear and panic in humans with bilateral amygdala damage (not freely available):

“Justin Feinstein did a study with those who had a damaged amygdala, the hub of the emotional system. They did not have normal fear responses. But if oxygen supplies were lowered and carbon dioxide supplies were increased, mimicking suffocation (increasing acidity of the blood) there were panic attacks.

Where in the world did those attacks come from? Certainly not from the usual emotional structures.

They believe it includes the brainstem! Because the lowering of oxygen supplies and adding carbon dioxide provoked the lower structures to sense the danger and reacted appropriately.

Very much like what happens to a fetus when the mother smokes during pregnancy and produces those same effects.”

Since those of us who chronically experience panic aren’t going into therapy over this weekend, what else can we do?

1. Stop looking at the John Hopkins Panic map.

2. Search out realistic news such as: “Change in [New York state] ICU admissions is actually a negative number for the first time since we started this intense journey.”

3. Stop clicking sensational headline links.

4. Question your information, and investigate multiple views. Trust has been lost:

  • Dr. Scott Jensen, a Minnesota physician for 35 years and state senator, on the inappropriate CDC / WHO guidelines for reporting COVID-19 deaths:

    “It’s ridiculous. The determination of cause of death is a big deal. The idea that we’re going to allow people to massage and game the numbers is a real issue because we’re going to undermine trust.

    I would never put down influenza as the cause of death. Yet that’s what we’re being asked to do here.”

  • The same day, Dr. Fauci arrogantly grouped physicians in with conspiracy theorists if they didn’t conform to these bordering-on-fraudulent CDC / WHO guidelines:

    “Every time we have a crisis of any sort, there’s always this popping-up of conspiracy theories. I think the deaths that we’re seeing are coronavirus deaths, and the other deaths are not being counted as coronavirus deaths.”

    Telling people to trust him – a bureaucrat who hasn’t been in active practice for over three decades – because he had far superior medical judgment than did practicing doctors who for years continuously see patients?

  • Consider the evidence.
  • Don’t accept lies you feel uneasy about. Trust your internal BS detector.

Which herd will you choose to belong to?

https://nypost.com/video/bison-stampede-terrorizes-family-trapped-in-car/

or

US doctors incentivized to diagnose everything as COVID-19

gettingwell4 Just me

To follow up Lowering US pneumonia death counts to increase COVID-19 death counts:

“Dr. Scott Jensen, a Minnesota physician and Republican state senator, told a local station he received a 7-page document coaching him to fill out death certificates with a COVID-19 diagnosis without a lab test to confirm the patient actually had the virus.

‘It’s ridiculous. The determination of cause of death is a big deal. The idea that we’re going to allow people to massage and game the numbers is a real issue because we’re going to undermine trust.

I would never put down influenza as the cause of death. Yet that’s what we’re being asked to do here.’

Dr. Jensen also disclosed that hospitals are paid more if they list patients with a COVID-19 diagnosis.

Senator Dr. Scott Jensen: ‘Right now Medicare is determining that if you have a COVID-19 admission to the hospital you get $13,000. If that COVID-19 patient goes on a ventilator you get $39,000, three times as much. Nobody can tell me after 35 years in the world of medicine that sometimes those kinds of things impact on what we do.'”

https://thespectator.info/2020/04/09/hospitals-get-paid-more-to-list-patients-as-covid-19-and-three-times-as-much-if-the-patient-goes-on-ventilator-video/

And the public has been told many times with prosecuted examples that Medicaid / Medicare fraud is a crime. On the plus side, COVID-19 must be the ultimate cure for deadly medical conditions, if no one dies of anything else anymore.

Cui bono questions as John Hopkins will be herding the US public toward the cliff April 6-10, 2020 draws to a close for the week:

  1. This change in medical reporting has had / will have what effects on the headlines we’ve seen and will see?
  2. Who has benefited / will benefit from (medical, economic, social, and political) reports on and actions taken with the change in medical reporting to: “COVID-19 being the underlying cause more often than not.”
  3. Who has suffered and will suffer from these reports and actions?

Do early experiences of hunger affect our behavior, thoughts, and feelings today?

gettingwell4 5+ stars Premium, Epigenetics, Primal Therapy , , , , , , ,

Reposted from five years ago.

A 2015 worldwide human study Hunger promotes acquisition of nonfood objects found that people’s current degree of hungriness affected their propensity to acquire nonfood items.

The researchers admitted that they didn’t demonstrate cause and effect with the five experiments they performed, although the findings had merit. News articles poked good-natured fun at the findings with headlines such as “Why Hungry People Want More Binder Clips.”

The research caught my eye with these statements:

“Hunger’s influence extends beyond food consumption to the acquisition of nonfood items that cannot satisfy the underlying need.

