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 U.S. 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 U.S. 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.”
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Statistical inferences vs. biological realities

A 2019 UCLA study introduced a derivative of the epigenetic clock named GrimAge:

“DNAm GrimAge, a linear combination of chronological age, sex, and DNAm-based surrogate biomarkers for seven plasma proteins and smoking pack-years, outperforms all other DNAm-based biomarkers, on a variety of health-related metrics.

An age-adjusted version of DNAm GrimAge, which can be regarded as a new measure of epigenetic age acceleration (AgeAccelGrim), is associated with a host of age-related conditions, lifestyle factors, and clinical biomarkers. Using large scale validation data from three ethnic groups, we demonstrate that AgeAccelGrim stands out among pre-existing epigenetic clocks in terms of its predictive ability for time-to-death, time-to-coronary heart disease, time-to-cancer, its association with computed tomography data for fatty liver/excess fat, and early age at menopause.”

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6366976/ “DNA methylation GrimAge strongly predicts lifespan and healthspan”


A miserable attempt at reporting the study’s findings included angles of superstition, fear-of-the-future, and suspicion-by-spurious-association:

“The research has already captured the attention of the life insurance industry. After all, a solid death date could mean real savings when it comes to pricing policies.

The hope is that if and when legitimate anti-aging drugs are developed, GrimAge could be used to test their effectiveness. In a world with functional anti-aging drugs, “doctors could test [your GrimAge number] and say, ‘You know what, you’re aging too quickly. Take this,'” Horvath said.”

https://onezero.medium.com/a-new-test-predicts-when-youll-die-give-or-take-a-few-years-2d08147c8ea6 “A New Test Predicts When You’ll Die (Give or Take a Few Years)”


A detailed blog post from Josh Mitteldorf provided scientific coverage of the study:

“Methylation sites associated with smoking history predicted how long the person would live more accurately than the smoking history itself. Even stranger, the methylation marks most closely associated with smoking were found to be a powerful indication of future health even when the sample was confined to non-smokers.

The DNAm GrimAge clock was developed in two stages, a correlation of a correlation. Curiously, the indirect computation yields the better result.

Horvath’s finding that secondary methylation indicators are more accurate than the underlying primary indicator from which they were derived is provocative, and calls out for a new understanding.”

https://joshmitteldorf.scienceblog.com/2019/03/05/dnam-grimage-the-newest-methylation-clock “DNAm GrimAge—the Newest Methylation Clock”


When there are logical disconnects in findings like the above, it’s time to examine underlying premises. As noted in Group statistics don’t necessarily describe an individual, an assumption required by statistical analyses is that each measured item in the sample is interchangeable with the next.

This presumption is often false, producing individually inapplicable results. For example, the review from earlier this week Immune memory vs. immune adaptation included this description of the adaptive immune system:

“To be effective, highly specific immune response requires huge diversity of receptors and antibodies, which is achieved by somatic rearrangement of gene segments. Recombination results in millions of TCR [T cell receptor] and antibody variants able to recognize and neutralize millions of various antigens.”

Standard statistics of millions of T cell receptor and antibody variants won’t represent their individually unique properties. Individual differences are their purpose and benefit to us.

The GrimAge study’s overreach was most apparent in stratifying educational attainment to develop correlations. As mentioned in Does a societal mandate cause DNA methylation? such statistics are poor evidence of each individual’s biological realities.

Neither derivatives of group statistics, nor correlations of correlations, seem to be the techniques needed to understand biological causes of effects. Commentators on the GrimAge study alluded to this point, but glossed it over:

“It remains a mystery why exactly the epigenetic clocks work, and whether age-related changes in DNA methylation contribute to the cause of aging or are a result of it.”

Immune memory vs. immune adaptation

This 2019 Dutch/German/Romanian perspective aimed for a better understanding of immune systems:

“Based on molecular, immunological, and evolutionary arguments, we propose that innate immune memory is a primitive form of immune memory present in all living organisms, while adaptive immune memory is an advanced form of immune memory representing an evolutionary innovation in vertebrates.

