The thalamus part of the limbic system has a critical period for connections

This highly-jargoned 2015 UK study found that connections made by the thalamus of the developing human fetus had a critical period of the last trimester of womb-life. Babies born before the 33rd week of gestation experienced thalamic disconnections compared with normal-term babies and adults. The disconnections increased with a shorter womb-life.

The thalamus of premature babies also developed stronger connections with areas of the face, lips, tongue, jaw, and throat. They presumably needed these connections for survival actions such as breathing and feeding that aren’t a part of the last trimester of womb-life.

The study confirmed that the structures of thalamic connections of normal-term babies were very similar to those of adults. The study added to the research that shows that human limbic systems and lower brains closely approximate their lifelong functionalities at the normal time of birth.


It was difficult to measure the thalamus at this stage of life with current technology, and the researchers had to discard over two-thirds of their results. The researchers recommended monitoring these premature babies for difficulties in later childhood that may be caused by their early-life experiences.

Why would this monitoring recommendation apply to just the study’s subjects? We know from other studies that a main purpose of thalamic connections is to actively control and gate information to and from the cerebrum.

Would it make sense for a medical professional to disregard any patient’s birth history if they had problems in their brain’s gating functions or connectivity?


One researcher said:

“The ability of modern science to image the connections in the brain would have been inconceivable just a few years ago, but we are now able to observe brain development in babies as they grow, and this is likely to produce remarkable benefits for medicine.”

This study’s results provided evidence for a principle of Dr. Arthur Janov’s Primal Therapy: the bases for disconnection from aspects of oneself are often set down during gestation. The “remarkable benefits for medicine” are more likely to be along the lines of what I describe in my Scientific evidence page.

http://www.pnas.org/content/112/20/6485.full “Specialization and integration of functional thalamocortical connectivity in the human infant”

Would you deprive your infant in order to be in a researcher’s control group?

This 2015 Harvard study found that exposing extremely premature babies to sounds of their mothers enlarged their auditory cortex.

The lead researcher stated:

“Our findings do not prove that the brains of these babies are necessarily better, and we cannot conclude that they will end up with no developmental disabilities.

We don’t know the advantages of having a bigger auditory cortex.”

It’s too bad that studies like this one have to take deprived infants and further deprive them for use as a control group. I suppose it’s possible that the control group members’ development could just be shifted, similar to the Maternal depression and antidepressants epigenetically change infant language development study.

However, given the findings of the Our early experiences are maintained and unconsciously influence us for years, if not indefinitely study, it’s also possible that the last trimester of womb life is a critical period for a child’s auditory cortex. If timely development doesn’t take place within the environment provided by the mother, there may not be another period to fully catch up on growth and learning, even given the effects of neural plasticity.

http://www.pnas.org/content/112/10/3152.full “Mother’s voice and heartbeat sounds elicit auditory plasticity in the human brain before full gestation”

How do we assess “importance” in our lives? An example from scientists’ research choices

This 2015 Virginia study found that scientists preferred research projects that had the potential to make:

“Deeper vs. broader contributions.

The scientists surveyed considered a hypothetical broader study, compared with an otherwise-comparable deeper study, to be riskier, a less-significant opportunity, and of lower potential importance.”

What were underlying motivations for subject scientists to become the Big Frogs in tiny puddles?

For example, if scientists recognized that there was an opportunity to positively influence a great number of human lives with a “broader” study, such as the hunger research proposed in Do the impacts of early experiences of hunger affect our behavior, thoughts, and feelings today? why would they prefer a “deeper” study such as starving fruit flies?


These researchers said that “scientists’ personal dispositions” accounted for this finding. I agree, but not for any of the specific reasons they stated.

Subjects’ “lower potential importance” judgments were key, and bear closer examination. The study’s supplementary material showed this consideration was made on a sliding scale in response to a question:

“Would you describe Project A (B) as potentially very important?”

The “lower potential importance” finding was an accumulation of each scientist’s personal judgment of a project described as:

“A broad project that spans several topical domains, including at least one that coincides with your area(s) of expertise and interest.

compared with:

“A focused and specialized project that fits your particular interests and leverages your deep expertise in a specific area.”

Weren’t personal judgments of the hypothetical project’s “potentially very important” aspect how each scientist predicted the project would make them feel important?

Given vague project descriptions in above quotations, I assert that their judgments’ contexts were “important to me” rather than “important to science” or “important to society” or important to some other context.


A relevant hypothesis of Dr. Arthur Janov’s Primal Therapy that applies to the “lower potential importance” finding is: the need to feel important is a defense against feeling unimportant due to early experiences of neglect.

Using principles referenced in the hunger post, the need to feel important is:

  1. A derivative need;
  2. A substitute for an unfulfilled need; and
  3. Caused by the impact of an early unmet need.

A corollary is that if an infant didn’t have early experiences of neglect, and their early needs were met, they likely wouldn’t develop derivative needs such as the need to feel important as they progressed through childhood, adolescence, and adulthood.