We conclude that a basic biologically based motivation can affect substantively unrelated behaviors that cannot satisfy the motivation.“

The concept of the quotes relates to a principle of Dr. Arthur Janov’s Primal Therapy – symbolic satisfaction of needs. Two fundamentals of Primal Therapy:

  1. The physiological impacts of our early unmet needs drive our behavior, thoughts, and feelings.
  2. The painful impacts of our unfulfilled needs impel us to be constantly vigilant for some way to fulfill them.

Corollary principles of Primal Therapy:

  • Our present efforts to fulfill our early unmet needs will seldom be satisfying. It’s too late.
  • We acquire substitutes now for what we really needed back then.
  • Acquiring these symbols of our early unmet needs may – at best – temporarily satisfy derivative needs.

But the symbolic satisfaction of derived needs – the symptoms – never resolves the impacts of early unfulfilled needs – the motivating causes:

  • We repeat the acquisition behavior, and get caught in a circle of acting out our feelings and impulses driven by these conditions.
  • The unconscious act-outs become sources of misery both to us and to the people around us.

As this study’s findings showed, there’s every reason for us to want researchers to provide a factual blueprint of causes for our hunger sensation effects, such as “unrelated behaviors that cannot satisfy the motivation.“

Hunger research objectives could include answering:

  • What enduring physiological changes occurred as a result of past hunger?
  • How do these changes affect the subjects’ present behaviors, thoughts, and feelings?

Hunger research causal evidence for the effect of why people acquire “items that cannot satisfy the underlying need” may include studying where to start the timelines for the impacts of hunger. The impacts potentially go back at least to infancy when we were completely dependent on our caregivers.

Infants can’t get up to go to the refrigerator to satisfy their hunger. All a hungry infant can do is call attention to their need, and feel pain from the deprivation of their need.

Is infancy far back enough, though, to understand the beginnings of potential impacts of hunger?

Lowering US pneumonia death counts to increase COVID-19 death counts

gettingwell4 4-5 stars Advanced knowledge, Immune system

To follow up CDC directs the US to attribute deaths from other causes to COVID-19, my sending its information to Tucker Carlson yesterday morning may have contributed to the information being broadcast nationally yesterday evening. The transcript at Tucker Carlson: Possible That Doctors Are Classifying Conventional Pneumonia Deaths As COVID Deaths, Increasing The Count included:

“For many years, the CDC has tracked the total number of Americans who die each week from pneumonia. For the last few weeks, that number has come in far lower than at the same moment in previous years.

How could that be? It seems entirely possible that doctors are classifying conventional pneumonia deaths as COVID-19 deaths. This would mean the epidemic is being credited for thousands of deaths that would have occurred if the virus never arrived here.”

Not sure where to find the information supporting “For the last few weeks, that number has come in far lower than at the same moment in previous years.”

Cui bono questions midway through John Hopkins will be herding the US public toward the cliff April 6-10, 2020:

  1. This change in medical reporting has had / will have what effects on the headlines we’ve seen and will see?
  2. Who has benefited / will benefit from (medical, economic, social, and political) reports on and actions taken with the change in medical reporting to: “COVID-19 being the underlying cause more often than not.”
  3. Who has suffered and will suffer from these reports and actions?

Sea Level

gettingwell4 Just me

Walked on the beach

sea level

remembering the last time I lived here 40+ years ago, experiencing Sea Level in concert back then, still listening to their instrumentals now, along with these:

It’s a lot like being little
And wanting a brand new toy
It’s a lot like being little
And wanting a baby boy
To call brother
And it hurts when you want it so bad

It’s a lot like being a young boy
Cannot make the team
It’s a lot like being a young girl
Cannot help but dream
Of a best friend’s brother
And it hurts when you want it so bad

When it’s love that you have lost
Baby that’s the worst hurt
That you’ll ever hurt
Waiting for a new love to come along
Maybe it’s just as bad

It’s a lot like being a man
With no one to call your own
It’s a lot like being a woman
Wanting a house and a home
To be a mother
And it hurts when you want it so bad

In the dreary world
That we’re living in
It’s fashionable to let nothing faze you

Yeah, you’re above it all
You’re fooling, fooling yourself
You’re living in a dream

So you close the door
You let nothing in
And yet you’re moving and not caring where you’ve been

Yeah, you’re above it all
And you remind me of myself
You’re living in a dream
Living in a dream

Young sports fans can end the COVID-19 herding of the population

gettingwell4 Just me

Let’s put together a few items:

  • Football / soccer is the most popular sport in the world.
  • People are passionate about their sports.
  • We are connected like never before.
  • Very few young people are at risk for COVID-19 complications.
  • Suppressing people’s physical movement causes resentment.
  • From the 1776 US Declaration of Independence: “Governments are instituted among men, deriving their just powers from the consent of the governed.”

Image from the US Library of Congress

Who will be first?

 

CDC directs the US to attribute deaths from other causes to COVID-19

gettingwell4 4-5 stars Advanced knowledge, Immune system

To follow up the If people don’t stand up for their rights, their rights will be forgotten point, which YouTube has taken down:

“We don’t die of the virus. We die of pneumonia.”

