Flatten the Panic Curve April 13-17, 2020

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

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

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.”

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.”

Deaths in Italy attributed to COVID-19

Why have so many coronavirus patients died in Italy? from the Telegraph today:

“According to Prof Walter Ricciardi, scientific adviser to Italy’s minister of health, the country’s mortality rate is far higher due to demographics – the nation has the second oldest population worldwide – and the manner in which hospitals record deaths.

‘The age of our patients in hospitals is substantially older – the median is 67, while in China it was 46,’ Prof Ricciardi says. ‘So essentially the age distribution of our patients is squeezed to an older age and this is substantial in increasing the lethality.

But Prof Ricciardi added that Italy’s death rate may also appear high because of how doctors record fatalities.

‘The way in which we code deaths in our country is very generous in the sense that all the people who die in hospitals with the coronavirus are deemed to be dying of the coronavirus.

On re-evaluation by the National Institute of Health, only 12 per cent of death certificates have shown a direct causality from coronavirus, while 88 per cent of patients who have died have at least one pre-morbidity – many had two or three,’ he says.”


Refactoring the current 4,825 deaths in Italy attributed to COVID-19 equals 579 (4,825 x .12). That number places Italy slightly above France’s 562 current total.

Evidence-based statements wouldn’t sufficiently frighten the herd, though. The article continued on to include now-obligatory, hyperbolic, unscientific WHO statements referencing a “miracle.”

Image from “Culture Audits: We Have Been Asking the Wrong Question”

Recover your sanity

Men, it has been well said:

  • Think in herds; it will be seen that
  • They go mad in herds, while
  • They only recover their senses slowly, one by one.

During the great plague, which ravaged all Europe between the years 1345 and 1350, it was generally considered that the end of the world was at hand.

‘But the facts, my dear fellow,’ said his friend, ‘the facts do not agree with your theory.’ ‘Don’t they?’ replied the philosopher, shrugging his shoulders, ‘then, tant pis pour les faits’ – so much the worse for the facts!”

Charles Mackay, 1841

https://www.gutenberg.org/ebooks/24518 “Memoirs of Extraordinary Popular Delusions and the Madness of Crowds”

Alfred Jacob Miller “Hunting buffalo” 1837

“Establishing the hidden communication networks in large self-organized groups facilitates a quantitative understanding of behavioral contagion.

An individual will be more likely to respond (is more susceptible) if it:

  • Is strongly connected to the initiator (short path length), and if it
  • Has neighbors which are strongly connected to each other.”

Why is it so difficult to live your own life?

Wander into creativity?

This 2019 US study investigated the context of creative ideas:

“Creative inspiration routinely occurs during moments of mind wandering. Approximately 20% of ideas occurred in this manner.

Although ideas that occurred while participants were both on task and mind wandering did not differ in overall quality, there were several dimensions on which they did consistently differ. Ideas that occurred while mind wandering were reported to be experienced with a greater sense of ‘aha’ and were more likely to involve overcoming an impasse.

The present findings are consistent with the view that spontaneous task-independent mind wandering represents a source of the inventive ideas that individuals have each day. This potential function of mind wandering may help to explain why a mental state that can be associated with significant negative outcomes is nevertheless so ubiquitous.”

“Would you say the idea felt like an ‘aha!’ moment?” and “How creative do you feel the idea was?” were the closest items to emotional measures. “How important do you think this idea is?” and several months later “How important has the idea proven to be overall?” were used to measure importance.

https://labs.psych.ucsb.edu/schooler/jonathan/sites/labs.psych.ucsb.edu.schooler.jonathan/files/pubs/0956797618820626.pdf “When the Muses Strike: Creative Ideas of Physicists and Writers Routinely Occur During Mind Wandering”

I came across this study from its reference in How Productivity Apps Can Make Us Less Productive (And Less Happy).


The study’s design missed opportunities to discover sources of creative ideas and feelings of importance. It focused on effects and intentionally disregarded causes, despite asserting that “mind wandering represents a source of inventive ideas.”