Are people motivated to act like the scientists who were subjects of this study? Do we make career and personal choices based on whether or not our work and other people make us feel important?

See my Welcome page and Scientific evidence page for further elaborations of this topic.

http://www.pnas.org/content/112/12/3653.full “Different personal propensities among scientists relate to deeper vs. broader knowledge contributions”

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

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

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

The research caught my eye with these statements:

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

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

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


I stated two fundamentals of Primal Therapy in An agenda-driven study on beliefs, smoking and addiction that found nothing of substance:

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

Corollary principles of Primal Therapy are:

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

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

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

In his book “Primal Healing” Dr. Arthur Janov gives two examples of critical periods only during which early needs can be satisfied:

  1. Being touched in the first months of life is crucial to a child’s development. The lack of close contact after the age of 5 wouldn’t have the same effect.
  2. Conversely, the need for praise at 6 months of age may not be essential, but it’s crucial for children at age 5.

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

Why not start with hunger research? Objectives of the research should include answering:

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

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

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

Is infancy far back enough, though, to understand the beginnings of potential impacts of hunger? The Non-PC alert: Treating the mother’s obesity symptoms positively affects the post-surgery offspring study referenced an older study of how the hunger of mothers-to-be had lifelong ill effects for the fetuses they carried during the Dutch hunger winter of 1944. The exposed children had epigenetic DNA changes from their mothers’ starvation, which resulted in relative obesity compared with their unexposed siblings.

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”

More from the researchers that found people had the same personalities at age 26 that they had at age 3

This 2014 research came from the Dunedin Study in New Zealand that has studied a group of over 1,000 people for 40+ years now. They first came to worldwide fame by finding that the study’s participants at age 26 largely had the same personality that each did at age 3.

The current study linked the participants’ childhood cognitive abilities and self-control to their current cardiac age.

Would a US doctor have the knowledge and foresight to understand that significant factors in a middle-aged patient’s cardiac health came from their early childhood, infancy, or womb life experiences?

http://www.pnas.org/content/111/48/17087.full “Credit scores, cardiovascular disease risk, and human capital”

One way that an infant unconsciously knows the emotions of the humans in their environment

This 2014 human study found one way that an infant unconsciously recognized the emotions of the humans in their environment:

“The current study provides neural evidence for the unconscious detection of emotion and gaze cues from the sclera in 7-mo-old infants.

Wide-open eyes, exposing a lot of white, indicate fear or surprise. A thinner slit of exposed eye, such as when smiling, expresses happiness or joy.”

The basis for finding that the subjects’ responses were unconscious was that the researchers determined that displaying images of eyes for 50 milliseconds fell below the threshold of infants’ conscious awareness.

http://www.pnas.org/content/111/45/16208.full “Unconscious discrimination of social cues from eye whites in infants”

If research provides evidence for the causes of stress-related disorders, why only focus on treating the symptoms?

This 2014 rodent research reliably induced many disorders common to humans. Here are some post-birth problems the researchers caused, primarily by applying different types of stress, as detailed in the study’s supplementary material:

Yet the researchers’ goal was to identify a brain receptor for:

“Novel therapeutic targets for stress-related disorders.”

In other words, develop new drugs to treat the symptoms.


Where are the studies that have goals to prevent these common problems being caused in humans by humans?

Where is the research on treatments to reverse the enduring physiological impacts to stress by treating the causes?


What do you think of this excerpt?

“Accumulating evidence suggests that traumatic events particularly during early life (e.g., parental loss or neglect) coupled with genetic factors are important risk factors for the development of depression and anxiety disorders.

Moreover, the brain is particularly vulnerable to the effects of stress during this period.

Maternal separation in rodents is a useful model of early-life stress that results in enduring physiological and behavioral changes that persist into adulthood, including increased hypothalamic–pituitary–adrenal (HPA)–axis sensitivity, increased anxiety, and visceral hypersensitivity.”

http://www.pnas.org/content/111/42/15232.fullGABAB(1) receptor subunit isoforms differentially regulate stress resilience”

Are stress-induced epigenetic changes to DNA inherited across generations?

This 2014 Geneva/Cambridge plant study ended by stating:

“The unequivocal demonstration of transgenerational transmission of environmentally-induced epigenetic traits remains a significant challenge.

One of the critical activities erasing stress memories is conserved between plants and mammals.”

However, the researchers didn’t demonstrate that their findings were broadly applicable for mammals or organisms other than the specific plant variety they studied. Possible reasons for these limited findings were given in a 2015 Australian study referenced by Mechanisms of stress memories in plants:

“The majority of DNA methylation analyses performed in plants to date have focused on Arabidopsis, despite being relatively depleted of TEs [transposable elements] (15–20% of the genome) and being poorly methylated compared to other plant genomes.

