Conserved epigenetic sensitivity to early life experience in the hippocampus

This 2012 human study was done by McGill University, whose researchers in Canada are at the forefront of epigenetic studies. The subject was epigenetic DNA methylation in the hippocampus of people who experienced abuse as children and who also committed suicide.

Comparisons were made with rats that were stressed in early life to identify genomic regions that are epigenetically changeable in response to a range of early life experiences.

http://www.pnas.org/content/109/Supplement_2/17266.full “Conserved epigenetic sensitivity to early life experience in the rat and human hippocampus”

How painful long-lasting memories are stored and why they are so strong

This 2014 rodent study provided evidence for a portion of the neurophysiology that underlies how painful long-lasting memories are stored and why they are so strong. The amygdala was the brain area studied.

The researchers were misguided in news coverage by focusing on solutions such as external mechanisms to forget these memories. The researchers should think in terms of how their research can help people who can help themselves instead of having something externally done to them.

After all, we’re humans who can participate in therapy, not lab rats who need to be fixed.

http://www.pnas.org/content/111/51/E5584.full “Hebbian and neuromodulatory mechanisms interact to trigger associative memory formation”

Early emotional experiences change our brains: Childhood maltreatment is associated with reduced volume in the hippocampus

This 2011 human study by the grandfather of hippocampus stress studies, Martin Teicher, quantified childhood maltreatment using the Adverse Childhood Experiences study and Childhood Trauma Questionnaire scores:

“The strongest associations between maltreatment and volume were observed in the left CA2-CA3 and CA4-DG [dentate gyrus] subfields, and were not mediated by histories of major depression or posttraumatic stress disorder.

These findings support the hypothesis that exposure to early stress in humans, as in other animals, affects hippocampal subfield development.”

The evidence is clear that early emotional experiences change our brains. There are seldom valid reasons for researchers to exclude emotional content when designing human brain studies, especially studies that involve the hippocampus.

http://www.pnas.org/content/109/9/E563.full “Childhood maltreatment is associated with reduced volume in the hippocampal subfields CA3, dentate gyrus, and subiculum”

Emotional memories and out-of-body–induced hippocampal amnesia

I was happy to see that the researchers in this 2014 Swedish human study included emotional memories when studying the hippocampus. They demonstrated that including emotional memories wasn’t that difficult to do.

In fact, this study’s researchers deemed emotional memories to be necessary in order to properly study the hippocampus, as evidenced by this statement about the experiment’s scripts:

“The selected life events had a moderate emotional level to ensure episodic long-term memory encoding.”

It made me wonder whether there are scientific bases for why other researchers go to such lengths to avoid including emotions in human memory studies.

Also:

“The experiments revealed two important findings. First, the behavioral results showed that episodic encoding of life events requires perceiving the world from the first-person perspective centered on one’s real body, and violations of this basic condition produced impaired episodic recall, indicative of fragmented encoding.

Second, the brain imaging data demonstrated that encoding events experienced out-of body specifically impacts the activation of the left posterior hippocampus during retrieval, suggesting an impaired hippocampal binding mechanism during encoding.

These findings are fundamentally important, as they suggest a link between the ongoing perceptual experiences of the body and the world from the first-person perspective and the hippocampal episodic memory system.”

To conclude:

“Given the apparent requirement of a natural first-person perspective between the body and the world for intact hippocampal memory function, a dissociative out-of-body experience during an acutely stressful event could, by itself, impair the encoding mechanism and produce fragmented, spatiotemporally disorganized memories.”

http://www.pnas.org/content/111/12/4421.full “Out-of-body–induced hippocampal amnesia”

Similarity in form and function of the hippocampus in rodents, monkeys, and humans

This 2013 study had something for the anti-evolutionists to chew on.

Is it anti-evolutionary for human brain and behavior researchers to not be informed by animal studies such as those that show prenatal hippocampal damage done to the fetus by the mother’s environment?

http://www.pnas.org/content/110/Supplement_2/10365.full “Similarity in form and function of the hippocampus in rodents, monkeys, and humans”

Are 50 Shades of Grey behaviors learned in infancy?

Ever wonder how someone could become attached to their early childhood abuser?

Ever wonder what underlying neurobiological conditions may account for the popularity of Fifty Shades of Grey?

This 2014 rodent study “Enduring good memories of infant trauma” linked below showed how trauma changed infants’ limbic system and lower brains. As adults, they derived a neurochemical benefit from re-experiencing the traumatic conditions:

“Trauma and pain experienced in infancy clearly led to higher rates of adult rat depression-like behavior..(but) the infant brain has limited ability to link trauma to fear areas in the brain, such as the amygdala.

These results are surprising because cues associated with trauma experienced as adults provoke fear and do not rescue depressive behavior.

It is possible that giving SSRI medications to children could be detrimental to mental health in adulthood,” Dr. Sullivan says. “We believe that our research offers the first evidence for the impact of serotonin pathways.

The infant trauma increases serotonin to produce brain programming of later life depression, and the infant trauma cue increases serotonin to alleviate the adult depressive like symptoms.”


As the study may apply to humans, let’s say that as an infant, someone was traumatized by a caregiver who, for example, bound them too tightly and left them alone for too long. What adult behaviors and other symptoms may develop as results? The person may:

  • Show depression-like symptoms that would strangely be alleviated by being bound tightly and left alone for an extended period.
  • Develop attachments to people who treated them poorly in a way that triggered them to re-experience their early childhood traumas.
  • Feel their mood lift when their infancy traumas were cued.
  • Be unable to explain and integrate with their cerebrum what was going on with their limbic system and lower brains.
  • Be caught in a circle of acting out their feelings and impulses, with unfulfilling results.

