If research doesn’t provide causal evidence for effects, can epigenetics be forced in to explain everything?

This 2015 UK bird study found that older mothers had female children who had fewer offspring than did the rest of the house sparrow population. The finding applied also to older fathers and their male children.

In general, if a study didn’t directly demonstrate cause and effect, it isn’t appropriate to force the use of epigenetics to explain everything. That’s what this study did with epigenetic inheritance.

Did the study:

“Demonstrate that this parental age effect..potentially is epigenetically inherited.”

by analyzing DNA across generations?

No!

The researchers ran some numbers that tested the effect of older foster parents where the model’s only other possible explanation was epigenetic inheritance.

Several other things about this study were off:

  • The researchers used the term “fitness” 28 times as shorthand to mean the number of offspring, but only twice was it explained as “reproductive fitness.” This was potentially misleading in some of the contexts of the term’s other uses. For example, several of the cited references used “fitness” in a different context.
  • The researchers went into a long exposition of telomeres, punctuated by citing 11 references, only to say:

    “However it is unclear how telomere dynamics could affect fitness.”

    The next sentence was:

    “An alternative explanation might be the accumulation of deleterious mutations as individuals age.”

    which was additionally irritating because “alternative” assumed that telomeres presented a factual explanation of the study’s findings in the first place. Was this section an artifact of a struggle with the reviewer?

After forcing epigenetic inheritance as an explanatory factor and potentially misleading readers about reproductive fitness and telomeres, the researchers had little basis to conclude that their research had “important implications.”

http://www.pnas.org/content/112/13/4021.full “Reduced fitness in progeny from old parents in a natural population”

An agenda-driven study on beliefs, smoking and addiction that found nothing of substance

The researchers of this 2014 Virginia Tech study said that they found something profound about beliefs and the brain and addiction and smoking.


I’ll assert the short versions of some relevant understandings before assessing the study.

1) A principle of Dr. Arthur Janov’s Primal Therapy is: we all have needs that start at the beginning of our lives. Our needs change as we grow.

If our basic needs aren’t satisfied anywhere along the way, we feel pain.

When the unmet needs are early in our lives and the painful conditions persist, enduring physiological changes may occur.

This basic truth is supported by the findings of much of the recent research I’ve curated on this blog, the references in those studies, and older research elsewhere.

2) Another fundamental of Primal Therapy is that the physiological impacts of these unmet needs drive our behavior, thoughts, and feelings.

The painful impacts of our unfulfilled needs impel us to be constantly vigilant for some way to fulfill them.

This is a richly insightful and truly empathetic method of interpreting people’s behaviors and expressions of thoughts and feelings.

3) A hypothesis of Primal Therapy is: a major function that our cerebrums have evolutionarily adapted is to use ideas and beliefs to repress pain and make us more comfortable.

I value this inference as an empathetic method of interpreting people’s expressions of thoughts and feelings. Click the Beliefs category to view samples of how beliefs, expectations, and predictions are studied using cerebral measurements.


So – what did this study contribute to science about beliefs and the underlying causes of addiction and smoking as found by measuring the subjects’ brains?

Nothing new, really. The study was all about the effects, the symptoms. There was nothing about:

  • Impelling physical conditions and causes,
  • What primarily drives people’s beliefs and addiction behaviors, and
  • What may permanently help someone with their need for the next cigarette.

I wonder what the study’s reviewer saw that factually advanced science.

Everybody already knew that beliefs can temporarily substitute for addicting substances, as well as temporarily change behaviors. It’s a foundation of AA and detox centers.

It’s also a foundation of AA and detox centers that these beliefs have to be constantly reinforced. That fact in and of itself demonstrates that underlying causes aren’t addressed in the AA and detox center approaches. The symptoms always bubble up, and require thought remedies and other interventions in order to stay suppressed.


The research provided details about an approach that wasn’t capable of anything more than temporarily suppressing symptoms. What does the following quote from the Significance statement sound like to you?