Experiments were subjectively biased for a framework that considered ideas as originating solely from a person’s thinking brain. A framework like Primal Therapy that demonstrated how ideas may arise as defenses against feelings wasn’t considered, although relevant.

Let’s use the finding “Ideas that occurred while mind wandering were more likely to involve overcoming an impasse” as an example for a Primal Therapy framework’s view:

  1. A person who has a seemingly unsolvable work problem probably encounters feelings of helplessness.
  2. Staying busy with tasks can distract them from these feelings.
  3. During times of less cognitive activity, though, these feelings can have more impetus.
  4. The resultant discomfort will trigger ideas to help ward off helpless feelings.

Regarding importance judgments, there are many needs a person develops and tries to satisfy as substitutes for real needs that weren’t fulfilled. I’ve focused on the need to feel important in blog posts such as Your need to feel important will run your life, and you’ll never feel satisfied.

A blood plasma aging clock

This 2019 Stanford human study developed an aging clock using blood plasma proteins:

“We measured 2,925 plasma proteins from 4,331 young adults to nonagenarians [18 – 95] and developed a novel bioinformatics approach which uncovered profound non-linear alterations in the human plasma proteome with age. Waves of changes in the proteome in the fourth, seventh, and eighth decades of life reflected distinct biological pathways, and revealed differential associations with the genome and proteome of age-related diseases and phenotypic traits.

To determine whether the plasma proteome can predict chronological age and serve as a “proteomic clock,” we used 2,858 randomly selected subjects to fine-tune a predictive model that was tested on the remaining 1,473 subjects. We identified a sex-independent plasma proteomic clock consisting of 373 proteins. Subjects that were predicted younger than their chronologic age based on their plasma proteome performed better on cognitive and physical tests.

The 3 age-related crests were comprised of different proteins. Few proteins, such as GDF15, were among the top 10 differentially expressed proteins in each crest, consistent with its strong increase across lifespan. Other proteins, like chordin-like protein 1 (CHRDL1) or pleiotrophin (PTN), were significantly changed only at the last two crests, reflecting their exponential increase with age.

We observed a prominent shift in multiple biological pathways with aging:

  • At young age (34 years), we observed a downregulation of proteins involved in structural pathways such as the extracellular matrix. These changes were reversed in middle and old ages (60 and 78 years, respectively).
  • At age 60, we found a predominant role of hormonal activity, binding functions and blood pathways.
  • At age 78, key processes still included blood pathways but also bone morphogenetic protein signaling, which is involved in numerous cellular functions, including inflammation.

These results suggest that aging is a dynamic, non-linear process characterized by waves of changes in plasma proteins that are reflective of a complex shift in the activity of biological processes.”

https://www.biorxiv.org/content/10.1101/751115v1.full “Undulating changes in human plasma proteome across lifespan are linked to disease”


A non-critical review of the study was published by the Life Extension Advocacy Foundation. Frequent qualifiers like “could,” “may,” and “possible” were consistent with the confirmation biases of their advocacy.

There were several misstatements of what the study did, including the innumerate:

  1. “used around half of the participant data to build a “proteomic clock”
  2. tested it on the other half of the participants
  3. a total of 3000 proteins”

Per the above study quotation, the numbers were actually:

  1. Closer to two thirds (2,858 ÷ 4,331), not “around half”;
  2. The other third (1,473 ÷ 4,331), not “the other half”; and
  3. 2,925 not 3000.

The final paragraph and other parts of the review bordered on woo. Did a review of the findings have to fit LEAF’s perspective?


In contrast, Josh Mitteldorf did his usual excellent job of providing contexts for the study with New Aging Clock based on Proteins in the Blood, emphasizing comparisons with epigenetic clock methodologies:

“For some of the proteins that feature prominently in the clock, we have a good understanding of their metabolic function, and for the most part they vindicate my belief that epigenetic changes are predominantly drivers of senescence rather than protective responses to damage.