These studies have lacked the resolution to provide the specific context and genomic location of the changes in DNA methylation.”

There are also significant differences in how epigenetic inheritance across generations may operate among different species per Epigenetic reprogramming in plant and animal development.


Neither the current study nor the above review addressed the behavioral aspect of stress-induced epigenetic inheritance across generations. For example, the behavior of a mother whose DNA was epigenetically changed by stress can induce the same epigenetic changes to her child’s DNA when her child is stressed per One way that mothers cause fear and emotional trauma in their infants:

“Our results provide clues to understanding transmission of specific fears across generations and its dependence upon maternal induction of pups’ stress response paired with the cue to induce amygdala-dependent learning plasticity.”

http://www.pnas.org/content/111/23/8547.full “Identification of genes preventing transgenerational transmission of stress-induced epigenetic states”

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”

Maternal depression and antidepressants epigenetically change infant language development

This 2012 human study found that infant language development accelerated when the depressed mother-to-be took antidepressants:

“Language acquisition reflects a complex interplay between biology and early experience.

Psychotropic medication exposure has been shown to alter neural plasticity and shift sensitive periods in perceptual development.”

Infant language development was delayed when the depressed mother-to-be didn’t take serotonin reuptake inhibitor medication:

“Prenatal depressed maternal mood and (S)SRI exposure were found to shift developmental milestones bidirectionally on infant speech perception tasks.”

Contrast this study with Problematic research with telomere length, which pretended that maternal depression had negligible epigenetic effects on the developing fetus, infant, and child.

http://www.pnas.org/content/109/Supplement_2/17221.full “Prenatal exposure to antidepressants and depressed maternal mood alter trajectory of infant speech perception”

Our early experiences are maintained and unconsciously influence us for years, if not indefinitely

This 2014 Montreal study provided more evidence of critical periods during human development:

“Clearly illustrates that early acquired information is maintained in the brain and that early experiences unconsciously influence neural processing for years, if not indefinitely.

We show that internationally adopted children (aged 9–17 years) from China, exposed exclusively to French since adoption (mean age of adoption, 12.8 mo), maintained neural representations of their birth language despite functionally losing that language and having no conscious recollection of it.

We show that neural representations are not overwritten and suggest a special status for language input obtained during the first year of development.”


YES! GIVE US MORE STUDIES LIKE THIS ONE!

http://www.pnas.org/content/111/48/17314.full “Mapping the unconscious maintenance of a lost first language”

Non-PC alert: Treating the mother’s obesity symptoms positively affects the post-surgery offspring

This 2013 Quebec human epigenetic study found that DNA methylation – chemical modification that causes genes to express differently – as durably detectable between siblings born before and after their mother’s gastric bypass surgery.

The younger, post-maternal-surgery siblings were found to have DNA indicating reduced risks of developing diabetes and heart disease when compared with the DNA of their older, pre-maternal-surgery siblings. The mothers’ average weight loss was 103 lbs.

It was notable to see this famous research reference cited:

“Prenatal exposure to famine during the Dutch hunger winter of 1944 is associated with obesity with less DNA methylation (“undermethylation”) of the imprinted insulin-like growth factor 2 (IGF2) gene in exposed offspring relative to their unexposed siblings.”

It was also notable to see the reactions to this non-politically-correct finding. For one example, this news article was in full-fledged denial, stating:

“Nor do investigators know whether a father’s weight loss might have a similar impact. It’s also possible that epigenetic inheritance wasn’t at play.”

Other news coverage expressed the memes that:

  • Pregnant women can abuse anything and everything with impunity without any consequent damage to their fetus, and
  • There wasn’t the tiniest chance that the mother was involved in any of their child’s adverse outcomes. When the child’s diverted developmental and behavioral consequences manifested, political correctness would dictate that these arose out of some unknown factors.

http://www.pnas.org/content/110/28/11439.full “Differential methylation in glucoregulatory genes of offspring born before vs. after maternal gastrointestinal bypass surgery”

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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A mother’s care affects the infant’s hippocampus structure and function through epigenetic regulation of genes

This 2012 McGill University rodent study found:

“Variations in maternal care in the rat affect hippocampal morphology and function as well as performance on hippocampal-dependent tests of learning and memory in the offspring.

Thus, in the rat, as in humans, social influences operate during early life to influence the structure and function of brain regions critical for cognitive capacity.

Variations in maternal care can influence hippocampal function and cognitive performance through the epigenetic regulation of genes.”

http://www.pnas.org/content/109/Supplement_2/17200.full “Variations in postnatal maternal care and the epigenetic regulation of metabotropic glutamate receptor 1 expression and hippocampal function in the rat”