“Our findings suggest that subjective beliefs can override the physical presence of a powerful drug like nicotine by modulating learning signals processed in the brain’s reward system.”

Any human therapeutic approach won’t supply the addicting substance. That leaves just beliefs and their required constant reinforcement.

The unsupported overconfidence of the researchers that:

“The implications of these findings may be far ranging”

led to one of the most ridiculous statements I’ve seen in a while:

“Just as drugs micromanage the belief state,” Montague said, “maybe we can micromanage beliefs to better effect behavior change in addiction.”

This hubris just added to the stench of an agenda.

Since smoking isn’t politically correct, I’d guess that it wasn’t that difficult for this study to be funded and promoted. It apparently wasn’t an obstacle that the research DETRACTED from science and didn’t really help people.

http://www.pnas.org/content/112/8/2539.full “Belief about nicotine selectively modulates value and reward prediction error signals in smokers”

Is it science, or is it a silly and sad farce when researchers “make up” missing data?

This 2014 French study was a parody of science.

The researchers “made up” missing data on over 50% of the men and over 47% of the women! All to satisfy their model that drove an agenda of the effects of adverse childhood experiences.

As an example of how silly and sad this was:

  • Two of the seven subject ages of interest were 23 and 33 consecutively, and
  • One of the nine factors was education level.

If I was a subject, and wasn’t around to give data at age 33 and later, how would the researchers have extrapolated a measurement of my education level of “high school” at age 23?

I’m pretty sure their imputation method would have “made up” education level data points for me of “high school” for ages 33 and beyond. I doubt that the model would have produced my actual education levels of a Bachelors and two Masters degrees at age 33.

Everything I said about the Problematic research on stress that will never make a contribution toward advancing science study applied to this study, including the “allostatic load” buzzword and the same compliant reviewer.

Studies like this both detract from science and are a misallocation of scarce resources. Their design and data aren’t able to reach levels where they can provide etiologic evidence.

Such studies also have limiting effects on how we “do something” about real problems, because the researchers won’t be permitted to produce findings that aren’t politically correct.

http://www.pnas.org/content/112/7/E738.full “Adverse childhood experiences and physiological wear-and-tear in midlife: Findings from the 1958 British birth cohort”

If a study didn’t measure feelings, then its findings may not pertain to genuine empathy

This 2014 UK study tried to show that empathetic actions were very context-dependent. It mainly studied causing overt pain to another person.

The lead researcher stated:

“We were interested in quantifying how much people care about others, relative to themselves. A lack of concern for others’ suffering lies at the heart of many psychiatric disorders such as psychopathy, so developing precise laboratory measures of empathy and altruism will be important for probing the brain processes that underlie antisocial behavior.”

The researchers didn’t provide direct evidence of genuine empathy – the subjects’ emotions of sensing and sharing the emotions of another person.

The study was designed to cause sensations of pain and draw conclusions about empathetic feelings. The subjects’ limbic system and lower brains were never measured, however.

Why did the researchers decide to only infer these feelings and sensations from actions and reports? Why wasn’t this inferred evidence confirmed with direct measurements of the brain areas that primarily process feelings and sensations?


  1. At no time during the experiment did the subjects see or hear or touch the person whom they caused pain. Wouldn’t it be difficult for the subjects to feel authentic empathy for a disembodied presence?
  2. We’re informed by the Task performance and beliefs about task responses are solely cerebral exercises study that it’s inaccurate to characterize subjects’ task responses as feelings.
  3. We know from the Problematic research: If you don’t feel empathy for a patient, is the solution to fake it? study that people’s cerebrums are easily capable of generating a proxy for empathy.

This study’s findings concerning empathy involved inauthentic empathy – the non-feeling, cerebral exercise, faking-it kind.

http://www.pnas.org/content/111/48/17320.full “Harm to others outweighs harm to self in moral decision making”

Problematic research on stress that will never make a contribution toward advancing science

This 2014 UK human study found:

“Type 2 diabetes is characterized by disruption of stress-related processes across multiple biological systems and increased exposure to life stress.”