Wyss-Coray compared the proteins in the new (human) proteome clock with the proteins that were altered in the (mouse) parabiosis experiments, and found a large overlap [46 proteins change in the same direction and define a conserved aging signature]. This may be the best evidence we have that the proteome changes are predominantly causal factors of senescence.

46 plasma proteins

Almost all the proteins identified as changing rapidly at age 78 are increasing. In contrast, a few of the fastest-changing proteins at age 60 are decreasing (though most are increasing). GDF15 deserves a story of its own.

The implication is that a more accurate clock can be constructed if it incorporates different information at different life stages. None of the Horvath clocks have been derived based on different CpG sites at different ages, and this suggests an opportunity for a potential improvement in accuracy.”

A commentator linked the below study:

https://www.sciencedirect.com/science/article/pii/S0092867419308323 “GDF15 Is an Inflammation-Induced Central Mediator of Tissue Tolerance” (not freely available)

which prompted his response:

“Thanks, Lee! This is just the kind of specific information that I was asking for. It would seem we should construct our clocks without GDF15, which otherwise might loom large.”

An epigenetic clock review by committee

This 2019 worldwide review of epigenetic clocks was a semi-anonymous mishmash of opinions, facts, hypotheses, unwarranted extrapolations, and beliefs. Diversity of viewpoints among the 21 coauthors wasn’t evident.

1. Citations of coauthors’ works seemed excessive, and they apologized for omissions. However:

  • Challenge 5 was titled “Single-cell analysis of aging changes and disease” and
  • Table 1 “Major biological and analytic issues with epigenetic DNA methylation clocks” had single-cell analysis as the Proposed solution to five Significant issues.

Yet studies such as High-Resolution Single-Cell DNA Methylation Measurements Reveal Epigenetically Distinct Hematopoietic Stem Cell Subpopulations were unmentioned.

2. Some coauthors semi-anonymously expressed faith that using current flawed methodologies in the future – only more thoroughly, with newer equipment, etc. – would yield better results. If all 21 coauthors were asked their viewpoints of Proposed solutions to the top three Significant issues of epigenetic clocks, what would they emphasize when quoted?

3. Techniques were praised:

“Given the precision with which DNA methylation clock age can be estimated and evolving measures of biological, phenotype-, and disease-related age (e.g., PhenoAge, GrimAge)..”

Exactly why these techniques have at times produced inexplicable results wasn’t examined, though. Two examples:

  • In Reversal of aging and immunosenescent trends, Levine PhenoAge methodology estimated that the 51-65 year old subjects’ biological ages at the beginning of the study averaged 17.5 years less than their chronological age. Comparing that to Horvath average biological age of 3.95 years less raised the question: exactly why did PhenoAge show such a large difference?
  • The paper mentioned GrimAge methodology findings about “smoking-related changes.” But it didn’t explain why GrimAge methylation findings most closely associated with smoking history also accurately predicted future disease risk with non-smokers.

Eluding explanations for these types of findings didn’t help build confidence in methodologies.

4. A more readable approach to review by committee could have coauthors – in at least one section – answer discussion questions, as Reversing epigenetic T cell exhaustion did with 18 experts.

https://genomebiology.biomedcentral.com/articles/10.1186/s13059-019-1824-y “DNA methylation aging clocks: challenges and recommendations”

A GWAS meta-analysis of two epigenetic clocks

This 2019 UK human study conducted a meta-analysis of genome-wide association studies of two epigenetic clocks using 13,493 European-ancestry individuals aged between ten and 98 years:

“Horvath-EAA, described in previous publications as ‘intrinsic’ epigenetic age acceleration (IEAA), can be interpreted as a measure of cell-intrinsic ageing that exhibits preservation across multiple tissues, appears unrelated to lifestyle factors, and probably indicates a fundamental cell ageing process that is largely conserved across cell types.