Innate immune responses have the capacity to be trained and thereby exert a new type of immunological memory upon reinfection. The central feature of trained innate immune cells is the ability to mount a qualitatively and quantitatively different transcriptional response when challenged with microbes or danger signals. Evidence supports the convergence of multiple regulatory layers for mediating innate immune memory, including changes in chromatin organization, DNA methylation, and probably non-coding RNAs such as microRNAs and/or long non-coding RNAs.

Two properties of the adaptive immune response are mediated by two fundamentally different types of mechanisms:

  1. The higher magnitude and speed of the response is mediated by epigenetic programming.
  2. The specificity of the response is insured by gene recombination of TCR [T cell receptor] and BCR [B cell receptor] and clonal expansion of specific cell subpopulations upon antigen recognition.

To be effective, highly specific immune response requires huge diversity of receptors and antibodies, which is achieved by somatic rearrangement of gene segments. Recombination results in millions of TCR and antibody variants able to recognize and neutralize millions of various antigens.”


The paper included speculations such as the “Evidence supports..probably non-coding RNAs” quoted above, and the penultimate sentence:

“One can envision that vaccines that are capable of inducing both forms of immune memory at the same time would be more effective.”

100% factual evidence is preferred. The paper’s overall information can only be as accurate as the paper’s least accurate information.

The lead author coauthored A dietary supplement that trains the innate immune system and a study referenced in Eat your oats.

https://www.sciencedirect.com/science/article/pii/S1931312818306334 “Innate and Adaptive Immune Memory: an Evolutionary Continuum in the Host’s Response to Pathogens” (not freely available)

Our brains are shaped by our early environments

This 2019 McGill paper reviewed human and animal studies on brain-shaping influences from the fetal period through childhood:

“In neonates, regions of the methylome that are highly variable across individuals are explained by the genotype alone in 25 percent of cases. The best explanation for 75 percent of variably methylated regions is the interaction of genotype with different in utero environments.

A meta-analysis including 45,821 individuals with attention-deficit/hyperactivity disorder and 9,207,363 controls suggests that conditions such as preeclampsia, Apgar score lower than 7 at 5 minutes, breech/transverse presentations, and prolapsed/nuchal cord – all of which involve some sort of poor oxygenation during delivery – are significantly associated with attention-deficit/hyperactivity disorder. The dopaminergic system seems to be one of the brain systems most affected by perinatal hypoxia-ischemia.

Exposure to childhood trauma activates the stress response systems and dysregulates serotonin transmission that can adversely impact brain development. Smaller cerebral, cerebellar, prefrontal cortex, and corpus callosum volumes were reported in maltreated young people as well as reduced hippocampal activity.

Environmental enrichment has a series of beneficial effects associated with neuroplasticity mechanisms, increasing hippocampal volume, and enhancing dorsal dentate gyrus-specific differences in gene expression. Environmental enrichment after prenatal stress decreases depressive-like behaviors and fear, and improves cognitive deficits.”


The reviewers presented strong evidence until the Possible Factors for Reversibility section, which ended with the assertion:

“All these positive environmental experiences mentioned in this section could counterbalance the detrimental effects of early life adversities, making individuals resilient to brain alterations and development of later psychopathology.”

The review’s penultimate sentence recognized that research is seldom done on direct treatments of causes:

“The cross-sectional nature of most epigenetic studies and the tissue specificity of the epigenetic changes are still challenges.”

Cross-sectional studies won’t provide definitive data on cause-and-effect relationships.