HOWEVER, the stress effects weren’t conclusively shown to be either a cause or consequence of type 2 diabetes. Correlation wasn’t causation.

Looking around for clues as to what went wrong, I found this data sample of cortisol in a small table that comprised the total amount of information in the supplementary material:

“Geometric means, adjusted for education, marital status, BMI, smoking status, use of statins, and time of day.”

It’s hubris for the researchers to state that they improved data measurements by averaging them after adjusting for all of the above six factors.

Maybe the problem was elsewhere, maybe in the study design. Wherever the problems were, they guaranteed that the researchers would NEVER find cause and effect.

But maybe that’s the point?

There appeared to be other agendas that ensured studies like these failed to make a contribution toward advancing science. The researchers inevitably used buzzwords such as “allostatic load” and cited the need for further studies (money). Everybody was okay with that, including the reviewer, and everybody kept their safe jobs.

Such studies also had limiting effects on how we “do something” about real problems because the researchers wouldn’t produce findings that weren’t politically correct.

http://www.pnas.org/content/111/44/15693.full “Disruption of multisystem responses to stress in type 2 diabetes: Investigating the dynamics of allostatic load”

Do researchers have to be cruel to our fellow primates to adequately research oxytocin?

This 2014 primate study found:

“Oxytocin increased infants’ affiliative communicative gestures and decreased salivary cortisol, and higher oxytocin levels were associated with greater social interest.”

One would have to take an anti-evolutionist stance and believe that primates do not feel what humans feel to consider this process to NOT be cruel:

“To test these macaques, we took advantage of ongoing experiments requiring infants to be separated from their mother on the day of birth. Infants were nursery-reared, housed individually, with a cloth surrogate mother. They could see and hear other infants, but could not touch them.”

We know that primate infants, like humans, need nourishment, transportation, warmth, protection, and socialization from their mothers. What level of findings about oxytocin can a research study make that would justify this deprivation?

It surely wasn’t the findings this study made. We knew without doing the study that getting oxytocin from a nebulizer would be nowhere near an acceptable substitute for a mother’s touch and care.

http://www.pnas.org/content/111/19/6922.full “Inhaled oxytocin increases positive social behaviors in newborn macaques”

Problematic research on oxytocin: If the study design excludes women, its findings cannot include women

This 2014 study’s findings that “the hormone oxytocin promotes group-serving dishonesty” can’t apply generally to humans because its subjects were ALL men.

Regarding oxytocin, the researchers certainly knew or should have known previous studies’ findings about sex differences, as did Is oxytocin why more women than men like horror movies? which cited:

“Oxytocin modulates brain activity differently in male and female subjects.”

Regarding differing reciprocal behaviors, the researchers also knew or should have been better informed about associated brain areas through studies such as Reciprocity behaviors differ as to whether we seek cerebral vs. limbic system rewards and its references.

And how could the study produce reliable, replicable evidence of:

Dishonesty to be plastic and rooted in evolved neurobiological circuitries”

when the researchers performed NO measurements of “neurobiological circuitries” that supported that finding?

What was the agenda in play here? What did the female Princeton reviewer see in this study that advanced science?

http://www.pnas.org/content/111/15/5503.full “Oxytocin promotes group-serving dishonesty”


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Who benefits when research with no practical application becomes a politically correct meme?

Do you take a risk, as this 2013 University of Texas/Yale study concluded, because you don’t foresee how you can avoid the risk?

By making this finding, the study essentially assigned the bases of a person’s risky decisions to their cerebrum.

I wasn’t persuaded. The conclusion was reached because the study’s design only engaged the subjects’ cerebrums with a video game task involving popping balloons. See Task performance and beliefs about task responses are solely cerebral exercises for a similar point.

If the researchers had instead designed a study that also engaged the subjects’ limbic system and lower brains, the findings may have been different.


Only one of the news articles covered this story with some accuracy, io9.com:

Helfinstein (the lead researcher) doesn’t see any direct, practical applications of the research. After all, people don’t spend their lives in fMRI scanners, so it’s not as if we can tell when people are going to make a risky decision in their day-to-day activities.”