Isn’t it curious that this acting-out behavior – driven by unconscious memories of traumatic conditions – is a subject for popular entertainment? It may have resonated with personal experiences of the people who read the books and watched the movie.


What about people who want to be relieved of their symptomatic behavior? Is it a justifiable practice:

  • To pass affected people over to talk therapies that aren’t interested in directly treating the cause – a neurobiological condition that exists in the limbic system and lower brains – only the symptoms?
  • To drug affected people with the neurochemicals that their condition makes scarce – the symptoms – instead of addressing the source?

A principle of Dr. Arthur Janov’s Primal Therapy is that people are capable of treating their own originating neurobiological conditions. One of the therapeutic results is that the patient is relieved of being caught in endless circles of acting-out behavior.

That way we can have our own lives, and not be driven by what happened during early stages of our lives.

http://www.pnas.org/content/112/3/881.full “Enduring good memories of infant trauma: Rescue of adult neurobehavioral deficits via amygdala serotonin and corticosterone interaction”

Making lasting memories: Remembering the significant

This 2013 article summarized 158 studies related to the roles of regions in the limbic system and memory:

“Episodic memory is the capacity to recall specific experiences and to re-experience individual events.

The findings of both animal and human studies provide compelling evidence that stress-induced activation of the amygdala and its interactions with other brain regions involved in processing memory play a critical role in ensuring that emotionally significant experiences are well-remembered.”

http://www.pnas.org/content/110/Supplement_2/10402.full “Making lasting memories: Remembering the significant”

Problematic research with telomere length

This 2014 study purportedly linked the effect of shorter telomere length in children to twin causes of a disadvantaged social environment and genetics. Two questionable areas were even more egregious than the study’s lack of a control group.

The first questionable area was that the researchers purposely measured telomere length using methods that couldn’t be directly compared with the telomere length measurements found in almost all other telomere studies. There was no attempt to make findings equivalent, no map with cited studies! They offered up rationale after rationale, but the direct incomparability with other studies remained.

The largest questionable area was the way the researchers produced the study’s concluding sentence:

“We suggest that an individual’s genetic architecture moderates the magnitude and direction of the physiological response to exogenous stressors.”

The researchers’ process deliberately skewed the sample of forty 9-year old boys. Next, they split this forty-member sample in half according to maternal depression! Maternal depression is an experimentally proven contributor to epigenetic changes that are detrimental to developing fetuses, infants, and young children.

The researchers asserted that the results of compounding their questionable choices represented something about stress and genetics in a larger population of children.

Of course, “an individual’s genetic architecture moderates the magnitude and direction of the physiological response to exogenous stressors.” These researchers didn’t do the work to determine whether it was the genetic architecture that the 9-year-olds were either epigenetically changed into or conceived.

I presume that this additional work on genetic architecture wasn’t pursued by the researchers because it may not produce the race-baiting headlines of the press coverage this study achieved. If the additional work pointed to epigenetic causes of adverse effects, the headline may have been non-politically correct like “Maternal depression and poor caregiving damages fetuses, infants, and young children.”

Was this study published to further an agenda? If so, did this study also represent a failure of the peer review process?

Was it predetermined that this study would be published in PNAS regardless of its methods? Were the researchers and reviewers even interested in advancing science?

http://www.pnas.org/content/111/16/5944.full “Social disadvantage, genetic sensitivity, and children’s telomere length”

Shorter telomere length in older men but not older women

This 2014 UK human study was the first on telomere length I’ve curated, so here’s some background information:

“Telomeres are..structures..that cap the ends of..chromosomes, protecting them from end-to-end fusion and degradation during cell division.

Human telomeric DNA naturally shortens with age during..cell divisions and as a result of oxidative attack.

At critical shortness, telomeres exhibit impaired function, leading to genomic instability, apoptosis, and cell senescence, often with altered transcriptional programming and mitochondrial dysfunction.

In humans, mutations that directly compromise telomere maintenance cause premature mortality and onset of a spectrum of diseases overlapping with the age-related diseases common in the population.

Shorter telomere length in white blood cells is linked and, in some cases, anticipates aging-related morbidity and mortality from conditions with immune system involvement, such as infectious diseases, cancer, and cardiovascular diseases, as well as risk factors, including hypertension, diabetes, obesity, and smoking.

A critical determinant of telomere length is the enzyme telomerase, which has the capacity to add..onto the..ends of telomeric DNA, extending telomere length and promoting genomic stability.

Acute mental stress appears to increase telomerase enzymatic activity at least transiently, and it has been suggested that high telomerase activity in conjunction with shorter telomere length may be indicative of a stressed system.”

The study put UK civil service men and women ages 54 through 76 through a series of stress tests. They found that men with longer telomeres had quicker recovery times than did men with shorter telomeres.

Men with shorter telomeres and low telomerase activity also had quicker recovery times than did men with shorter telomeres and high telomerase activity:

“In addition, we found that the (shorter telomeres and high telomerase activity men) had blunted reactivity to acute stress in diastolic blood pressure, heart rate, and cortisol.”

No telomere-based differences occurred with women:

“The explanation for the sex difference in response profiles in our study is not clear. Hormonal processes are unlikely to be directly responsible, because women in this study were postmenopausal.”

http://www.pnas.org/content/111/12/4519.full “Shorter telomeres with high telomerase activity are associated with raised allostatic load and impoverished psychosocial resources”