The question that remains to be examined is: How can humans best address these early-life causes to ameliorate their lifelong effects?

https://onlinelibrary.wiley.com/doi/full/10.1111/dmcn.14182 “Early environmental influences on the development of children’s brain structure and function” (not freely available)

A therapy to reverse cognitive decline

This 2018 human study presented the results of 100 patients’ personalized therapies for cognitive decline:

“The first examples of reversal of cognitive decline in Alzheimer’s disease and the pre-Alzheimer’s disease conditions MCI (Mild Cognitive Impairment) and SCI (Subjective Cognitive Impairment) have recently been published..showing sustained subjective and objective improvement in cognition, using a comprehensive, precision medicine approach that involves determining the potential contributors to the cognitive decline (e.g., activation of the innate immune system by pathogens or intestinal permeability, reduction in trophic or hormonal support, specific toxin exposure, or other contributors), using a computer-based algorithm to determine subtype and then addressing each contributor using a personalized, targeted, multi-factorial approach dubbed ReCODE for reversal of cognitive decline.

An obvious criticism of the initial studies is the small number of patients reported. Therefore, we report here 100 patients, treated by several different physicians, with documented improvement in cognition, in some cases with documentation of improvement in electrophysiology or imaging, as well.”

https://www.omicsonline.org/open-access/reversal-of-cognitive-decline-100-patients-2161-0460-1000450-105387.html “Reversal of Cognitive Decline: 100 Patients”


The lead author commented on Josh Mitteldorf’s informative post A cure for Alzheimer’s? Yes, a cure for Alzheimer’s!:

  1. “We have a paper in press, due to appear 10.22.18 (open access, JADP, I’ll send a copy as soon as available), showing 100 patients with documented improvement – some with MRI volumetrics improved, others with quantitative EEG improvements, others with evoked response improvements, and all with quantitative cognitive assessment improvement. Some are very striking – 12 point improvements in MoCA, for example – others less so, but all also have subjective improvement. Hopefully this will address some of the criticisms that we haven’t documented improvement in enough people.
  2. We were just turned down again for a randomized, controlled clinical trial, so on the one hand, we are told repeatedly that no one will believe that this approach works until we publish a randomized, controlled study, and on the other hand, we’ve been turned down (first in 2011/12, and now in 2018), with the complaint that we are trying to address more than one variable in the trial (as if AD is a single-variable disease!). Something of a catch-22. We are now resubmitting (unfortunately, the IRBs are not populated by functional medicine physicians, so they are used to seeing old-fashioned drug studies), and we’ll see what happens.
  3. I’ve been extending the studies to other neurodegenerative diseases, and it has been impressive how much of a programmatic response there seems to be in these “diseases.”
  4. I agree with you that there are many features in common with aging itself.
  5. You made a good point that APP is a dependence receptor, and in fact it functions as an integrating dependence receptor, responding to numerous inputs (Kurakin and Bredesen, 2015).
  6. In the book and the publications, we don’t claim it is a “cure” since we don’t have pathological evidence that the disease process is gone. What we claim is “reversal of cognitive decline” since that is what we document.
  7. As I mentioned in the book, AD is turning out to be a protective response to multiple insults, and this fits well with the finding that Abeta has an antimicrobial effect (Moir and Tanzi’s work). It is a network-downsizing, protective response, which is quite effective – some people live with the ongoing degenerative process for decades.
  8. We have seen several cases now in which a clinical trial of an anti-amyloid antibody made the person much worse in a time-dependent manner (each time there was an injection, the person would get much worse for 5-10 days, then begin to improve back toward where he/she was, but over time, marked decline occurred), and this makes sense for the idea that the amyloid is actually protecting against pathogens or toxins or some other insult.
  9. It is important to note that we’ve never claimed that all people get better – this is not what we’ve seen. People very late in the process, or who don’t follow the protocol, or who don’t address the various insults, do not improve. It is also turning out to be practitioner dependent – some are getting the vast majority of people to improve, others very few, so this is more like surgery than old-fashioned prescriptive medicine – you have to do a somewhat complicated therapeutic algorithm and get it right for best results.
  10. I’m very interested in what is needed to take the next step in people who have shown improvement but who started late in the course. For example, we have people now who have increased MoCA from 0 to 9 (or 0 to 3, etc.), with marked subjective improvement but plateauing at less than normal. These people had extensive synaptic and cellular loss prior to the program. So what do we need to raise the plateau? Stem cells? Intranasal trophic support? Something else?
  11. I haven’t yet seen a mono-etiologic theory of AD or a mono-therapeutic approach that has repeatedly positive results, so although I understand that there are many theories and treatments, there doesn’t seem to be one etiology to the disease, nor does there seem to be one simple treatment that works for most. It is much more like a network failure.”