In contrast, Hannum-EAA, referred to in previous studies as ‘extrinsic’ epigenetic age acceleration (EEAA), can be considered a biomarker of immune system ageing, explicitly incorporating aspects of immune system decline such as age-related changes in blood cell counts, correlating with lifestyle and health-span related characteristics, and thus yielding a stronger predictor of all-cause mortality.

The meta-analysis of Horvath-EAA identified ten independent associated SNPs [single nucleotide polymorphisms], doubling the number reported to date, and highlighted 21 genes involved in Horvath-based epigenetic ageing. Four of the ten Horvath-EAA-associated SNPs are mQTL [methylation quantitative trait loci] for CpGs used in the Horvath/Hannum epigenetic clocks. A possible interpretation of this is that the functional mechanism by which these SNPs influence the rate of biological ageing is via altering methylation levels.

Father’s age at death, a rough proxy for lifespan, was nominally significantly correlated with both EAA measures, and parents’ age at death was additionally correlated with Hannum-EAA. Aside from these, genetic correlations with age-related traits were surprisingly few: it is possible that this could reflect an overly conservative correction for the multiple tests carried out, or low statistical power, rather than a genuine lack of correlations.

Genetic correlation analysis should be restricted to GWAS with a heritability Z-score of 4 or more, on the grounds of interpretability and power, so the Horvath-based results particularly should be interpreted with caution.”


A non-apologetic way to explain the above graphic is that NONE of these 218 “health and behavioral traits” were any more associated with the studied genetic measurements than would be expected by chance!

Fervent believers in the GWAS methodology’s capability to exactly predict individual phenotypes eventually become victims of the scientific method. These GWAS researchers griped about “overly conservative correction, or low statistical power” and other predictable shortfalls, and ended a long limitations statement with:

“While we have identified a number of SNPs and genes significantly associated with EAA, including genes already known to be related to ageing, the analyses presented here fall short of providing a mechanistic explanation for how these variants and genes act to influence biological age.”

Outside of beliefs, it’s hard to understand why research money keeps pouring into the GWAS dead end. If these researchers and their employing institution and sponsors want to make a difference in human lives, they need to get busy in other areas.

These researchers were employed by the same institution that couldn’t be bothered to scrape together six more weeks of funds to study the transgenerational damaging effects of acetaminophen – an analgesic available to billions of people – in Epigenetics research that was designed to fall one step short of wonderful.

https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1008104 “A meta-analysis of genome-wide association studies of epigenetic age acceleration”

Restrict information in the name of science?

A Stanford researcher was annoyed that we live in the 21st century, and advocated we return to previous centuries’ information-flow check valves of wise old men. No doubt the publishers of and subscribers to the Journal of the American Medical Association applauded the same old tired prescription.

Ten instances of the word “should” in the final two paragraphs provided ample evidence of the paper’s intent. Mirroring the current political climate – projecting – accusations made of others were items the accusers were guilty of themselves, such as:

“When these scientists act as investigators in the hundreds of observational studies that they publish, or as editors and peer reviewers in evaluating submissions from others, would they tolerate publishing analyses and funding proposals that might contradict their belief system?”

https://jamanetwork.com/journals/jama/fullarticle/2753533 “Neglecting Major Health Problems and Broadcasting Minor, Uncertain Issues in Lifestyle Science”


One of the paper’s references included an informative graphic:

“A histogram of the total number of rumor cascades in our data across the seven most frequent topical categories.”

https://science.sciencemag.org/content/359/6380/1146 “The spread of true and false news online”


I’ll borrow from the curation of another Stanford paper Online dating cuts out the middlemen in conclusion:

“Are there examples where it wouldn’t potentially improve a person’s life to choose their information sources? Friends, family, and other social groups – and religious, educational, and other institutions – have had their middlemen/guarantor time, and have been found lacking.

Make your own choices for your one precious life.”

Perinatal stress and sex differences in circadian activity

This 2019 French/Italian rodent study used the PRS model to investigate its effects on circadian activity:

“The aim of this study was to explore the influence of PRS on the circadian oscillations of gene expression in the SCN [suprachiasmatic nucleus of the hypothalamus] and on circadian locomotor behavior, in a sex-dependent manner.