Compare that with the majority of the news coverage that hijacked the study’s findings to try to develop a politically correct meme:

“Many health-relevant risky decisions share this same structure, such as when deciding how many alcoholic beverages to drink before driving home or how much one can experiment with drugs or cigarettes before developing an addiction.”

The study found that “risk taking may be due, in part, to a failure of the control systems necessary to initiate a safe choice.” The brain areas were “primarily located in regions more active when preparing to avoid a risk than when preparing to engage in one.” These areas included the “bilateral parietal and motor regions, anterior cingulate cortex, bilateral insula, and bilateral lateral orbitofrontal cortex.”

Notice that just one of the studied brain areas (the anterior cingulate cortex) is part of the limbic system or lower brains, although the bilateral insula connects to the limbic system. Yet the limbic system and lower parts of the brain are most often the brain areas that drive real-world risky behaviors such as smoking, drug use, sexual risk taking, and unsafe driving.

A video game task of popping balloons that engaged the cerebrum was NOT informative to the cause-and-effect of the emotions and instincts and impulses from limbic system and lower brains that predominantly drive risky behavior.

Who may benefit from the misinterpretations and misdirections of the study’s findings? We can take clues from the five applicable NIH grants (UL1-DE019580, RL1MH083268, RL1MH083269, RL1DA024853, PL1MH083271) and the researchers’ statement:

“We were able to predict choice category successfully in 71.8% of cases.”

Anybody ever read Philip K. Dick?

http://www.pnas.org/content/111/7/2470.full “Predicting risky choices from brain activity patterns”

Can psychologists exclude the limbic system and adequately study awareness and social cognition?

This 2014 Princeton human study was proof that cognitive researchers are stuck in the cerebrum. That and gadgets.

The researchers didn’t measure limbic system or lower brain areas, yet from their use of cartoon faces and magnetically zapping their subjects’ brains they proclaimed:

“The findings suggest a fundamental connection between private awareness and social cognition.”

For just one example of the gross omissions of the study’s design, look at the limbic system’s part in “social cognition” for The amygdala is where we integrate our perception of human facial emotion.

And it’s a very limited scope of “private awareness” that excludes conscious awareness of what’s in our own feeling, instinctual, and impulsive levels of consciousness.

http://www.pnas.org/content/111/13/5012.full “Attributing awareness to oneself and to others”


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Can a study exclude the limbic system and adequately find how we process value?

This 2014 human study was notable for defining away the limbic system and lower brain from consideration in processing positive and negative stimuli for value.

However, the researchers didn’t fully reveal their biases until the last paragraph of the supplementary material, where they were obligated to comment on a previous study that included the limbic system. Good for the reviewer if that was how the researchers became obligated to deal with the previous study.

It isn’t difficult to include the limbic system in studies of value. For example, the Teenagers value rewards more and are more sensitive to punishments than are adults study found:

  • Cerebral areas increased activity when the expected value of the reward increased.
  • Limbic system areas increased activity when the expected value of the reward decreased.

http://www.pnas.org/content/111/13/5000.full “Disentangling neural representations of value and salience in the human brain”

Problematic research that excluded the most influential human epigenetic environments

This 2014 ivy league human study found that what appeared to be genetic links may have been epigenetic responses to our environment.

Curiously, none of the news articles covering this study highlighted the lack of the most influential environments on epigenetic DNA changes:

  • The mother’s prenatal environment provided for the fetus, and
  • The family environment during infancy and early childhood.

This omission may have been because the study intentionally didn’t support such an interpretation. Here’s a partial explanation from the study’s supplementary material of the “family fixed-effects model” the researchers developed:

“The family fixed-effects model blocks both genetic factors and parental characteristics/behaviors that are common to family members (e.g., siblings), including unmeasured factors; therefore, from the perspective of confounding, the fixed-effect specification is preferred.”

