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

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:

This change in medical reporting has had / will have what effects on the headlines we’ve seen and will see?

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.”

Who has suffered and will suffer from these reports and actions?

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

To follow up the If people don’t stand up for their rights, their rights will be forgotten point:

“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.”


How probable is it now that US deaths from pneumonia will NOT be attributed to COVID-19?

This change in medical reporting has had / will have what effects on the headlines we’ve seen and will see?

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.”

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

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.”

Changing an inflammatory phenotype with broccoli sprouts

This follow up to Growing a broccoli sprouts Victory Garden is what’s gone on during Week 1 of starting to grow broccoli sprouts for a “30 grams of fresh broccoli sprouts incorporated daily into the diet” [1] program.

Day 0 – I’ve tried many things to cure chronic inflammation over the years, basing most of my actions on what’s proven to work for other people. These treatments have helped but haven’t completely worked for me. I’ve continued them with the hypothesis that they may have positive synergistic interactions with daily eating 30 grams of broccoli sprouts / 17 mg of sulforaphane.

Day 0 treatments included two dozen supplements I’ve taken since turning 50, a diet low in advanced glycation end products started last year [2], and naproxen (a nonsteroidal anti-inflammatory drug). The chronically inflamed spots are the left thumb base (arthritis), tendons outside the left ankle (peroneal tendinosis), and left knee tendonitis, all probably consequences of playing golf for 40+ years.

Day 1 – The vertical farming equipment is a Deluxe Kitchen Crop 4-Tray Seed Sprouter Model VKP1200 made by VICTORIO Kitchen Products. I soak one tablespoon of organic broccoli seeds for 12 hours. Take them out of the stackable trays for a twice-daily rinsing, which is counter to directions of pouring water into the tower top. Microwave the Day 3 broccoli sprouts daily per [3]. Run its tray through the dishwasher (but no heat cycle). Put the tray back in rotation for Day 0.

Day 2 – Threw away one of my crutches, naproxen, as taking it had become more of a habit than a necessity. I’d been taking 220 mg twice daily for years until two weeks ago, when I switched to once daily.

Sulforaphane increases “several endogenous antioxidant compounds via the transcription factor Nrf2 [nuclear factor erythroid 2-related factor 2, discovered in 1994]. Of the phytochemicals with Nrf2 inducer capacity, Brassica-derived SFN [sulforaphane] is the most potent naturally occurring biomolecule known at this time.

Another transcription factor, NF-κB, which is associated with inflammatory pathways is downregulated by SFN. This dual action of SFN is especially intriguing in that Nrf2 and NF-κB interact via their own ‘cross talk’.” [4]

Day 3 – Stopped taking 2 mg of sulforaphane in the form of a broccoli sprout extract capsule, and 200 mg of a diindolyl methane (DIM) capsule daily. DIM was raised 195% from Day 0 to Day 70 after daily intake of broccoli sprouts in [1], noting: “The anti-inflammatory effects observed with broccoli sprouts intake are likely due to the combined effects of all the hydrolysis products of glucosinolates.” Don’t need either supplement when broccoli sprouts supply them.

The next supplement I might drop is N-Acetyl-Cysteine (NAC), the precursor to our endogenous antioxidant glutathione. I take a 600 mg capsule twice daily.

[4] goes on and on about sulforaphane / glutathione interactions. For example: “Several well-studied Nrf2-dependent target genes of possible relevance are those encoding synthesis of glutathione (GSH)” in Section 5.2. SFN as a Redox Modulator that included Figure 6 below, and in Section 6. SFN: Its Redox-Modulating Effects:

Day 4 – I’d seen studies of broccoli sprouts that ranged from 3-days old (the most frequent age) to 8-days old. Before [5], I hadn’t found analyses of broccoli sprout age differences in sulforaphane contents, and only a few studies of sulforaphane differences among broccoli sprout cultivated varieties.

Day 5 – I’ve eaten sprouts at 3 – 5 days old, and haven’t noticed a taste difference after microwaving per [3]. Here’s what they look like at Days 0, 1, 2, and 3:

Day 6 – Are you ready to change your phenotype?