Research on transcriptional rhythms has shown that more than half of all genes in the human and rodent genome follow a circadian pattern. We focused on genes belonging to four functional classes, namely the circadian clock, HPA axis stress response regulation, signaling and glucose metabolism in male and female adult PRS rats.

Our findings provide evidence for a specific profile of dysmasculinization induced by PRS at the behavioral and molecular level, thus advocating the necessity to include sex as a biological variable to study the set-up of circadian system in animal models.”

“There was a clear-cut effect of sex on the effect of PRS on the levels of activity:

  • During the period of lower activity (light phase), both CONT and PRS females were more active than males. During the light phase, PRS increased activity in males, which reached levels of CONT females.
  • More interestingly, during the period of activity (dark phase), male PRS rats were more active than male CONT rats. In contrast, female PRS rats were less active than CONT females.
  • During the dark phase, CONT female rats were less active than CONT male rats.

The study presented evidence for sex differences in circadian activity of first generation offspring that was caused by stress experienced by the pregnant mother:

“Exposure to gestational stress and altered maternal behavior programs a life-long disruption in the reactive adaptation such as:

  •  A hyperactive response to stress and
  • A defective feedback of the hypothalamus-pituitary-adrenal (HPA) axis together with
  • Long-lasting modifications in stress/anti-stress gene expression balance in the hippocampus.”

It would advance science if these researchers carried out experiments to two more generations to investigate possible transgenerational epigenetic inheritance of effects caused by PRS. What intergenerational and transgenerational effects would they possibly find by taking a few more months and extending research efforts to F2 and F3 generations? Wouldn’t these findings likely help humans?


One aspect of the study was troubling. One of the marginally-involved coauthors was funded by the person described in How one person’s paradigms regarding stress and epigenetics impedes relevant research. Although no part of the current study was sponsored by that person, there were three gratuitous citations of their work.

All three citations were reviews. Unlike study researchers, reviewers aren’t bound to demonstrate evidence from tested hypotheses. Reviewers are free to:

  • Express their beliefs as facts;
  • Over/under emphasize study limitations; and
  • Disregard and misrepresent evidence as they see fit.

Fair or not, comparisons of reviews with Cochrane meta-analyses of the same subjects consistently show the extent of reviewers’ biases. Reviewers also aren’t obligated to make post-publication corrections for their errors and distortions.

As such, reviews can’t be cited for reliable evidence. Higher-quality studies that were more relevant and recent than a 1993 review could have elucidated points.

Sucking up to the boss and endorsing their paradigm was predictable. Since that coauthor couldn’t constrain themself to funder citations only in funder studies, it was the other coauthors’ responsibilities to edit out unnecessary citations.

https://www.frontiersin.org/articles/10.3389/fnmol.2019.00089/full “Perinatal Stress Programs Sex Differences in the Behavioral and Molecular Chronobiological Profile of Rats Maintained Under a 12-h Light-Dark Cycle”

Would you return a lost wallet?

The researchers in this 2019 Swiss/US study intentionally “lost” > 17,000 wallets under experimental conditions:

“We conducted field experiments in 40 countries to examine whether people act more dishonestly when they have a greater economic incentive to do so, and we found the opposite to be true. Citizens were more likely to return wallets that contained relatively larger amounts of money. Neither nonexperts nor professional economists were able to predict this result.

When people stand to heavily profit from engaging in dishonest behavior, the desire to cheat increases but so do the psychological costs of viewing oneself as a thief.”


The study did well in some aspects, including publicity. However:

1. The researchers admitted in the final paragraph:

“Using average reporting rates across countries, we find substantial variation in rates of civic honesty, ranging from 14 to 76%. This variation largely persists even when controlling for a country’s gross domestic product, suggesting that other factors besides a country’s wealth are also at play.”