When the preferred model blocked the most important environments in which epigenetic DNA changes occur, what environments remained?

“These results suggest genetic influences on complex traits like obesity can vary over time, presumably because of global environmental changes that modify allelic penetrance.”

Although a finding attributing “global environmental changes” made more funding available to the researchers, it was rightly an outlier from the majority of epigenetic studies.

This finding made me start a negative rating for studies that DETRACT from science!

Why was the reviewer okay with the study’s model omitting the most important factors in human development? The study’s model defined away both the:

  • Out-of-favor genetic factors, and the
  • Predominant but nonpolitically-correct epigenetic factors

in order to manufacture a politically-correct epigenetics meme!

How else to interpret this statement, if not intended to generate a meme?

“Our results underscore the importance of interpreting any genetic studies with a grain of salt and leave open the possibility that new genetic risk factors may be seen in the future due to different genetically driven responses to our ever-changing environment.”

http://www.pnas.org/content/112/2/354.full “Cohort of birth modifies the association between FTO genotype and BMI”

Problematic research: If you don’t feel empathy for a patient, is the solution to fake it?

If you don’t experience empathy for another person, this 2014 Harvard study showed how to use your cerebrum to manipulate your limbic system into displaying a proxy of empathy.

Is this what we want from our human interactions? To have a way to produce an emotion the same way that an actor would as they read their lines?

The focus here was on how to finesse the effect of “no empathy.” Because the researchers didn’t define a lack of genuine empathy as a symptom of a fundamental problem, they absolved themselves from investigating any underlying causes.

Nice trick in the academic world.


In the real world, in which we are feeling human beings, what may be a cause of no empathy?

Let’s say that someone is in a position that helps people. They have daily encounters where they may be expected to be empathetic, but they seldom have these feelings for others.

One hypothesis of Dr. Arthur Janov’s Primal Therapy is the condition’s origin may be that in the past, the person needed help as a matter of survival, and they weren’t helped. Their unconscious memories of being helpless impel them to act out being helpful in their current life.

The person’s frequent reaction to any hint in the present of the agony of not receiving help back when they desperately needed it is to act out what they needed to have done back then. Helping others also gives them momentary distraction from such painful memories. But the relief is transitory, so they repeat the process.

Let’s say that the person’s unconscious needs pressed on them, and they made a career choice of actively helping people. They’re usually too caught up in their own thoughts and feelings and behavior, however, to sense the feelings of the people they’re helping in the present.

The person knows that something isn’t right, but they don’t know what the problem is. They see indicators such as: their actions that should feel fulfilling aren’t, they seldom feel empathy, and so on.


Primal Therapy allows patients to therapeutically address the origins of such conditions. A symptom such as lack of empathy for others will resolve as historical pains are ameliorated.

Or we can do as this study suggested: produce an inauthentic display – and thereby ignore the lack of empathy as a symptom – and never address the causes of no empathy.

http://www.pnas.org/content/111/12/4415.full “Episodic simulation and episodic memory can increase intentions to help others”

Problematic research on hardwired differences in human male and female brains

At the risk of wading into a quagmire, it’s hard to take this 2013 Pennsylvania study’s findings seriously, that there were new and significant hardwired differences in human male and female brains in addition to what we already knew. The authors didn’t explain all the factors involved in why they found what they did.

For example, can we raise kids in our culture along typical gender roles and biases, then at ages 12-14, say that the differences in their brains are solely due to their genders? To do so would be to ignore what’s known about epigenetic and environmental influences in shaping the brain.

Here’s an ancient (2011), 90-minute, poor-quality-of-science panel discussion of the subject that included the author of Is the purpose of research to define opportunities for interventions?


Kevin Mitchell had the last word in his 2017 post Debunking the male-female brain mosaic where he both exposed this and other conceptual fallacies, and explained how framing and data cherry-picking can mislead accurate analysis. Feel free to apply what he said to the above video and to the below study.


http://www.pnas.org/content/111/2/823.full “Sex differences in the structural connectome of the human brain”

Problematic research: Feigning naivety of the impact of prenatal, infancy and early childhood experiences

What I found curious in this 2012 UK review of 82 studies was the reviewer’s reluctance to highly regard a human’s life before birth, during infancy, and in early childhood.