The CDC at https://www.cdc.gov/nchs/nvss/covid-19.htm has been issuing guidance to merge deaths from other causes into a WHO code U07.1 that assigns COVID-19 as the primary cause of death. For example, click the March 24, 2020 “Notification of new ICD code introduced for COVID-19” guidance to see:

“The underlying cause depends upon what and where conditions are reported on the death certificate. However, the rules for coding and selection of the underlying cause of death are expected to result in COVID-19 being the underlying cause more often than not.“

Click the April 2, 2020 “New Releases: Final Guidance and Provisional Death Counts” guidance to see:

“Provisional counts for COVID-19 deaths are based on a current flow of mortality data in the National Vital Statistics System (NVSS), and will include:

  • A weekly provisional count of deaths in the United States due to COVID-19
  • A provisional count of deaths from all causes
  • Percent of previous year’s deaths (the number of deaths received compared to the number of deaths expected based on data from previous years)
  • Pneumonia deaths (excluding pneumonia deaths involving influenza)

Pneumonia deaths are included in the provisional counts because deaths due to COVID-19 may be misclassified as pneumonia deaths in the absence of positive test results, and pneumonia may appear on death certificates as a comorbid condition. Thus, increases in pneumonia deaths may be an indicator of excess COVID-19-related mortality.”

  1. How probable is it now that US deaths from pneumonia will NOT be attributed to COVID-19?
  2. This change in medical reporting has had / will have what effects on the headlines we’ve seen and will see?
  3. Who has benefited / will benefit from (medical, economic, social, and political) reports on and actions taken with the change in medical reporting to: “COVID-19 being the underlying cause more often than not.”
  4. Who has suffered and will suffer from these reports and actions?

If people don’t stand up for their rights, their rights will be forgotten

gettingwell4 4-5 stars Advanced knowledge, Beliefs, Epigenetics, Immune system, Memory, Stress

YouTube took down this interview and a follow-on interview It was known to everybody that the lockdown would cause a catastrophe.

Here’s an interview last week with a German epidemiologist, Professor Wittkowski, who isn’t on a government payroll:

“First of all the elderly and fragile should be separated from the population where the virus is circulating. Everyone else, especially the children, should keep going to school, because they will be the primary impetus for herd immunity.

Flattening the curve prolongs the time a virus stays in the population. People staying indoors keeps the virus healthy.

Like every other respiratory disease, without government intervention, the pandemic would already be over like it’s over in China and South Korea. Except, both in China and South Korea, social distancing started very close to the peak. By keeping the virus from running its course, they are now having a second wave of cases. It will keep on if we don’t let it complete.

There’s nothing to be scared about. This is a flu epidemic like others, maybe more severe. What’s changed is the internet. People get their information in a few seconds, rather than a week.

Tracking a respiratory disease is impossible. Even in times of social distancing. Nature has ways to make sure we survive.

The standard for AIDS reporting, i.e., the date of infection separated from the date of reporting, is not being followed.

If we had herd immunity now, we wouldn’t have a second wave in the fall. Herd immunity typically lasts for a couple of years. If we prevent herd immunity, it is certain that a second wave will occur.

Testing doesn’t stop anything. Antibody testing will give us estimates of herd immunity, which would be useful.

We don’t die of the virus. We die of pneumonia.

The downside of starting containment is that we should not believe that we are more intelligent than mother nature when we were evolving. Mother nature was pretty good at making sure we were a good match for the diseases that we happened to see virtually every year.

I think people, especially in the United States, are more docile than they should be. People should talk with their politicians, question them, ask them to explain. Because if people don’t stand up to their rights, their rights will be forgotten.”

In the name of COVID-19: Digital currencies with government surveillance

gettingwell4 Just me

To follow up Waiting to be officially denied, the UK Financial Times published Rushing out untested digital finance fixes for Covid-19 is folly (requires a subscription) on March 31, 2020:

“Due to the protracted nature of the 2008 global financial crisis, the world’s most powerful money-printing institutions were already at the limits of unconventional policy when this crisis struck.

Democratic Congresswoman Rashida Tlaib proposed a permanent Treasury-managed digital public currency wallet system. An early version of the alternative $2tn Coronavirus Aid Relief and Economic Security (CARES) act, which passed last week, considered rolling out Fed-managed digital dollar wallets to all US residents, citizens and businesses to facilitate cash distributions.

Government surveillance is a real concern. Apple’s digital dominance already makes it hard for consumers to decline privacy compromises terms in exchange for access to its products.

Imagine how much harder that choice would be if the consumer had to sign up for a data-tracking CBDC [central bank digital currency], or waive her right to a government-funded handout or vaccine?”

We see news stories about Michigan’s congressional representative, other people rushing agendas in the US, Thailand, South Korea, Singapore, China, Taiwan, EU, IMF, UK, or any number of people desperate to create panic to grab even more power.