Yet the paper’s first page contained the above graphic, which used each country’s GDP as a dependent variable! Wasn’t a behavioral economics study of honesty required to present their data honestly, and use factors that were experimentally significant?

2. “Other factors..at play” were relegated to the supplementary materials. The paper was only three-and-a-half pages long, so there was room for further explanations.

Here’s one comment on cultural differences from a Chinese PhD student:

“Biased design. In China (and Asian countries), people seldom use email, and our merit is to leave things untouched (“路不拾遗“:no one picks up lost articles in the street (idiom)).”

3. The study design had nothing to do with avoiding taxes, but three of the four sentences in the paper’s first paragraph did. This impressed as pointless.

https://science.sciencemag.org/content/365/6448/70 “Civic honesty around the globe” (not freely available)

Wikipedia is a poor source of information on advanced glycation end products (AGEs)

A link to Wikipedia is usually on the first page of search results. The Wikipedia post on AGEs lacks the evidence that a reader may infer from its text.

For example, the second paragraph of the AGEs post, Dietary Sources, contained the following text and references:

  1. “However, only low molecular weight AGEs are absorbed through diet, and vegetarians have been found to have higher concentrations of overall AGEs compared to non-vegetarians. [4]
  2. Therefore it is unclear whether dietary AGEs contribute to disease and aging, or whether only endogenous AGEs (those produced in the body) matter. [5]
  3. This does not free diet from potentially negatively influencing AGE, but implicates dietary AGE may be less important than other aspects of diet that lead to elevated blood sugar levels and formation of AGEs. [4] [5]”

[4] https://www.sciencedirect.com/science/article/pii/S0278691513004444 “Advanced glycation end products in food and their effects on health” (not freely available) 2013 Denmark.

Please note on this linked page that a German researcher took the time to correct one bias of the Danish reviewers, citing evidence from his studies that:

“The deleterious effects of food-derived AGEs in subjects with type 2 diabetes mellitus are proven.”

[5] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3257625 “Dietary Advanced Glycation End Products and Aging” 2010 US.


Both of these references were reviews.

Unlike study researchers, reviewers aren’t bound to demonstrate evidence from tested hypotheses. Reviewers are free to:

  • Express their beliefs as facts;
  • Over/under emphasize study limitations; and
  • Disregard and misrepresent evidence as they see fit.

Reviewers also aren’t obligated to make post-publication corrections for their errors and distortions. For example, the Danes didn’t correct their review with any findings the German researcher presented.

As such, reviews can’t be cited for reliable evidence.


A sample of other problems with each of the Wikipedia sentences:

1. “However, only low molecular weight AGEs are absorbed through diet, and vegetarians have been found to have higher concentrations of overall AGEs compared to non-vegetarians. [4]”

The first part of sentence 1 came from the review’s abstract:

“Only LMW AGEs..may be absorbed from the gut and contribute to the body burden of AGEs.”

But the reviewers didn’t support their abstract’s statement with direct evidence from any study!

2. “Therefore it is unclear whether dietary AGEs contribute to disease and aging, or whether only endogenous AGEs (those produced in the body) matter. [5]”

The “therefore” of sentence 2 was misplaced. Sentence 1 didn’t attempt to explain whether “dietary AGEs contribute to disease and aging” or “only endogenous AGEs matter.”

Since sentence 2 wasn’t a consequence of sentence 1, the Wikipedia contributor(s) needed to support sentence 2 with evidence. Citing an “unclear” 2010 reference [5] ignored dozens of studies that provided better clarity.

3. “This does not free diet from potentially negatively influencing AGE, but implicates dietary AGE may be less important than other aspects of diet that lead to elevated blood sugar levels and formation of AGEs. [4] [5]”

Wikipedia contributors tend to cite irrelevant references rather than get flagged with “citation needed.” The value judgment of sentence 3 was an example of this intentionally misleading masquerade.

“Dietary AGE may be less important..” wasn’t unequivocally supported by studies referenced in either review, and didn’t represent an authoritative body of evidence. Contrast those weasel words with:

“The deleterious effects of food-derived AGEs in subjects with type 2 diabetes mellitus are proven.”