References in order of citation:

[1] 2018 Effects of long-term consumption of broccoli sprouts on inflammatory markers in overweight subjects

[2] 2016 Dr. Vlassara’s AGE-Less Diet: How a Chemical in the Foods We Eat Promotes Disease, Obesity, and Aging and the Steps We Can Take to Stop It

[3] 2020 Microwave cooking increases sulforaphane level in broccoli curated in Microwave broccoli to increase sulforaphane levels

[4] 2019 Sulforaphane: Its “Coming of Age” as a Clinically Relevant Nutraceutical in the Prevention and Treatment of Chronic Disease

[5] 2020 3-day old broccoli sprouts have the optimal yields

3-day old broccoli sprouts have the optimal yields

This 2020 Chinese study compared the contents of 3, 5, and 7-day old broccoli sprouts:

“The objective of this study was:

  1. To optimize the extraction conditions of SF [sulforaphane] from seeds and sprouts at the same time to ensure the maximum SF yields from them;
  2. To compare the SF yields, total flavonoid (TF) contents, and total phenolic (TP) contents from broccoli seeds and sprouts (after 3, 5, and 7 days germination respectively) of six different cultivated varieties; and
  3. To evaluate and compare the the stability and bioaccessibility of SF, TF and TP from broccoli seeds and sprouts upon in vitro gastrointestinal digestion; total antioxidant activities of samples before and after digestion were also investigated in this section.

Most varieties obtained the maximum SF, TP and TF contents in sprouts on day 3. SF contents in sprouts were 46% – 97% of seeds, whereas TP and TF contents in sprouts were 1.12 – 3.58 times higher than seeds among varieties.

After in vitro digestion, broccoli sprouts from MNL variety kept considerable SF, TF, and TP contents, as well as antioxidant capacities, with all values higher than seeds.

SF from seeds and sprouts both showed high bioaccessibility values of 0.91 and 1.00, respectively. The high bioaccessibility of SF in vitro experiments provide an additional evidence for its efficient utilization, as many previous researches have reported a high bioavailability of SF in vivo.”


This study provided higher measures of sulforaphane in vitro bioaccessibility compared with previous studies of in vivo bioavailability.

It was good to read a definitive study that addressed both broccoli sprout age and cultivated variety for optimizing sulforaphane. The need was there. As the study authors put it:

“From the perspective of comparison methods, broccoli varieties, and germination processes, there is still lack of a systematic comparison of SF yields and other bioactive compounds contents between broccoli seeds and sprouts.”

https://www.sciencedirect.com/science/article/pii/S0308814620300637 “Sulforaphane and its antioxidative effects in broccoli seeds and sprouts of different cultivars” (not freely available)

Growing a broccoli sprouts Victory Garden

To follow up How much sulforaphane is suitable for healthy people? I’ve started growing broccoli sprouts, and a “30 grams of fresh broccoli sprouts incorporated daily into the diet” [1] program. I loosely follow [2]‘s sprouting guidelines. One preparation difference is microwaving per [3]‘s findings as follows:

I put broccoli sprouts into a small casserole dish, add enough water to cover them, then cook in my 1000W microwave on full power for 90 seconds. I immediately dump the broccoli sprouts into a colander and spray with cold water to stop heating at the desired temperature. A linear interpolation of Table S1 would place its temperature after 95 seconds on full 1000W power close to but not exceeding the 60°C goal:

(1000W / 950W) x (((108s -90s) / (60°C – 50°C)) * (95s – 90s))) + 50°C = 59.5°C

The first batch of broccoli sprouts was a mild, cabbage-tasting side dish to the home-style chicken soup on page 238 of [4].

The a priori hypotheses:

    1. 30 grams of fresh broccoli sprouts will not have “51 mg (117 μmol)” of glucoraphanin [1] because they “Used the elicitor methyl jasmonate (MeJA) by priming the seeds as well as by spraying daily. MeJA at concentrations of 156 μM act as stressor in the plant and enhances the biosynthesis of the phytochemicals glucosinolates. Compared to control plants without MeJA treatment, the content of compounds as the aliphatic glucosinolate glucoraphanin was enhanced up to 70%.” 117 μmol / 1.70 = 69 μmol is the expected glucoraphanin amount in 30 grams weight of fresh broccoli sprouts.
    2. One measurement [5] of how much sulforaphane is present in fresh broccoli sprouts before microwaving is 100 μmol / 111 g = .9 μmol / g. (.9 x 30 g) = 27 μmol is the expected sulforaphane amount in 30 grams of fresh broccoli sprouts.
    3. Microwaving the raw broccoli sprouts will convert the 69 μmol of glucoraphanin to 69 μmol of sulforaphane. Last week a [3] coauthor agreed to make the data available to facilitate calculations. While I’m waiting…The study said the Figure 3 HL60 sulforaphane amount was 2.45 μmol / g. Eyeball estimates of the below Figure 3 control (raw broccoli florets) are a sulforaphane amount of .2 μmol / g and a glucoraphanin amount of 2.2 μmol / g. I assume that the broccoli florets and sprouts glucoraphanin-to-sulforaphane conversions would be the same. A roughly 1-to-1 glucoraphanin-to-sulforaphane conversion of ~2.2 μmol / g + a sulforaphane amount of ~.2 μmol / g is ~2.4 μmol / g of sulforaphane. Note the Figure 3 detrimental effects that continuing cooking for a few more seconds to HL70 (70°C), had on its sulforaphane contents, dropping it below even the control (raw) content!
    4. The estimated sulforaphane amount would be 96 μmol (27 from item 2 + 69 from item 3). This would be a 17 mg weight of sulforaphane (96 / 5.64) [6]. This dosage is comparable to a 2017 clinical pilot study [7] and seven other completed clinical trial dosages of 100 μmol (17.3 mg) listed in [8].
    5. I’ve been sitting around a lot since returning from Milano, Italy, on February 24, 2020, and probably weigh around 75 kg. The estimated dosage represents 96 μmol / 75 kg = 1.28 μmol / kg, which is comparable to the 1.36 μmol / kg average of [1]. (The study provided the subjects’ mean weight in Table 1 as “85.8 ± 16.7 kg.” The average dosage per kg body weight was 117 μmol / 85.8 kg = 1.36 μmol / kg.)
    6. Don’t have a practical estimate of the amount of sulforaphane I metabolize from post-microwave glucoraphanin. Both [7] and [8] cited a 2012 study that found: “Some conversion of GRN to SFN can occur in response to metabolism by the gut microflora; however, the response is inefficient, having been shown to vary ‘from about 1% to more than 40% of the dose.’”
    7. Don’t have a practical estimate of the “internal dose.” [8]