At a specific level:

  • “There doesn’t seem to be one etiology to the disease,
  • nor does there seem to be one simple treatment that works for most.
  • We don’t have pathological evidence that the disease process is gone.”

For general concepts, however:

  • “AD is turning out to be a protective response to multiple insults,
  • It is a network-downsizing, protective response, which is quite effective.
  • The amyloid is actually protecting against pathogens or toxins or some other insult.”

For a framework of an AD cure to be valid, each source of each insult that evoked each “protective response” should be traced.

Longitudinal studies would be preferred inside this framework. These study designs would investigate evidence of each insult’s potential modifying effect on each “protective response” that could affect the cumulative disease trajectory of each individual.

In many cases, existing study designs would be adequate if they extended their periods to the end of the subjects’ natural lifetimes. One AD-relevant example would be extending the prenatally-restraint-stressed model used in:

The framework would also encourage extending studies to at least three generations to investigate evidence for transgenerational effects, as were found in:

Epigenetic transgenerational inheritance mechanisms that lead to prostate disease

This 2019 Washington rodent study found:

“Ancestral exposure to the toxicant vinclozolin induces an epigenetic transgenerational increase in susceptibility to prostate pathology in F3 [male great-grandchildren] generation rats. These results are in agreement with previous studies which found a transgenerational increase in rates of prostatic epithelial atrophy, cystic hyperplasia, and prostatitis in the transgenerational F3 and F4 [male great-great-grandchildren] generations after exposure of F0 [great-great-grandmother] generation pregnant rats to vinclozolin. These effects were accompanied by transgenerational changes in mRNA expression in F3 generation ventral prostate epithelial cells.

A number of previous transgenerational studies have shown no ventral prostate histopathology or disease detected. Therefore, observations suggest ancestral exposure specificity in the ability to induce the transgenerational inheritance of prostate disease.

There was also no increase in prostate histopathology in the directly exposed F1 [male children] or F2 [male grandchildren] generation vinclozolin lineage rats compared to controls.

prostate pathology

The mechanism by which epigenetic transgenerational inheritance affects prostate epithelium involves control of gene expression by DNA methylation and lncRNAs. It will be necessary to determine the exact gene targets of these epigenetic modifications to determine further mechanisms.

Future studies need to investigate if similar mechanisms are at work in human males who have adult-onset BPH or prostate cancer. Ancestral exposures to toxicants and epigenetic transgenerational inheritance may contribute to the development of prostate disease in men today.”


The study’s above bolded sentence added to the evidence that epigenetic effects may skip generations. A study by the same group, Epigenetic transgenerational inheritance of ovarian disease, found in females:

There was no increase in ovarian disease in direct fetal exposed F1 or germline exposed F2 generation vinclozolin or DDT lineage rats compared to controls.

A disturbance in the paradigm of child abuse referenced other studies that found generation-skipping effects.

Serious researchers are closer to discovering evidence for precise mechanisms of epigenetic transgenerational inheritance. It’s well past time that other researchers performing studies like Burying human transgenerational epigenetic evidence take their work seriously enough to truly investigate human evidence for epigenetic transgenerational inheritance.

What are more important funding priorities than such human studies?

https://www.nature.com/articles/s41598-019-38741-1 “Environmental Toxicant Induced Epigenetic Transgenerational Inheritance of Prostate Pathology and Stromal-Epithelial Cell Epigenome and Transcriptome Alterations: Ancestral Origins of Prostate Disease”