Good job, Wikipedia contributors! You used lower-quality reviews to promote misunderstandings that DETRACTED from science.


Wikipedia’s premise is that since the group knows more about any subject than does any individual, everyone is entitled to contribute. The results are usually incoherent narratives that often substitute opinions for evidence.

The second paragraph of the Exogenous section of the Wikipedia glycation post provided an example:

  • Assertions of the first and third sentences needed citations. Did the contributor(s) think these would be unexamined?
  • Someone contributed a cancer reference as the fourth sentence, although it had little to do with the preceding sentences.
  • The fifth sentence was informative on exogenous glycations and AGEs. An editor would have removed “recently” and “recent” though, because the cited source was dated 2005.

Do delusions have therapeutic value?

This 2019 UK review discussed delusions, aka false beliefs about reality:

“Delusions are characterized by their behavioral manifestations and defined as irrational beliefs that compromise good functioning. In this overview paper, we ask whether delusions can be adaptive notwithstanding their negative features.

We consider different types of delusions and different ways in which they can be considered as adaptive: psychologically (e.g., by increasing wellbeing, purpose in life, intrapsychic coherence, or good functioning) and biologically (e.g., by enhancing genetic fitness).”

https://onlinelibrary.wiley.com/doi/full/10.1002/wcs.1502 “Are clinical delusions adaptive?”


A. Although section 4’s heading was Biological Adaptiveness of Delusions, the reviewers never got around to discussing evolved roles of brain areas and beliefs (delusions). One mention of evolutionary biology was:

“Delusions are biologically adaptive if, as a response to a crisis of some sort (anomalous perception or overwhelming distress), they enhance a person’s chances of reproductive success and survival by conferring systematic biological benefits.”

B. Although section 5’s heading was Psychological Adaptiveness of Delusions, the reviewers didn’t connect feelings and survival sensations as origins of beliefs (delusions) and behaviors. They had a few examples of feelings:

“Delusions of reference and delusions of grandeur can make the person feel important and worthy of admiration.”

and occasionally sniffed a clue:

“Some delusions (especially so‐called motivated delusions) play a defensive function, representing the world as the person would like it to be.”

where “motivated delusions” were later deemed in the Conclusion section to be a:

“Response to negative emotions that could otherwise become overwhelming.”

C. Feelings weren’t extensively discussed until section 6 Delusions in OCD and MDD, which gave readers an impression that feelings were best associated with those diseases.

D. In the Introduction, sections 4, 5, and 7 How Do We Establish and Measure Adaptiveness, the reviewers discussed feeling meaning in life, but without understanding:

  1. Feelings = meaning in life, as I quoted Dr. Arthur Janov in The pain societies instill into children:

    “Without feeling, life becomes empty and sterile. It, above all, loses its meaning.

  2. Beliefs (delusions) defend against feelings.
  3. Consequentially, the stronger and / or more numerous beliefs (delusions) a person has, the less they feel meaning in life.

E. Where, when, why, and how do beliefs (delusions) arise? Where, when, why, and how does a person sense and feel, and what are the connections with beliefs (delusions)?

F. The word “sense” was used 29 times in contexts such as “make sense” and “sense of [anxiety, coherence, control, meaning, purpose, rational agency, reality, self, uncertainty]” but no framework connected biological sensing to delusions. Papers from other fields have detailed cause-and-effect explanations and predecessor-successor diagrams for every step of a process. Not this one.


Regarding any therapeutic value of someone else’s opinion of a patient’s delusions:

I’ll reuse this quotation from the Scientific evidence page of Dr. Janov’s 2011 book “Life Before Birth: The Hidden Script that Rules Our Lives” p.166:

“Primal Therapy differs from other forms of treatment in that the patient is himself a therapist of sorts. Equipped with the insights of his history, he learns how to access himself and how to feel.