I don’t have a laboratory in my kitchen 🙂 and won’t have quantified results.


References in order of citation:

[1] 2018 Effects of long-term consumption of broccoli sprouts on inflammatory markers in overweight subjects

[2] 2017 You Need Sulforaphane – How and Why to Grow Broccoli Sprouts

[3] 2020 Microwave cooking increases sulforaphane level in broccoli curated in Microwave broccoli to increase sulforaphane levels

fsn31493-fig-0003-m

[4] 2016 Dr. Vlassara’s AGE-Less Diet: How a Chemical in the Foods We Eat Promotes Disease, Obesity, and Aging and the Steps We Can Take to Stop It

[5] 2016 Effect of Broccoli Sprouts and Live Attenuated Influenza Virus on Peripheral Blood Natural Killer Cells: A Randomized, Double-Blind Study

[6] 2020 https://pubchem.ncbi.nlm.nih.gov/compound/sulforaphane lists sulforaphane’s molecular weight as 177.3 g / mol. A 1 mg weight of sulforaphane equals a 5.64 μmol sulforaphane amount (.001 / 177.3).

[7] 2019 Sulforaphane: Its “Coming of Age” as a Clinically Relevant Nutraceutical in the Prevention and Treatment of Chronic Disease

[8] 2019 Broccoli or Sulforaphane: Is It the Source or Dose That Matters? Note that a coauthor didn’t disclose their business’ conflict of interest for an effectively promoted commercial product.

Using COVID-19 as a cover story

One aspect of the coronavirus is how it’s being used for economic upheavals that weren’t previously acceptable. The view from a Hong Kong analyst:

From March 2020 MMT is now a reality:

“Under cover of the ‘coronacrisis’, we are now witnessing the introduction of Modern Monetary Theory (MMT), which isn’t modern and isn’t a theory.

The dollars that the government will inject into the Fed’s Special Purpose Vehicles (SPVs) were previously created out of nothing when the Fed monetised Treasury securities. So, the Fed creates money out of nothing. This money then goes to the government. The government then deposits some of this money into the Fed’s new SPVs, and based on this injection of ‘capital’ the Fed creates a lot more money out of nothing.

No longer will governments feel constrained by their abilities to tax the population and borrow from bond investors. From now on they will act like they have unrestricted access to a bottomless pool of money.”

The Coming Great Inflation from October 2019 showed that current developments were already in the works:

“The difference between money and every other economic good is that money is on one side of almost every economic transaction. Consequently, there is no single number that can accurately represent the price (purchasing power) of money, meaning that even the most honest and rigorous attempt to calculate the ‘general price level’ will fail. This doesn’t imply that changes in the supply of money have no effect on money purchasing power, but it does imply that the effects of changes in the money supply can’t be explained or understood via a simple equation.

The economic effects of a money-supply increase driven by commercial banks making loans to their customers will be very different from the economic effects of a money-supply increase driven by central banks monetising assets. ‘Main Street’ is the first receiver of the new money in the former case and ‘Wall Street’ is the first receiver of the new money in the latter case. This alone goes a long way towards explaining why the QE programs of Q4-2008 onward had a much greater effect on financial asset prices than on the prices that get added together to form the Consumer Price Index.

Due to the combination of the false belief that large increases in the supply of money have only a minor effect on the purchasing power of money and the equally false belief that the economy would benefit from a bit more ‘price inflation’, it’s a good bet that central banks and governments will devise ways to inject a lot more money into the economy in reaction to future economic weakness.”