There was no lack in 2012 of animal studies to draw from to inferentially hypothesize how a human fetal environment causes the fetus to adapt with enduring epigenetic changes.

To take just one study that I won’t curate on this blog because it’s too old:

Weinstock M (2008) The long-term behavioural consequences of prenatal stress. Neurosci Biobehav Rev 32:1073–1086, “Stress, [to the pregnant mother] in rodents as well as nonhuman primates, produces behavioral abnormalities [in the pup], such as

  • an elevated and prolonged stress response,
  • impaired learning and memory,
  • deficits in attention,
  • altered exploratory behavior,
  • altered social and play behavior, and
  • an increased preference for alcohol.”

Yet the reviewer posed the question:

“There is a need to determine just what epigenetic changes do and do not account for. Put succinctly, do they explain individual differences in response to adversity and do they account for variations in health and behavior outcomes?”

I suspect that the cause of this feigned naivety was the political incorrectness of adequately placing importance in the human fetus’ experience of the development environment provided by their mother.

The PC view would have us pretend that there aren’t lasting adverse effects from human prenatal, infancy, and early childhood experiences.

The follow-on pretense to this PC view would be that later-life consequences aren’t effects, but are instead, mysteries due to “individual differences.”

http://www.pnas.org/content/109/Supplement_2/17149.full “Achievements and challenges in the biology of environmental effects”


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Is this science, or a PC agenda? Problematic research on childhood maltreatment and its effects

This 2013 Wisconsin human study’s goal was to assess effects of childhood trauma using both functional MRI scans and self-reported answers to a questionnaire. The families of the study’s subjects (64 18-year-olds) participated with researchers before some of the teenagers were born.

How could the teenagers give answers that described events that may have taken place early in their lives, before their cerebrums were developed, around age 4? Even if the subjects were old enough to remember, would they give accurate answers to statements such as:

“My parents were too drunk or high to take care of the family.

Somebody in my family hit me so hard that it left me with bruises or marks.”

knowing that affirmative answers would prompt a visit to their family from a government employee?

Although some data may have been available, data from the teenagers’ prenatal, birth term, infancy, and early childhood wasn’t part of the study design. Intentional dismissal of early influencing factors ignored applicable research!

No

Was the study’s limited window due to the political incorrectness of placing importance in the development environment provided by the subjects’ mothers? The evidence was there for those willing to see.


One clue of ignored early traumatic events was provided by the lead researcher’s quote in news coverage:

“These kids seem to be afraid everywhere,” he says. “It’s like they’ve lost the ability to put a contextual limit on when they’re going to be afraid and when they’re not.”

This finding of “fear without context” possibly described the later-life effects of traumas that were encountered in utero and during infancy. A pregnant woman’s terror and fear can register on the fetus’ lower brain and the amygdala from the third trimester onward.

Storing a memory’s context is one of the functions that the hippocampus performs. Because the hippocampus develops later than the amygdala, though, it would be unable to provide a context for any earlier feelings and sensations such as fear and terror.

The researchers attempted to place the finding of unfocused fear into later stages of child development without doing the necessary research. They tried to force this finding into the subjects’ later development years by citing rat fear-extinction and other marginally related studies.

But citing these studies didn’t make them applicable to the current study. Cause and effect wasn’t demonstrated by noting various “is associated with” findings.


Was this science? Was it part of furthering an agenda like protecting publicly funded jobs?

Was this study published to make a contribution to science? Were the peer reviewers even interested in advancing science?

And what about the 64 18-year-old subjects? If the lead researcher’s statement was accurate, did these teenagers receive help that addressed what they really needed?

http://www.pnas.org/content/110/47/19119.full “Childhood maltreatment is associated with altered fear circuitry and increased internalizing symptoms by late adolescence”


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