The therapist does not heal him; the therapist is only the catalyst allowing the healing forces to take place. The patient has the power to heal himself.

Another way Dr. Janov wrote this was on p.58 of his 2016 book Beyond Belief as quoted in Beyond Belief: The impact of merciless beatings on beliefs:

NO ONE HAS THE ANSWER TO LIFE’S QUESTIONS BUT YOU. How you should lead your life depends on you, not outside counsel.

We do not direct patients, nor dispense wisdom upon them. We have only to put them in touch with themselves; the rest is up to them.

Everything the patient has to learn already resides inside. The patient can make herself conscious. No one else can.”

Why do we believe obvious lies?

Here are two accounts of this weekend’s news from real journalists, neither of whom are fans of the current US president.

Matt Taibbi of Rolling Stone
https://taibbi.substack.com/p/russiagate-is-wmd-times-a-million
“It’s official: Russiagate is this generation’s WMD”

He cited intentional misreporting (lying) multiple times from the New York Times, Washington Post, CNN, Wall Street Journal, MSNBC, Mother Jones; and from NBC, ABC, McClatchy, New Yorker, New York Magazine, Bloomberg, BuzzFeed, Slate, Yahoo, Fortune, Guardian; and from numerous US congressmen and senators. Most of these false stories have still not yet been corrected or retracted.

  • “Recapping: the reporter who introduced Steele to the world (his September 23, 2016 story was the first to reference him as a source), who wrote a book that even he concedes was seen as “validating” the pee tape story, suddenly backtracks and says the whole thing may have been based on a Las Vegas strip act, but it doesn’t matter because Stormy Daniels, etc.
  • When explosive #Russiagate headlines go sideways, the original outlets simply ignore the new development, leaving the “retraction” process to conservative outlets that don’t reach the original audiences.
  • The Russiagate era has so degraded journalism that even once “reputable” outlets are now only about as right as politicians, which is to say barely ever, and then only by accident.
  • Authorities have been lying their faces off to reporters since before electricity! It doesn’t take much investigation to realize the main institutional sources in the Russiagate mess – the security services, mainly – have extensive records of deceiving the media.
  • As noted before, from World War I-era tales of striking union workers being German agents to the “missile gap” that wasn’t (the “gap” was leaked to the press before the Soviets had even one operational ICBM) to the Gulf of Tonkin mess to all the smears of people like Martin Luther King, it’s a wonder newspapers listen to whispers from government sources at all.”


Glenn Greenwald of The Intercept
https://twitter.com/ggreenwald

  1. “Can’t the people who got rich exploiting liberal #Resistance fears by feeding them false conspiracies at least content themselves to their bulging bank accounts from the scam they pulled off & have one day of silence where they don’t try to pretend that they were right all along?
  2. If you’re just going to let stuff like this go – unexamined, unacknowledged, and unaccounted for – don’t expect anyone to be remotely sympathetic to the fact that public trust in big media is nonexistent and politicians benefit by making journalists their enemies.
  3. And just for future reference: documenting the falsehoods, baseless conspiracies, and deceitful narratives being peddled without dissent by the major corporate media isn’t “blogging” or “media criticism.” It’s journalism. It’s reporting. And it’s vital.
  4. Nothing kills journalism worse than cowardly group-think, and it’s worse than ever since they’re congregated in the same places in Brooklyn and the West Coast and petrified of saying anything that makes them unpopular among their peers.
  5. Check every MSNBC personality, CNN law “expert,” liberal-centrist outlets and #Resistance scam artist and see if you see even an iota of self-reflection, humility or admission of massive error.
  6. I wrote this with @GGreenwald in November 2016, warning Russiagate was being used to attack, smear, and censor alternative media. Those blacklisted alternative media ended up being correct about Russiagate – while the corporate media spread actual fake news.
  7. There should be major accountability in the US media and in the intelligence community they united with to drown US political discourse for 2 years straight in unhinged conspiratorial trash, distracting from real issues. That’s what should happen as a first step. But it won’t.”